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Sodium and Hypertension Still a Controversy in 1986

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Summary

Interpopulation studies support the hypothesis of a causal relationship between sodium consumption and arterial hypertension. However, although this association has been contradicted by intrapopulation studies, the correlation between sodium and hypertension appears to be genetically determined, as there are both sodium-sensitive and sodium-resistant individuals.

Sodium is essential for the maintenance of extracellular and plasma volume equilibrium. It is controlled metabolically by the interaction of several biological systems such as the renin-angiotensin-aldosterone system, the sympathetic nervous system, and the kallikrein-kinin and prostaglandin systems. Thus, sodium has a definite role in the mechanism involved in the pathophysiology of the predominantly volume-dependent forms of arterial hypertension.

Recently, different structural substances with natriuretic effects have been identified. Natriuretic hormone is a non-peptide substance which inhibits the Na,K-ATPase in response to extracellular volume increase. This hormone acts on the renal tubular cells reducing sodium reabsorption, and at an arteriolar level elevating peripheral resistance by increasing smooth muscle tension. Mammalian atria contain various precursors of biologically active peptides, with potent natriuretic and diuretic effects. They are released in response to volume loading and atrial stretch. Although some data suggest an important role for these natriuretic substances in fluid volume and blood pressure control, their place in physiology and in abnormal clinical states should be more definitively clarified in the next few years.

Résumé

Les études interpopulations renforcent l’hypothèse d’une relation causale entre la consommation de sodium et l’hypertension artérielle. Cette corrélation est contredite par les études intrapopulations, elle semble toutefois génétiquement déterminée puis qu’il existe à la fois des individus sodium-sensibles et des individus sodium-résistants.

Le sodium est essentiel au maintien de l’équilibre des volumes extracellulaire et plasmatique. Il est métaboliquement contrôlé par l’interaction de plusiers systèmes biologiques tels que le système aldostérone-rénine-angiotensine, le système nerveux autonome, les systèmes prostaglandines et kallikréine-kinines. Ainsi, le sodium joue un rôle précis dans le mécanisme qui intervient dans la physiopathologie des hypertensions artérielles essentiellement volume-dépendantes.

Récemment, on a identifié différentes substances natriurétiques. L’hormone natriurétique est une substance non peptidique qui inhibe la Na, K-A TPase en réponse à une augmentation du volume extracellulaire. Cette hormone agit sur les cellules tubulaires rénales provoquant une diminution de la réabsorption du sodium et au niveau artériolaire, élevant les résistances périphériques par augmentation de la contraction des muscles lisses. L’oreillette des mammifères contient divers précurseurs des peptides biologiquement actifs, qui majorent les effets natriurétique et diurétique. Ils sont libérés en réponse à un accroissement des volumes et à une distension auriculaires. Un certain nombre de données suggère que ces substances natriurétiques tiennent un rôle important dans le contrôle des volumes liquidiens et de la pression sanguine. Cependant, leur rôle exact dans la physiologie et les états cliniques pathologiques devraient être plus clairement précisé dans les prochaines années.

Zusammenfassung

Bevölkerungsstudien stützen die Hypothese einer kausalen Beziehung zwischen Natriumverbrauch und arterieller Hypertonie. Wenn auch dieser Assoziation in Bevölkerungsstudien widersprochen wurde, scheint jedoch die Korrelation zwischen Natrium und Hypertonie genetisch bestimmt zu sein, da es sowohl Natrium-sensitive als auch Natrium-resistente Personen gibt.

Natrium ist für die Aufrechterhaltung des Gleichgewichts von extrazellulärem und Plasma-Volumen erforderlich. Es wird metabolisch durch die Interaktion verschiedener biologischer Systeme, wie das Renin-Angiotensin-Aldosteron-System, das sympathische Nervensystem sowie das Kalikrein-Kinin und das Prostaglandin-System kontrolliert. Damit besitzt das Natrium eine definitive Rolle bei dem Mechanismus, der an der Pathophysiologie der vornehmlich Volumenabhängigen Formen der arteriellen Hypertonie beteiligt ist.

