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, Volume 28, Supplement 1, pp 98–111 | Cite as

Endocrine Physiology of Electrolyte Metabolism

  • Keith G. Dawson
Section 2: Mechanism and Physiological Significance of Electrolyte Disturbances

Summary

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions.

Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and pros-taglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by β1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II.

Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified nalriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide).

Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure.

Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion.

Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected.

The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.

Keywords

Renin Aldosterone Renin Release Renin Secretion Calcio 

Résumé

Classiquement, l’ion sodium s’est vu attribué la première place, voire une place exclusive par rapport au autres ions, dans la pathologie cardiovasculaire. Récemment, d’autres ions tels que le chlore, le potassium, le magnésium et le calcium ont trouvé leur place dans les mécanismes de l’hypertension, les arythmies cardiaques et les désordres métaboliques. On s’est de même intéressé aux commandes endocriniennes de l’équilibre ionique qui impliquent des actions hormonales classiques mais aussi des phénomènes de neurotransmission et des effets cellulaires inhabituels d’hormones endocrines.

Des études montrent que le contrôle du système rénine-angiotensine-aldostérone dépend non seulement du taux de calcium dans le cytosol mais aussi de la présence de l’ion chlore et des prostaglandines dans la macula densa. La libération de rénine est stimulée par l’hyperpolarisation des cellules juxtaglomérulaires induite par les agonistes β1, la parathormone, le glucagon, le magnésium et une faible concentration du cytosol en calcium. La libération de rénine est inhibée par des concentrations élevées de calcium, potassium et angiotensine II.

Faisant suite à la libération de rénine, la régulation hormonale stimule l’activité de l’enzyme de conversion par le cortisol et les prostaglandines (PGE2). Joue aussi un rôle dans le contrôle hormonal l’hormone antidiurétique, qui provoque une dilution des électrolytes extracellulaires et augmente les résistances périphériques. Un facteur natriurétique récemment isolé de l’oreillette semble avoir une action diurétique du même type que celle du furosémide.

Le rôle des autres électrolytes a été soigneusement examiné. Le chlore peut être déterminant dans la réabsorption rénale de sodium en fonction des taux plasmatiques des prostaglandines. Le calcium est un régulateur indispensable de la sécrétion d’adrénaline, de rénine, d’aldostérone. De même, les variations de l’ion calcium servent à la contraction musculaire lisse. Sa concentration dans l’organisme est réglée par la parathormone et la vitamine D. De plus, une alimentation riche en calcium joue un rôle protecteur contre l’hypertension, tandis que les inhibiteurs calciques diminuent la pression artérielle.

Les systèmes endocriniens jouent un rôle capital dans la protection contre l’élévation brutale de la kaliémie par le biais de l’insuline et de la modulation adrénergique de la distribution extrarénale du potassium. Il est admis que l’aldostérone est la mécanisme de régulation retardée de l’excrétion de potassium.

Les concentrations de magnésium chutent en cas d’hyperaldostéronisme, d’hyperparathyroïdisme et d’acidocétose diabétique ainsi que de malnutrition. Si une hypokaliémie coexiste, elle peut rester réfractaire tant que l’hypomagnésémie n’est pas corrigée.

L’ensemble de ces actions hormonales et électrolytiques sont donc un élément important de régulation du système cardiovasculaire.

Zusammenfassung

Historisch stand das Natrium-Ion in bezug auf kardiovaskuläre Erkrankungen, vielleicht andere Ionen ausschlieβend, im Vordergrund. In letzter Zeit fanden andere Ionen, wie Chlorid, Kalium, Magnesium und Kalzium, steigende Beachtung hinsichtlich Hypertonie, Herzarrhythmien und metabolischer Störungen. Endokrine Faktoren, die diese Ionen kontrollieren, fanden ebenfalls zunehmende Beachtung; zu ihnen zählen klassische Hormonwirkungen ebenso wie die Neurotransmission und parakrine hormonelle Wirkungen.

