Position Paper: Vasoconstriction and Volume Factors in Renovascular Hypertension
Interest in the pathogenesis of renovascular hypertension has remained strong since Goldblatt’s famous experiment in 1934 where by constricting one renal artery, he produced hypertension that was reversed by clamp removal or nephrectomy. The role of a pressor mechanism via the renin-angiotensin system in this type of hypertension has been vigorously supported and refuted with equally convincing arguments over the years. In support of renin’s contribution to the development and maintenance of renovascular hypertension are the facts that it can be readily produced experimentally by clamping of one renal artery, thus stimulating oversecretion of renin (1); it is frequently characterized by high levels of plasma renin activity (PRA) (2); it can frequently be cured by removal or revascularization of the affected kidney (3); it can be prevented (4) or reversed (5, 6) by administration of various angiotensin inhibitors after the experimental procedure that produces severe stenosis of the renal artery. Against renin’s role are the findings that PRA is sometimes found to be in the normal or even subnormal range (7), and there is no correlation between PRA levels and the degree of hypertension (8); that corrective or ablative surgery is not always successful in curing hypertension (3); that angiotensin blockade does not always produce a fall in blood pressure (5, 9)—in fact, the competitive antagonists of angiotensin II that possess partial agonistic effects may occasionally increase, rather than decrease, the arterial pressure, a reaction characteristic of the low-renin hypertension state attributed to sodium overload (10).
KeywordsRenal Artery Renal Artery Stenosis Renovascular Hypertension Renovascular Disease Renal Artery Disease
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- 12.Buggy J, Fink GD, Johnson AK, Brody MJ (1977) Prevention of the development of renal hypertension by anteroventral third ventricular tissue-lesions. Circ Res 25 (Suppl I): 110–117Google Scholar
- 17.Fasciolo JC, Risler NR, Totel G (1972) Corticotensins: Pressor peptides from the kidney. In: Genest J, Koiw E (eds) Hypertension 1972. Springer, Berlin, pp 177–182Google Scholar
- 19.Maxwell MH, Lupu AN, Viskoper RJ, Aravena LA, Waks UA (1977) Mechanism of hypertension during the acute and intermediate phases of the one- clip two-kidney model in the dog. Circ Res 25 (Suppl I): 24–28Google Scholar
- 29.Hatzinikolaou P, Gavras H (1980) Sodium induced elevation of blood pressure in the anephric state (abstr). Clin Res 28: 329AGoogle Scholar
- 30.Gavras H, Liang C, Brunner HR (1978) Redistribution of regional blood flow after inhibition of the angiotensin converting enzyme. Circ Res 43 (Suppl I): 59–63Google Scholar
- 33.Lupu AN, Maxwell MH, Kaufman JJ (1977) Mechanisms of hypertension during the chronic phase of the one-clip, two-kidney model in the dog. Circ Res 25 (Suppl I): 57–61Google Scholar
- 34.Dauda G, Möhring J, Hofbauer KG, Homsy E, Miksche U, Orth H, Gross F (1973) The vicious circle in acute malignant hypertension of rats. Clin Sci Mol Med 45: 251S–255SGoogle Scholar
- 38.Streeten DHP, Anderson GH (1979) Outpatient experience with saralasin. Kidney Int 15: S-44–S-52Google Scholar