Kürzlich wurden verschiedene strukturelle Substanzen mit natriuretischen Effekten identifiziert. Das natriuretische Hormon ist eine nicht peptidartige Substanz, die die Na, K-A TPase in Reaktion auf einen Anstieg des extrazellulären Volumens hemmt. Dies Hormon wirkt auf die Zellen der Nierentubuli, indem es die Natriumresorption reduziert und auf Höhe der Arteriolen den peripheren Widerstand durch Erhöhung des Tonus der glatten Muskulatur erhöht. Der Herzvorhof von Säugetieren enthält verschiedene Vorstufen von biologisch-aktiven Peptiden mit potenten natriuretischen und diuretischen Effekten. Sie werden als Reaktion auf eine Volumenüberladung und Dehnung des Vorhofs freigesetzt. Wenn auch einige Daten eine wichtige Rolle für diese natriuretische Substanzen bei der Kontrolle des Flüssigkeitsvolumens und Blutdrucks vermuten lassen, sollte ihre Bedeutung in der Physiologie und abnormen klinischen Zuständen in den nächsten paar Jahren definitiv geklärt werden.

Resumen

Los estudios interpoblación confirman la relación causal entre consumo de sodio e hipertensión arterial. Aunque esta asociación ha sido negada por otros estudios intrapoblación, la cor-relación entre sodio e hipertensión parece estar determinada genéticamente al haber individuos sodiosensibles y sodiorresistentes.

El sodio es esencial para el mantenimiento del equilibrio del volumen extracelular y el plasmatico, controlado metabólicamente por la interaccion de varios sistemas biológicos, tales como el de renina-angiotensina-aldosterona, el sistema nervioso simpâtico y los sistemas calicreína-cinina y prostaglandina. Así pues, el sodio desempeña una función bien definida en el mecanismo fisiopatológico de las formas de hipertensión arterial, en su mayor parte dependientes del volumen.

Recientemente se han identificado diferentes sustancias estructurales con efectos natriuréticos. La hormona natriurética es una sustancia no peptídica que inhibe la Na, K-A TPasa en respuesta al aumento de volumen extracelular. Esta hormona actúa sobre las células tubulares rénales reduciendo la reabsorción de sodio y elevando la resistencia periférica en las asteriolas por aumento de la tension del músculo liso. Las aurículas de mamífero contienen diversos precursores de péptidos biológicamente activos con potentes efectos natriuréticos y diuréticos, que se liberan en respuesta a la carga de volumen y a la dilatación auricular. Aunque algunos datos parecen confirmar la importancia de estas sustancias natriuréticas en el control del volumen líquido y de la presión arterial, su función en fisiología y en los estados clínicos anómalos debera determinarse con mayor precisión en el futuro.

Resumo

Estudos interpopulacionais sustentam a hipótese de que o consumo de sódio tem relação causal com a hipertensão arterial. Entretanto, embora os estudos intrapopulacionais tenham contradito uma tal associação, a correlação entre o sódio e hipertensão parece ser genéticamente determinada, uma vez que há indivíduos sensíveis e indivíduos resistentes ao sódio.

O sódio é essencial para a manutenção do equiliíbrio do volume plasmático e extracelular. Ele é controlado metabolicamente pela interação de diversos sistemas biológicos, tais como o sistema renina-angiotensina-aldosterona, o sistema nervoso simpático e os sistemas calicreínaquinina e prostaglandina. Assim sendo, o sódio tem papel definido no mecanismo implicado na fisiopatologia das formas de hipertensão arterial predominantemente dependentes do volume.

Recentemente, identificou-se diversas substâncias estruturais com efeitos natriuréticos. O hormônio natriurético é uma substância não-peptídica que inibe a Na-K-A TPase como reação a um aumento do volume extracelular. Este hormônio a tua nas células tubulares renais, reduzindo a reabsorção do sódio, e, num nível arteriolar, elevando a resistência periférica por meio de um aumento da tensão de músculo liso. Os átrios de mamíferos contêm diversos precursores de peptídeos biologicamente ativos, dotados de poderosos efeitos natriuréticos e diuréticos. Eles são liberados em reação ao aumento do volume e ao estiramento dos átrios. Embora alguns dados surgiram que estas substâncias natriuréticas tenham um papel importante no controle do volume de fluido e da pressão sanguínea, o seu desempenho nafisiologia e nos estados clínicos anormals deveria ser esclarecido de forma mais definida nos próximos anos.