Studien zeigen, daβ die Kontrolle des Renin-Angiotensin-Aldosteronsystems durch die Kalziumspiegel im Cytosol der juxtaglomerulären Zellen ebenso wie durch Chloridionen und Prostaglandine in der Macula densa erfolgt. Die Renin-Freisetzung wird durch eine durch β1-Agonisten, Nebenschilddrüsenhormon, Glukagon, Magnesium und erniedrigtes Cytosol-Kalzium induzierte Hyperpolarisation der juxtaglomerulären Zelle stimuliert. Die Freisetzung von Renin wird durch erhöhtes Kalzium, Kalium und Angiotensin II gehemmt.

Der Reninfreisetzung folgend, umfaβt die Hormonregulation die Stimulation der Converting-Enzym-Aktivität durch Kortison und Prostaglandin (PGEz). Zu anderen hormonellen Kontrollmechanismen zählt das anti-diuretische Hormon, das eine Verdünnung der extrazellulären Elektrolyte und eine Erhöhung des peripheren Widerstandes bewirkt. Ein kürzlich identifizierter, aus Vorhofkammern isolierter natriuretischer Faktor, scheint ein potentes Diuretikum mit Furosemid-ähnlichen Wirkungen zu sein.

Andere Elektrolyte wurden genauer untersucht. Chlorid kann eine dominierende, Prostaglandin-abhängige Rolle für die rénale Natrium-Reabsorption spielen. Kalzium wurde als grundlegender Regulator von Hormonen wie Noradrenalin, Renin und Aldosteron erkannt. Ebenso sind Änderungen der Kalziumionenkonzentration das Mittel, durch das Kontraktion glatter Muskeln beeinfluβt wird. Nebenschilddrüsenhormon und Vitamin D regulieren die Spiegel dieses Ions im Körper. Zusätzlich scheint eine hohe Kalziumaufnahme mit der Nahrung eine protektive Rolle gegen Bluthochdruck zu spielen, während Kalziumantagonisten den Blutdruck reduzieren.

Das endokrine System besitzt eine wichtige Schutzfunktion in bezug auf akute Erhöhungen des Serum-Kaliums; mit Hilfe von Insulin und der adrenergen Modulation kann Kalium extrarenal aus dem Serum entfernt werden. Aldosteron wurde als verzögerter Regulator der Kaliumausscheidung erkannt.

Magnesiumspiegel sinken bei Hyperaldosteronismus, bei Hyperparathyreose und Ketoazidose ebenso wie bei Mangelernährungszuständen. Ein begleitender Kaliummangel kann therapierefraktär sein, bis die Hypomagne-siämie korrigiert ist.

Die integrierte Wirkung dieser Hormone und Elektrolyte kann daher für die Regulation des kardiovaskulären Systems von gröβter Wichtigkeit sein.

Sommario

Storicamente è stata data una grande importanza allo ione sodio in relazione alle malattie cardiovascolari, forse accantonando gli effetti di altri ioni. Recentemente è stata posta un’attenzione sempre maggiore su altri ioni, fra cui il cloro, il potassio, il magnesio ed il calcio, in relazione all’ipertensione, alle aritmie cardiache e alle alterazioni metaboliche. Anche i fattori endocrini che controllano questi ioni sono stati fatti oggetto di una crescente attenzione, e fra essi ricordiamo i classici effetti degli ormoni, gli effetti dei neurotrasmettitori e gli effetti secondari degli ormoni stessi.

Alcuni studi suggeriscono che il controllo del sistema renina-angiotensina-aldosterone è influenzato dai livelli di calcio nel cito-plasma delle cellule iuxtaglomerulari e dai livelli di cloro e di prostaglandine nella macula densa. La liberazione di renina è stimolata dall’iperpolarizzazione delle cellule iuxtaglomerulari indotta dai β-1-agonisti, dall’ormone paratiroideo, dal glucagone, dal magnesio e da bassi livelli di calcio citoplasmatico. La liberazione di renina è inibita da elevati livelli di calcio, di potassio e di angiotensina II.

Successivamente alla liberazione di renina, la regolazione ormonale include la stimolazione dell’attività dell’enzima di conversione da parte del cortisolo e delle prostaglandine (PGE2). Fra gli altri controlli ormonali ricordiamo l’ormone antidiuretico, che détermina una diluizione degli elettroliti extracellulari ed un aumento delle resistenze periferiche. Un fattore natriuretico di recente identificazione, isolato dagli atri cardiaci, sembra agire come potente diuretico, con effetti simili a quelli della furosemide.

