Abstract
The study of primary hypertensiona has now entered a new phase in which the genome is becoming the principal focus research. Movement in this promising direction requires overcoming not only technical and technological problems. It has become evident that the choice of the loci where genomic abnormalities should be searched for will largely determine to what extent our understanding of the nature of hypertension corresponds to reality. The key chain of the pathogenesis may serve as a guide for the most efficient search for gene abberations.
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Berk BC, Vallega G, Muslin AJ, Gordon HM, Canessa M, Alexander RW (1989) Spontaneously hypertensive rat vascular smooth muscle cells in culture exhibit growth Na+/H+ exchange. Clin Invest 83: 822–829
Berridge MJ (1984) Inositol triphosphate and diacrylglycerol as a second messenger. Biochem J 220: 345–360
Boriskina GM, Gulak PV, Postnov YV (1978) Phosphoinositide in the erythrocyte membrane of rats with spontaneous and renal hypertension. Experientia 34: 744
Canessa M, Adragna N, Solomon HS, Connoly TM, Tosteson DC (1980) Increased sodium-lithium countertransport in red cells of patients with essential hypertension. N Engl J Med 302: 772–776
Dimitrov D, Resink TJ, Müller FB, Bühler FR (1986) Altered platelet phosphatidyl inositol metabolism in essential hypertension. J Hypertens 4 [Suppl 6]: 346–348
Garay RP, Meyer PA (1979) A new test showing abnormal net Na+ and K+ fluxes in erythrocytes of essential hypertensive patients. Lancet 1: 349–353
Guyton AC (1980) Circulatory physiology. III. Arterial pressure and hypertension. Saunders, Philadelphia
Heagerty AM, Ollerenshaw JD, Swales JD (1986) Abnormal vascular phosphoinositide hydrolysis in the spontaneously hypertensive rat. Br J Pharmacol 89: 803–807
Jones AW (1973) Altered ion transport in vascular smooth muscle from spontaneously hypertensive rats. Influence of aldosterone, norepinephrine and angiotensin. Circ Res 33: 563–572
Kotelevtsev YV, Orlov SN, Pokudin NI, Agnayev VM, Postnov YV (1987) Genetic analysis of Na+, K+-cotransport calcium content and blood pressure in (SHR x WKY)FZ hybrids. Bull Exp Biol Med 103: 456–458
Kotelevtsev YV, Brashishkite DA, Spitkovsky DD, Kiselev FL, Postnov YV (1988) Interstrain restriction fragment length polymorphism of c-fos and c-src oncogene loci in spontaneously hypertensive and normotensive rats. J Hypertens 6: 781–799
Kotelevtsev YV, Spitkovsky DD, Orlov SN, Postnov YV (1989) Interstrain restriction fragment length polymorphism in the c-src correlates with Na, K-cotransport and calcium content in hybrid rat erythrocytes. J Hypertens 7 [Suppl 6]: 112–113
Lang GF (1950) Hypertension. Medgiz, Moscow (in Russian )
Livne A, Veitch R, Grinstein S, Balfe JW, Marquez-Julio A, Rothstein A (1987) Increased platelet Na+ H+ exchange rates in essential hypertension: application of a novel test. Lancet 1: 533–536
Marche P, Kutouzov S, Girard A, Elghozi JL, Meyer P, Ben-Ishay (1985) Phosphoinositide turnover in erythrocyte membranes in human and experimental hypertension. J Hypertens 3: 25–30
Orlov SN, Postnov IY, Pokudin NI, Kukharenko VY, Postnov YV (1989) Na+ H+ exchange and other ion-transport systems in erythrocytes of essential hypertensives and spontaneously hypertensive rats: a competative analysis. J Hypertens 7: 781–788
Pickering GW (1977) Personal views on mechanisms of hypertension. In: Genest J, Koiw E, Kuchel O (eds) Hypertension. Physiopathology and treatment. McGraw-Hill, New York, pp 598–606
Postnov YV (1987) Membrane defect in primary hypertension: a reflection of altered cellular oncogene function? Kardiologija 27 (11): 98–102
Postnov YV, Orlov SN (1979) Alteration of cell membranes in hypertension: role of altered membrane control over intracellular calcium. In: First joint US-USSR symposium of hypertension. National Institute of Healthy, pp 182–193
Postnov YV, Orlov SN (1984) Cell membrane alteration as a source of primary hypertension. J Hypertens 2: 1–6
Postnov YV, Orlov SN (1985) Ion transport across plasma membrane in primary hypertension. Physiol Rev 65: 904–945
Postnov YV, Orlov SN, Gulak PV, Shevchenko AS (1976) Altered permeability of the erythrocyte membrane for sodium and potassium in spontaneously hypertensive rats. Pflügers Arch 365: 257–263
Postnov YV, Orlov SN, Shevchenko AS, Adler AM (1977) Altered sodium permeability, calcium binding and Na-K-ATPase activity in the red blood cell membrane in essential hypertension. Pflügers Arch 371: 263–269
Postnov YV, Orlov SN, Pokudin NI (1981) Alteration of the intracellular calcium pool of adipose tissue in spontaneously hypertensive rats. No effect of peripheral immunosympathectomy. Pflügers Arch 390: 256–259
Postnov YV, Kravtsov GM, Orlov SN, Kotelevtsev YV, Pokudin NI, Postnov IY (1987) Regulation by protein kinase C of erythrocyte shape, volume and passive, sodium permeability: alteration in essential hypertension. J Hypertens 5 [Suppl 5]: 257–259
Postnov YV, Kravtsov GM, Orlov SN, Pokudin NI, Postnov IY, Kotelevtsev YV (1988) Effect of protein kinase C activation on cytoskeleton and cation transport in human erythrocytes. Reproduction of some membrane abnormalities revealed in essential hypertension. Hypertension 12: 267–273
Shlager G, Chang-Shin (1989) The role of dominance and epistasis in the genetic control of blood pressure in rodent models of hypertension. In: 6th International Symposium on SHR and related studies, Iowa City, p 32
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Postnov, Y.V. (1991). Cell Membrane Alteration in Primary Hypertension: An Evidence of Its Genomic Source. In: Berg, K., Bulyzhenkov, V., Christen, Y., Corvol, P. (eds) Genetic Approaches to Coronary Heart Disease and Hypertension. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76891-0_3
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DOI: https://doi.org/10.1007/978-3-642-76891-0_3
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