Riassunto

Gli studi tra popolazioni confermano l’ipotesi di un rapporto causale ira consumo di sodio e ipertensione arteriosa. Tuttavia, sebbene questo rapporto sia stato smentito da studi intrapopolazione, la correlazione tra sodio e ipertensione appare geneticamente determinata, poichè vi sono sia individui sodio—sensibili che sodio-resistenti. Il sodio è essenziale per il mantenimento dell’equilibrio del volume plasmatico ed extracellulare. È controllato metabolicamente dall’inter azione di diversi sistemi biologici, come il sistema renina—angiotensina—aldosterone, il sistema nervoso simpatico e i sistemi callicreina—chinina e prostaglandinico. Pertanto il sodio ha un ruolo preciso nei meccanismi fisiopatologici delle forme di ipertensione arteriosa di tipo prevalentemente volume—dipendente. Recentemente sono state identificate differenti sostanze con effetti natriuretici. Vormone natriuretico è una sostanza non peptidica che inibisce la Na, K—ATPasi in risposta ad aumenti del volume extracellulare. Questo ormone agisce sulle cellule dei tubuli renali riducendo il riassorbimento di sodio e a livello arteriolare aumentando la tensione della muscolatura liscia. Gli atri dei mammiferi contengono vari precursori di peptidi biologicamente attivi, con potenti effetti natriuretici e diuretici. Queste sostanze vengono liberate in risposta ad aumenti di volume o a distensione atriale. Sebbene alcuni dati suggeriscano l’importanza di queste sostanze natriuretiche nel controllo dei volumi e della pressione arteriosa, il loro ruolo e in condizioni fisiologiche e patologiche dovrebbe essere meglio chiarito nei prossimi anni.

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References

  • Aderounmu AF, Salako LA. Abnormal cation composition and transport in erythrocytes from hypertensive patients. European Journal of Clinical Investigation 9: 369–375, 1979

    Article  CAS  PubMed  Google Scholar 

  • Allen FM, Sherril JW. The treatment of arterial hypertension. Journal of Metabolic Research 2: 429–545, 1922

    Google Scholar 

  • Ambard L, Beaujard E. Causes de l’hypertension arterielle. Archives Generales de Médicine 1: 520–533, 1904

    Google Scholar 

  • Ambrosioni E, Tartagni F, Montebugnoli L, Magnani B. Intralymphocytic sodium in hypertensive patients: A significant correlation. Clinical Science 57: S325–S327, 1979

    Google Scholar 

  • Bealer S, Haywood JR, Johnson AK, Gruber KA, Buckalew VM, Brody MJ. Impaired natriuresis and secretion of natriuretic hormone (NH) in rats with lesions of the anteroventral 3rd ventricle (AV3V) region. Federation Proceedings 38(3): 1232, 1979

    Google Scholar 

  • Blaustein MP. Sodium ions, calcium ions, blood pressure regulation and hypertension: A reassessment and a hypothesis. American Journal of Physiology 232: C165–C173, 1977

    CAS  PubMed  Google Scholar 

  • Blaustein MP. Sodium transport and hypertension: where are we going? Hypertension 6: 445–453, 1983

    Article  Google Scholar 

  • Blaustein MP, Hamlyn JM. Role of a natriuretic factor in essential hypertension: an hypothesis. Annals of Internal Medicine 98(Part 2): 785–792, 1983

    CAS  PubMed  Google Scholar 

  • Borenstein HB, Cupples WA, Sonnenberg H, Veress AT. The effects of natriuretic atrial extracts on renal hemodynamics and urinary excretion in anesthetized rats. Journal of Physiology (London) 334: 133–140, 1983