Altri elettroliti sono stati oggetto di più attento studio. Il cloro può svolgere un ruolo determinante nel riassorbimento renale di sodio, in relazione alla concentrazione delle prostaglandine. Il calcio è stato riconosciuto come regolatore di base della secrezione di ormoni quali la noradrenalina, la renina e l’aldosterone. Inoltre gli ioni calcio sono coinvolti nei meccanismi che permettono di effettuare la contrazione del muscolo liscio. l’ormone paratiroideo e la vitamina D regolano il livello corporeo di questo ione. Sembra inoltre che un elevato apporto di calcio con la dieta svolga un ruolo protettivo nei confronti dell’ipertensione, mentre i calcioantagonisti sembrano ridurre la pressione arteriosa.

Meccanismi endocrini svolgono un ruolo essenziale nel proteggere contro aumenti acuti della potassiemia, per mezzo dell’azione insulinica e della modulazione adrenergica sulla distribuzione extrarenale di potassio. ’E noto che I’aldosterone svolge il ruolo di regolatore tardivo nell’escrezione del potassio.

I livelli di magnesio si riducono nell’iperaldosteronismo, nell’iperparatiroidismo, nella chetoacidosi diabetica e negli stati di malnutrizione. Una consistente carenza di potassio può essere refrattaria alla terapia fino a che non venga corretta la ipomagnesiemia. Pertanto l’azione integrata di questi ormoni e di questi elettroliti ricopre un ruolo di essenziale importanza nella regolazione dell’apparato cardiovascolare.

Resumen

Históricamente, el ión de sodio a recibido la mayor atención relatión con la patología cardiovascular, con perjuicio, quizás, de otros iones. Mas recientemente, se está prestando cada vez más atención a los otros iones, como el cloruro, potasio, magnesio y calcio, en relatión con la hipertensión, las arritmias cardiacas y las alteraciones metabólicas. También los factores endocrinos que controlan estos iones han recibido una atención progresivamente mayor; entre ellos se incluyen las acciones hormonales clásicas, as( como la neurotransmisión y las acciones hormonales paracrinales.

Una serie de estudios ha venido a indicar que el control del sistema renina-angiotensina-aldosterona reside en las concentraciones citoplasmâticas de calcio en las células yuxtaglomerulares, así como del ión de cloruro y prostaglandinas en la macula densa. La liberatión de renina se estimula mediante la hiperpolarización de las células yuxtaglomerulares, inducida por los agonistas β1,, PTH, glucagón, magnesio y baja concentration de calcio en el citosol. La liberation de renina se inhibe por concentraciones elevadas de calcio, potasio y angiotensina II.

Tras la liberación de la renina, la regulation hormonal comprende la estirnulación del enzima convertidor mediante cortisol y prostaglandina E2 (PGE2). Otros controles hormonales comprenden la ADH, que da lugar a la dilución de los electrolitos extracelulares y a una mayor resistencia periférica. Un factor natriurético recientemente identificado, aislado de las auriculas cardiacas, parece ser un potente diurético, con acción similar a la de la furosemida.

También se han sometido otros electrôlitos a un estudio intenso. Así, es posible que el cloruro desempeñe un papel importante en la reabsorción renal de sodio, en función de los niveles de prostaglandinas. Por otra parte, el calcio se ha identificado como regulador bàsico de la secreción de hormonas tales como la noradrenalina, la renina y la aldosterona, y los cambios en la concentration de iones de calcio hacen posible la contraction del músculo liso. La PTH y la vitamina D regulan la concentración de este ión en el organismo. Además de lo dicho, parece ser que la ingestion elevada de calcio desempeña un papel protector contra la hipertensión, mientras que los bloqueadores de los canales de calcio parecen reducir la tensión arterial.

Los sistemas endocrinos desempeñan un importante papel protector contra los aumentos repentinos del potasio sérico mediante la action de la insulina y la modulación adrenérgica de la excretión extrarrenal de potasio. Por su parte, la aldosterona ha sido identificada como el regulador de la excretión retardada de potasio.

Los niveles de magnesio descienden en los casos de hiperaldosteronismo, hiperparatiroidismo y cetoacidosis diabética, asi como en los estados de desnutrición. Es posible que una eventual deficiencia de potasio concomitante sea refractaria al tratamiento, hasta que se corrija la hipomagnesemia.

Así pues, la action integrada de estas hormonas y electrólitos es de la mayor importancia en la regulation del sistema cardiovascular.

Resumo

Ao longo da história, deu-se uma proeminência ao íon do sódio em relação às doenças cardiovasculares, o que talvez tenha excluido a importância de outros íons. Recentemente, outros ions, entre os quais o cloro, o potdssio, o magnésio e o cálcio têm recebido cada vez mais atenção em relação à hipertensão, arritmias cardiacas e distúrbios metabólicos. Os fatores endocrinos que controlam estes ions também têm recebido crescente atenção; estes incluem as ações hormonais clássicas bem como a neuro-transmissão e as ações hormonais nas quais a secreção duma célula endrócrina influencia a de outra célula endrôcrina de outra classe.

Hd estudos que indicam que o contrôle do sistema de renina-angiotensina-aldosterone reside nas concentrações de cálcio nos líquidos intra-celulares das células justaglomerulares, bem como do íon de cloro e das prostaglandinas na mácula densa. A secreção de renina é estimulada pela hiperpolarização da célula justaglomerular induzida por ativadores de β1, pelo hormônio da paratireóide, pelo glucagon, pelo magnésio e por uma baixa concentração de cálcio no líquido intracelular. A secreçõ de renina é inibida por uma alla concentração de cálcio, de potássio e de angiotensina II.

Subsequentemente à secreção de renina, a regulação hormonal inclui o estímulo da atividade da enzima de conversão por meio do cortisol e da prostaglandina (PGE2). Uma outra forma de controle hormonal é a produção por parte do hormônio antidiurético de uma diluição dos eletrólitos extracelulares e uma resistência periférica aumentada. Um fator natriurético recentemente isolado do átrio cardíaco parece ser um diurético potente, com ações semelhantes à do frusemide (furosemide).

Outros eletrólitos foram mais minuciosamente examinados. O cloro pode desempenhar um papel dominante na reabsorção renal do sódio, dependendo das concentrações de prostaglandina. O cálcio foi reconhecido como sendo um regulador básico da secreção de hormônios como a noradrenalina, a renina e o aldosterone. Além disso, a contração do músculo liso é efetuada por meio de mudanças de íons de cálcio. O hormônio da paratireóide e a vitamina D regulam a concentração deste íon no organismo. Também ficou aparente que um alto consumo de cálcio na dieta alimentar tem efeito protetor contra a hipertensão, enquanto que os bloqueadores dos canais de calcio baixam a pressão sanguínea.

Os sistemas endócrinos desempenham um papel importante na proteção contra elevações agudas da concentração de potássio no sero por meio da ação da insulina e da modulação adrenérgica da eliminação de potássio extrarrenal. O aldosterone é reconhecido como sendo um regulador retardador da excreção de potássio.

As concentrações de magnésio baixam no quadro de hiperaldosteronismo, hiper-paratireoidismo e de queto-acidose diabética, bem como em estados de mal-nutrição. Uma deficiência de potássio co-existente pode ser refratária a toda terapia até que a hipomagnesemia tenha sido corrigida.

A ação integrada destes hormônios e eletrólitos é consequentemente de importância primordial na regulação do sistema cardiovascular.