    CAS  Google Scholar 

  • Briggs JP, Steipe B, Schubert G, Schnermann J. Micropuncture studies of the renal effects of atrial natriuretic substance. Pflugers Archives 395: 271–276, 1982

    Article  CAS  Google Scholar 

  • Brody MJ, Johnson AK. Role of the anteroventral third ventricle region in fluid and electrolyte balance, arterial pressure regulation and hypertension. In Martini & Ganong (Eds) Frontiers in endocrinology, pp. 249–292, Raven Press, New York, 1980

    Google Scholar 

  • Burnett Jr JC, Granjer JP, Opgenorth TJ. Effects of synthetic natriuretic factor on renal function and renin release. American Journal of Physiology 247: F863–F866, 1984

    CAS  PubMed  Google Scholar 

  • Callaway CW. Nutritional factors and blood pressure control: an assessment. Annals of Internal Medicine 98 (Part 2): 884–890, 1983

    CAS  PubMed  Google Scholar 

  • Chaves-Ribeiro JM, Rumjaneck RD, Oigman W, Noronha A, Francischetti EA. Ativação da Na+K+ATPase da fração microsomal renal de rato pela angiotensina. Revista Brasileira de Pesquisas Médicas e Biológicas 5(4): 123–127, 1972

    Google Scholar 

  • Currie MG, Geller DM, Cole BR, Siegel NR, Fok KF et al. Purification and sequence analysis of bioactive atrial peptides (atriopeptins). Science 223: 67–69, 1984

    Article  CAS  PubMed  Google Scholar 

  • Dahl LK, Heine M, Tassinari L. Effects of chronic salt ingestion: evidence that genetic factors play an important role in susceptibility to experimental hypertension. Journal of Experimental Medicine 115: 1173–1190, 1962

    Article  CAS  PubMed  Google Scholar 

  • Dahl LK, Knudsen KD, Heine M, Leitl G. Effects of chronic excess salt ingestion: genetic influence on the development of salt hypertension in parabiotic rats: evidence of a humoral factor. Journal of Experimental Medicine 126: 687–699, 1967

    Article  CAS  PubMed  Google Scholar 

  • Daniel EE, Grover AK, Kwan CY. Isolation and properties of plasma membrane from smooth muscle. Federation Proceedings 41: 2898–2904, 1982

    CAS  PubMed  Google Scholar 

  • Dawber TR, Kannel WB, Kagan A, Donabedian RK, McNamara PM, Pearson G. Environmental factors in hypertension. In Stamler et al. (Eds) The epidemiology of hypertension, pp. 255–288,, Grune & Straton, New York, 1967

    Google Scholar 

  • de Bold AJ, Borenstein HB, Veress AT, Sonnenberg H. A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats. Life Science 28: 89–94, 1981

    Article  Google Scholar 

  • de Wardener HE, MacGregor GA. Dahl’s hypothesis that a saluretic substance may be responsible for a sustained rise in arterial pressure: its possible role in essential hypertension. Kidney International 18: 1–9, 1980

    Article  PubMed  Google Scholar 

  • de Wardener HE, MacGregor GA. The relation of a circulating transport inhibitor (The natriuretic hormone?) to hypertension. Medicine 62: 310–326, 1983

    PubMed  Google Scholar 

  • Edmondson RPS, Thomas RD, Hilton PJ, Patrick J, Jones NF. Abnormal leukocyte sodium composition and sodium transport in essential hypertension. Lancet 1: 1003–1005, 1975

    Article  CAS  PubMed  Google Scholar 

  • Flynn TG, de Bold ML, de Bold AJ. The amino acid sequence of an atrial peptide with potent diuretic and natriuretic properties. Biochemistry Biophysics Research Communication 117: 859–865, 1983

    Article  CAS  Google Scholar 

  • Folkow B. Physiological aspects of primary hypertension. Physiological Reviews 62: 347–504, 1982

    CAS  PubMed  Google Scholar 

  • Forrester TE, Alleyne GAO. Leukocyte electrolytes and sodium efflux rate constants in the hypertension of pre-eclampsia. Proceedings of the 7th Scientific Meeting of the International Society of Hypertension. New Orleans: International Society of Hypertension, p. 35, 1980

  • Freeman RH, Davis JO, Vari RC. Renal response to atrial natriuretic factor in conscious dogs with caval constriction. American Journal of Physiology 248: R495–R500, 1985

    CAS  PubMed  Google Scholar 

  • Freis ED. Salt, volume and the prevention of hypertension. Circulation 53: 589–595, 1976

    Article  CAS  PubMed  Google Scholar 

  • Friedman SM. Monovalent and divalent ions in vascular tissue. Annals of Internal Medicine 98 (Part 2): 753–758, 1983

    CAS  PubMed  Google Scholar 

  • Garay RP, Meyer P. A new text showing abnormal net Na+ and K+ fluxes in erythrocytes of essential hypertensive patients. Lancet 1: 349–352, 1979

    Article  CAS  PubMed  Google Scholar 

  • Genest J. Volume hormones and blood pressure. Annals of Internal Medicine 98: 744–749, 1983

    CAS  PubMed  Google Scholar 

  • Gleibermann L. Blood pressure and dietary salt in human populations. Nutrition 2: 143–156, 1973

    Google Scholar 

  • Goodfriend TL, Elliot ME, Atlas SA. Actions of synthetic atrial natriuretic factor on bovine adrenal glomerulosa. Life Science 35: 1675–1682, 1984

    Article  CAS  Google Scholar 

  • Grollman A, Hariison T, Mason MF, Baxter J, Grampton J, Reichoman F. Sodium restriction in the diet for hypertension. JAMA 129: 533–537, 1945

    Article  Google Scholar 

  • Gruber KA, Whitaker JM, Buekalew Jr VM. Endogenous digitalislike substance in plasma of volume expanded dogs. Nature 28: 743–745, 1980

    Article  Google Scholar 

  • Gudmundsson O, Herlitz H, Jonsson O, Hedner T, Anderson O, Berglund G. Blood pressure and intra-erythrocyte sodium during normal and high salt intake in middle-aged men: relationship to family history of hypertension and neurogenic and hormonal variables. Clinical Science 66: 427–433, 1984

    CAS  PubMed  Google Scholar 

  • Haddy FJ. Abnormalities of membrane transport in hypertension. Hypertension 5 (Suppl. V): V66–V72, 1983a

    CAS  PubMed  Google Scholar 

  • Haddy FJ. Sodium-potassium pump in low renin hypertension. Annals of Internal Medicine 98 (Part 2): 781–784, 1983b

    CAS  PubMed  Google Scholar 

  • Haddy FJ, Overbeck HW. The role of humoral agents in volume expanded hypertension. Life Science 19: 935–948, 1976

    Article  CAS  Google Scholar 

  • Heagerty AM., Bing RF, Milner M, Thurston H, Swales JD. Leucocyte membrane sodium transport in normotensive populations: dissociation of abnormalities of sodium efflux from raised blood pressure. Lancet 2: 894–896, 1982

    Article  CAS  PubMed  Google Scholar 

  • Henningsen NC, Mattson S, Nosslin B, Nelson D, Ohlsson O. Abnormal whole body and cellular (erythrocytes) turnover of 22Na+ in normotensive relatives of probands with established essential hypertension. Clinical Science 57: 3215–3245, 1979

    Google Scholar 

  • Kangawa K, Fukuda A, Matsuo H. Structural identification of β and γ human atrial natriuretic polypeptides. Nature 313: 397–400, 1985

    Article  CAS  PubMed  Google Scholar 

  • Kawasaki T, Delea CS, Bartter FC, Smith H. The effect of highsodium and low-sodium intakes on blood pressure and other related variables in human subjects with idiopathic hypertension. American Journal of Medicine 64: 193–198, 1978

    Article  CAS  PubMed  Google Scholar 

  • Kempner W. Treatment of kidney disease and hypertensive vascular disease with rice diet. North Carolina Medical Journal 5: 125–133, 1944

    Google Scholar 

  • Kleinen HD, Maack T, Atlas SA, Januszewicz A, Sealey JE, Laragh JH. Atrial natriuretic factor inhibits angiotensin, norepinefrine and potassium induced vascular contractility. Hypertension 6 (Suppl.I): 1143–1147, 1984