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References

  1. Abboud, H.E.; Luke, R.G.; Galla, J.H. and Kotchen, T.A.: Stimulation of renin by acute selective chloride depletion in the rat. Circulation Research 44: 815–821 (1979).PubMedCrossRefGoogle Scholar
  2. Akera, T. and Brody, T.M.: Myocardial membranes: Regulation and function of the sodium pump. Annual Review of Physiology 44: 375–388 (1982).PubMedCrossRefGoogle Scholar
  3. Alexander, J.C: Summary of worldwide captopril experience in patients with severe treatment-resistant hypertension; in Laragh et al. (Eds) Frontiers in Hypertension Research, pp. 529–531 (Springer, New York 1981).CrossRefGoogle Scholar
  4. Awan, N.A. and Mason, D.T.: Vasodilator therapy of severe congestive heart failure: The special importance of angiotensin converting enzyme inhibition with captopril. American Heart Journal 104(5 Pt. 2): 1127–1136(1982).PubMedCrossRefGoogle Scholar
  5. Ayachi, S.: Increased dietary calcium lowers blood pressure in the spontaneously hypertensive rat. Metabolism 28: 1234–1238 (1979).PubMedCrossRefGoogle Scholar
  6. Bigg, R.P. and Chia, R.: Magnesium deficiency. Role in arrhythmias complicating acute myocardial infarction. Medical Journal of Australia 1: 346–348 (1981).Google Scholar
  7. Blaustein, M.P.: The inlerrelationship between sodium and calcium fluxes across all membranes. Reviews of Physiology, Biochemistry and Pharmacology 70: 32–82 (1974).Google Scholar
  8. Blaustein, M.P.: Sodium ions, calcium ions, blood pressure regulation and hypertension. A reassessment and a hypothesis. American Journal of Physiology 232: C165–C173 (1977).PubMedGoogle Scholar
  9. Bohr, D.F.: Vascular smooth muscle: Dual effect of calcium. Science 139: 597–599(1963).PubMedCrossRefGoogle Scholar
  10. Briggs, J.; Kriz, W. and Schnermann, J.: Intracardiac localization of atrial natriuretic substance. (Abstract) Circulation 68: III–43(1983).Google Scholar
  11. Brody, M.J. and Johnson, A.K.: Role of the anteroventral third ventricle region in fluid and electrolyte balance, blood pressure regulation and hypertension; Martini and Ganong (Eds) Frontiers in Neuroendocrinology, pp. 249–292 (Raven Press, New York 1980).Google Scholar
  12. Brown, M.J.; Brown, D.C. and Murphy, M.B.: Hypokalemia from beta:-receptor stimultion by circulating epinephrine. New England Journal of Medicine 309: 1414–1419 (1983).PubMedCrossRefGoogle Scholar
  13. Cantin, M.: Relationship of juxtaglomerular apparatus and adrenal cortex to biochemical and extracellular fluid volume changes in magnesium deficiency. Laboratory Investigation 22: 558–568 (1970).PubMedGoogle Scholar
  14. Cantin, M. and Huet, M.: Histochemistry and ultrastructure of the juxtaglomerular apparatus in magnesium-deficient rats. Canadian Journal of Physiology and Pharmacology 51: 834–844 (1973).CrossRefGoogle Scholar
  15. Capponi, A.M. and Vailotin, M.B.: Renin release by rat kidney slices incubated in vitro: Role of sodium and of K+ and β-adrenergic receptors, and effect of vincristine. Circulation Research 29: 200–203 (1976).CrossRefGoogle Scholar
  16. Conn, J.W.: Primary aldosteronism, a new clinical syndrome. Journal of Laboratory and Clinical Medicine 45: 3–17 (1955).PubMedGoogle Scholar
  17. Cowley, A.W.; Smith, M.J.; Manning Jr, R.D. and Lohmeier, T.E.: Pressor and volume effects of vasopressin; in Laragh, et al. (Eds) Frontiers in Hypertension Research, pp. 373–380 (Springer, New York 1981).CrossRefGoogle Scholar
  18. Davis, J.O.; Higgins, J.T. and Urquhart, J.: Relation of renin and angiotensin II to aldosterone secretion and sodium excretion; in Baulieu and Robel (Eds) Aldosterone, pp. 175–186 (Black-well Scientific Publications, Oxford 1964).Google Scholar
  19. deBold, A.J.; Borenstein, H.B.; Veress, A.T. and Sonnenberg, H.: A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats. Life Sciences 28: 89–94(1981).CrossRefGoogle Scholar
  20. deBold, A.J. and Flynn, T.G.: Cardionatrin I — a novel heart peptide with potent diuretic and natriuretic properties. Life Sciences 33: 297–302 (1983).CrossRefGoogle Scholar
  21. DiBona, G.F.: Neural mechanisms of volume regulation. Annals of Internal Medicine 98: 750–752 (1983).PubMedGoogle Scholar
  22. Dominguez, J.H.; Gray, R.W. and Lemann, J.: Dietary phosphate deprivation in women and men: Effects on mineral and acid balances, parathormone and the metabolism of 25-OH-vitamin D. Journal of Clinical endocrinology and Metabolism 43: 1056–1068 (1976).PubMedCrossRefGoogle Scholar
  23. Dyckner, TV, Helmers, C. and Wester, P.O.: Initial serum potassium level, early arrhythmias and previous diuretic therapy in acute myocardial infarction. International Journal of Cardiology 2: 146–148 (1982).PubMedCrossRefGoogle Scholar
  24. Dzau, V.J.; Colucci, W.S.; Williams, G.H.; Curfman, G.; Keggs, L. and Hollenberg, N.K.: Sustained effectiveness of converting enzyme inhibition in patients with severe congestive heart failure. New England Journal of Medicine 302: 1373–1379 (1980).PubMedCrossRefGoogle Scholar
  25. Dzau, V.J.; Packer, M.; Lilly, L.S.; Swartz, S.L.; Hollenberg, N.K. and Williams, G.H.: Prostaglandins in severe congestive heart failure. Relation to activtion of the renm-angiotensin system and hyponatremia. New England Journal of Medicine 310: 347–352 (1984).Google Scholar
  26. Erdös, E.G. and Yang, H.Y.T.: Kininases, in Erdös (Ed.) Handbook of Experimental Pharmacology, pp. 298–323 (Springer, New York 1970).Google Scholar
  27. Fray, J.C.S.: Stimulus-secretion coupling of renin. Role of hemodynamic and other factors. Circulation Research 47: 458–492 (1980).Google Scholar
  28. Ganong, W.F.: Sympathetic effects on renin secretion: Mechanism and physiological role. Advances in Experimental Biology and Medicine 17: 17–32 (1972).CrossRefGoogle Scholar
  29. Garcia, R.; Thebault, G. and Geness, J.: Effect of partially purified atrial natriuretic factor (ANF) on rat and rabbit vascular smooth muscle. (Abstract.) Clinical and Investigative Medicine 6: 56 (1983).Google Scholar
  30. Gerber, J.G.: Indomethacin-induced rises in blood pressure. Annals of Internal Medicine 99: 555–559 (1983).PubMedGoogle Scholar
  31. Ginn, H.E.: Ade, R.; McCallum, T. and Fregley, M.: Aldosterone secretion in magnesium-deficient rats. Endocrinology 80: 969–971 (1967).PubMedCrossRefGoogle Scholar
  32. Goldberg, J.P.; Schrier, R.W.; Gardenswartz, M.L.H. and Berl, T.: In vivo role of cellular calcium (Ca) uptake in the response to systemic vasoconstrictors. (Abstract.) Clinical Research 28: 549A (1980).Google Scholar
  33. Habener, J.R. and Potts Jr, J.R.: Relative effectiveness of magnesium and calcium on secretion and biosynthesis of parathyroid hormone in vitro. Endocrinology 98: 197–202 (1976).PubMedCrossRefGoogle Scholar
  34. Hiramatsu, K.; Yamagishi, F.; Kubota, T. and Yamada, T.: Acute effects of the calcium antagonist nifedepine, on blood pressure, pulse rate, and the renin-angiotensin-aldosterone system in patients with essential hypertension. American Heart Journal 104: 1346–1350(1982).PubMedCrossRefGoogle Scholar
  35. Horton, R.; Zipser, R. and Fichman, M.: Prostaglandins, renal function and vascular regulation. Medical Clinics of North America 65: 891–914 (1981).PubMedGoogle Scholar
  36. King, R.G. and Stanbury, S.W.: Magnesium metabolism in primary hyperparathyroidism. Clinical Science 39: 281 -303 (1970).PubMedGoogle Scholar