    Google Scholar 

  • Langford HG, Watson RL. Electrolytes and hypertension. In Paul (Ed) Epidemiology and control of hypertension, pp. 119–130, Stratton Intercontinental Medical Book Corporation, New York, 1975

    Google Scholar 

  • Laragh JH. Calcium metabolism and calcium channel blockers for understanding and treating hypertension. American Journal of Medicine 77 (Suppl. 6B): 1–23, 1984

    CAS  PubMed  Google Scholar 

  • Laragh JH, Pecker MS. Dietary sodium and essential hypertension:some myths, hopes and truths. Annals of Internal Medicine 98 (Part 2): 735–743, 1983

    CAS  PubMed  Google Scholar 

  • Ledingham JGG. Dietary salt and hypertension. Cardiovascular Reviews and Reports 3: 399–408, 1982

    Google Scholar 

  • Linden RJ. Atrial reflexes in renal function. American Journal of Cardiology 44: 879–883, 1979

    Article  CAS  PubMed  Google Scholar 

  • Ljungman S, Aurell M, Hartford M, Wikstrand J, Wilhelmsen L, Berglund G. Sodium excretion and blood pressure. Hypertension 3: 318–326, 1981

    Article  CAS  PubMed  Google Scholar 

  • Lowenstein FW. Blood pressure in relation to age and sex in the tropics and subtropics. Lancet 1: 389–392, 1961

    Article  Google Scholar 

  • Luetscher JA, Axelrod BJ. Increased aldosterone output during sodium deprivation in normal men. Proceedings of the Society for Experimental Biology and Medicine 87: 650–653, 1954

    CAS  PubMed  Google Scholar 

  • Luft FC, Weinberger MH. Sodium intake and essential hypertension. Hypertension 4 (Suppl. III): 14–19, 1982

    CAS  Google Scholar 

  • Luft FC, Weinberger MH, Grim CE, Fineberg NS, Miller JZ. Sodium sensitivity in normotensive human subjects. Annals of Internal Medicine 98 (Part 2): 758–762, 1983

    CAS  PubMed  Google Scholar 

  • Maack T, Marion DN, Camargo MJF, Kleinen HD, Laragh JH et al. Effects of auriculin (ANF) on blood pressure, renal function and the renin-angiotensin-aldosterone system in dogs. American Journal of Medicine 77: 1069–1075, 1984

    Article  CAS  PubMed  Google Scholar 

  • MacGregor GA. Sodium is more important than calcium in essential hypertension. Hypertension 7: 628–637, 1985

    Article  CAS  PubMed  Google Scholar 

  • MacGregor GA, Fenton S, Alaghband-Zadeh J, Markandu ND, Roulston JE, de Wardener HE. Evidence for a raised concentration of a circulating sodium transport inhibitor in essential hypertension. British Medical Journal 283: 1355–1357, 1981

    Article  CAS  PubMed  Google Scholar 

  • Mann GV, Schaffer RD, Rich A. Physical fitness and immunity to heart disease in Masai. Lancet 2: 1308–1310, 1965

    Article  CAS  PubMed  Google Scholar 

  • Miall WE, Oldham PD. Factors influencing arterial blood pressure in the general population. Clinical Science 17: 409–444, 1958

    CAS  PubMed  Google Scholar 

  • Murphy RJF. The effect of ‘rice diet’ on plasma volume and extra-cellular fluid space in hypertensive subjects. Journal of Clinical Investigation 29: 912–917, 1950

    Article  CAS  PubMed  Google Scholar 

  • Needleman P, Adams SP, Cole BR, Currie MG, Geller D, et al. Atriopeptins as cardiac hormone. Hypertension 7: 469–482,1985

    Article  CAS  PubMed  Google Scholar 

  • Nemeh MN, Gilmore JP. Natriuretic activity of human and monkey atria. Circulation Research 53: 420–423, 1983

    Article  CAS  PubMed  Google Scholar 

  • Nicholls MG. Atrial natriuretic polypeptides: relationship with the renin-angiotensin-aldosterone system. In Robertson (Ed) Ace report 21, Gower Medical Publishing Ltd, New York, 1985

    Google Scholar 

  • Page LB. Hypertension and atherosclerosis in primitive and acculturating societies. In Hunt et al. (Eds) Hypertension update: mechanisms, epidemiology, evaluation and management, pp. 1–12, HLS Press, Bloomfield, New Jersey 1980

    Google Scholar 

  • Page LB, Danion A, Moellering Jr RC: Antecedents of cardiovascular disease in six Solomon Island societies. Circulation 49: 1132–1146, 1974

    Article  CAS  PubMed  Google Scholar 

  • Pickering G. Salt intake and essential hypertension. Cardiovascular Reviews & Reports 1: 13–17, 1980

    Google Scholar 

  • Pollock DM, Banks RD. Effect of atrial extract on renal function in the rat. Clinical Science 65: 47–55, 1983

    CAS  PubMed  Google Scholar 

  • Rasmussen H. Cellular calcium metabolism. Annals of Internal Medicine 98 (Part 2): 809–816, 1983

    CAS  PubMed  Google Scholar 

  • Richards AM, Nicholls MG, Espiner EA, Ikram H, Yandle TG, et al. Effects of α-human atrial natriuretic peptide in essential hypertension. Hypertension 7: 812–817, 1985

    Article  CAS  PubMed  Google Scholar 

  • Saper CB, Standaert DB, Currie MG, Schwartz D, Geller DM, Needleman P. Atriopeptin-immunoreactive neuron in the brain: presence of cardiovascular regulatory areas. Science 227: 1047–1049, 1985

    Article  CAS  PubMed  Google Scholar 

  • Seikurt EE. Effects of pulse pressure and mean arterial pressure modifications on renal hemodynamics and electrolyte and water excretion. Circulation 4: 541–557, 1951

    Article  Google Scholar 

  • Selye H, Stone H, Timiras PS, Schaffenburg C. Influence of sodium chloride upon the action of desoxycorticosterone acetate. American Heart Journal 37: 1009–1016, 1949

    Article  CAS  PubMed  Google Scholar 

  • Shaper AG. Cardiovascular disease in the tropics: III. Blood pressure and hypertension. British Medical Journal 3: 805–807, 1972

    Article  CAS  PubMed  Google Scholar 

  • Siegel G, Schneider W. Anions, cations, membrane potential and relaxation. In Vanhautte and Leusen (Eds) Vasodilatation, pp. 285–298, Raven Press, New York, 1981

    Google Scholar 

  • Snadjar RM, Rapp JP. Atrial natriuretic factor in Dahl rats. Hypertension 7: 775–782, 1985

    Article  Google Scholar 

  • Sonnenberg H, Cupples WA. Intrarenal localization of the natriuretic effect of the cardiac atrial extracts. Canadian Journal of Physiology and Pharmacology 60: 1149–1152, 1982

    Article  CAS  PubMed  Google Scholar 

  • Sonnenberg H, Milojevic S, Chong CK, Veress AT. Atrial natriuretic factor: reduced cardiac content in spontaneously hypertensive rats. Hypertension 5: 672–675, 1983

    Article  CAS  PubMed  Google Scholar 

  • Tobian L. Human essential hypertension: implications of animal studies. Annals of Internal Medicine 98 (Part 2): 729–734, 1983

    CAS  PubMed  Google Scholar 

  • Tobian L, Binion JT. Tissue cations and water in arterial hypertension. Circulation 5: 754–758, 1952

    Article  CAS  PubMed  Google Scholar 

  • Weder AB, Torretti BA, Julius S. Racial differences in erythrocyte cation transport. Hypertension 6: 115–123, 1984

    Article  CAS  PubMed  Google Scholar 

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Francischetti, E.A., Genelhu, V. & Oigman, W. Sodium and Hypertension Still a Controversy in 1986. Drugs 31 (Suppl 4), 29–39 (1986). https://doi.org/10.2165/00003495-198600314-00005

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