  37. Klein, W.; Brandt, D.; Vrecko, K. and Harringer, M.: Role of calcium antagonists in the treatment of essential hypertension. Circulation Research 52: 1174–1181 (1983).Google Scholar
  38. Kotchen, T.A.: Galla, J.H.; Guthrie, G.P. and Luke, R.G.: Regulation of renin by chloride. Journal of Cardiovascular Medicine 4: 475–479 (1979).Google Scholar
  39. Kotchen, T.A.; Lake, R.G.; Ott, C.E.; Galla, J.H. and Whites-carver, B.G.S.: Effect of chloride on renin and blood pressure responses to sodium chloride. Annals of Internal Medicine 98: 817–822 (1983).PubMedGoogle Scholar
  40. Langer, G.A.: Sodium-calcium exchange in the heart. Annual Review of Physiology 44: 435–439 (1982).PubMedCrossRefGoogle Scholar
  41. Levine, T.B.; Franciosa, J.A. and Cohn, J.N.: Acute and long-term response to an oral converting-enzyme inhibitor, captopril, in congestive heart failure. Circulation 62: 35–41 (1980).PubMedCrossRefGoogle Scholar
  42. Lifschitz, M.D. and Stein, J.H.: Renal vasoactive hormones; in Brenner and Rector (Eds) The Kidney, pp. 650–720 (W.B. Saunders, Philadelphia 1981).Google Scholar
  43. Mader, J.J. and Iseri, L.T.: Spontaneous hypomagnesemia, alkalosis and tetany due to hypersecretion of corticosterone-like mineralocorticoid. American Journal of Medicine 19: 976–988 (1955).PubMedCrossRefGoogle Scholar
  44. McCarron, D.A.: Low serum concentrations of ionized calcium in patients with hypertension. New England Journal of Medicine 307: 226–228 (1982).PubMedCrossRefGoogle Scholar
  45. McCarron, D.A. Divalent cations, anions and blood pressure calcium and magnesium nutrition in human hypertension. Annals of Internal Medicine 98 (Part 2): 800–805 (1983).PubMedGoogle Scholar
  46. McDonald, T.F.: The slow inward calcium current in the heart. Annual Review of Physiology 44: 425–434 (1982).PubMedCrossRefGoogle Scholar
  47. McGiff, J.C. and Spokas, E.G.: Position paper: Regulation of blood pressure by prostaglandin-kinin interactions; in Laragh et al. (Eds) Frontiers in Hypertension Research pp. 105–113 (S ringer. New York 1981).CrossRefGoogle Scholar
  48. Mendelsohn, F.A.; Lloyd, C.J.; Kachel, C. and Funder, J.W.: Glucocorticoid induction of angiotensin converting enzyme production from bovine endothelial cells in culture and rat lung in vivo. Clinical and Experimental Pharmacology and Physiology 7 (Suppl.): 57–62 (1982).Google Scholar
  49. Miura, K.; Abe, Y. and Yamamoto, K.: Hypotensive action of angiotensin converting enzyme inhibitor (SQ 14,225) in nephrectomized dogs. Journal of Pharmacology and Experimental Therapeutics 222: 246–250 (1982).PubMedGoogle Scholar
  50. Nemech, M.N. and Gilmore, J.P.: Natriuretic activity of human and monkey atria. Circulation Research 53: 420–423 (1983).CrossRefGoogle Scholar
  51. Oldham, S.B.; Fischer, J.A.; Capen, C.C.; Sizemore, G.W. and Arnand, CD. Dynamics of parathyroid secretion in virto. American Journal of Medicine 50: 650–657 (1971).PubMedCrossRefGoogle Scholar
  52. Osborn, J.L.; Noordewier, B.; Hook, J.B. and Bailie, M.D.: anism of prostaglandin E2 stimulation of renin secretion. Proceedings of the Society for Experimental Biology and Medi-“cine 159: 249–252 (1978).Google Scholar
  53. Rasmussen, H.: Cellular calcium metabolism. Annals of Internal Medicine 98: 809–816 (1983).PubMedGoogle Scholar
  54. Reinhart, P.H.; Taylor, W.M. and Bygrave F.L.: Calcium ion fluxes induced by the action of adrenergic agonists in perfused rat iiver. Brochemicai Journal 208: 619–630(1982).Google Scholar
  55. Resnick, L.M.; Laragh, J.H.; Sealey, J.E. and Alderman, M.H.: Divalent cations in essential hypertension. Relations between serum ionized calcium, magnesium and plasma renin activity. New England Journal of Medicine 309: 888–891 (1983).Google Scholar
  56. Rosa, R.M.; Silva, P.; Young, J.B.; Landsberg, L.; Brown, R.S.; Rowe, J.W. and Epstein, F.H.: Adrenergic modulation of extrarenal potassium disposal. New England Journal of Medicine 302: 431–434 (1980).PubMedCrossRefGoogle Scholar
  57. Ryzen, E.; Elbaum, N.; Singer, F.R. and Rude, R.K.: Parenteral magnesium loading as a means of diagnosing magnesium deficiency. (Abstract.) 8th International Conference on Calcium Regulting Hormones, Kobe, Japan, p. 148 (October 1983).Google Scholar
  58. Sonnenberg, H.; Cupples, W.A.; deBold, A.J. and Veress, A.T.: Intrarenal localization of the natriuretic effect of cardiac atrial extract. Canadian Journal of Physiology and Pharmacology 60: 1149–1152(1982).PubMedCrossRefGoogle Scholar
  59. Silva, P. and Spokes, K.: Sympathetic system in potassium homeostasis. American Journal of Physiology 241: FI 5I–F155 (1981).Google Scholar
  60. Solomon, R.J. and Cole, A.G.: Importance of potassium in patients with acute myocardial infarction. Acta Medica Scandinavica 647 (Suppl): 87–93 (1981).PubMedGoogle Scholar
  61. Steiness, E.: Diuretics, digitalis and arrhythmias. Acta Medica Scandinavica 647 (Suppl.): 75–78 (1981).PubMedGoogle Scholar
  62. Sternheim, W.; Dalakos, T.G.; Streeten, D.H.; Fox, L. and Speller, P.J.: Action of L-epinephrine in the renin-aldosterone system and on urinary electrolyte excretion in man. Metabolism 31: 979–984(1982).PubMedCrossRefGoogle Scholar
  63. Stokes, J.B.: Effect of prostaglandin E2 on chloride transport across the rabbit thick ascending limb of Henle: Selective inhibition of the medullary portion. Journal of Clinical Investigation 64: 495–502 (1979).PubMedCrossRefGoogle Scholar
  64. Sutton, R.A.L.: Plasma magnesium concentration in primary hyperparathyroidism. British Medical Journal 1: 529–533 (1970).PubMedCrossRefGoogle Scholar
  65. Swartz, S.L.; Williams, G.H.; Hollenberg, N.K.; Moore, T.J. and Dluhy, R.: Converting enzyme inhibition in essential hypertension: The hypotensive response does not reflect only reduced angiotensin II formation. Hypertension 1: 106–111 (1979).PubMedCrossRefGoogle Scholar
  66. Tannen, R.L.: Effects of potassium on blood pressure control. Annals of Internal Medicine 98: 773–780 (1983).PubMedGoogle Scholar
  67. Targonovnik, J.H.: Rodman, J.S. and Sherwood, L.M.: Regulation of parathyroid hormone secretion in vitro: Quantitative aspects of calcium and magnesium ion control. Endocrinology 88: 1477–1482 (1971).CrossRefGoogle Scholar
  68. Thurau, K.: Intrarenal action of angiotensin; in Page and Bumous (Eds) Handbook of Experimental Pharmacology, pp. 475–489 (Springer, New York 1974).Google Scholar
  69. Vandongen, R.; Peart, W.S. and Boyd, G.W.: Adrenergic stimulation of renin secretion in the isolated perfused rat kidney. Circulation Research 32: 290–296 (1973).PubMedCrossRefGoogle Scholar
  70. Wallach, S.: Physiologic and critical interrelations of hormones and magnesium, consideration of thyroid, insulin corticosteroids, six steroids and catecholamines; in Cantin and Seeley (Eds) Magnesium in Health and Disease, pp. 241–258 (Spectrum Publications, New York 1980).Google Scholar
  71. Watson, M.L.; Goodman, R.P.; Gill, JR.; Branch, R.A.; Brash, A.R. and Fitzgerald, G.A.: Endogenous prostacyclin synthesis is decreased during activation of the renin-angiotensin system in man. Journal of Clinical Endocrinology and Metabolism 58: 304–308 (1984).PubMedCrossRefGoogle Scholar

Copyright information

© ADIS Press Limited 1984

Authors and Affiliations

  • Keith G. Dawson
    • 1
  1. 1.Division of EndocrinologyUniversity of British ColumbiaVancouver

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