New Insights Into the Pathophysiology of Renovascular Hypertension

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New Insights Into the Pathophysiology of Renovascular Hypertension J. Carlos Romero, M.D., Ariel E. Feldstein, Martin G. Rodriguez-Porcel, M.D., M.S., Aleix Cases-Amenos, M.D., PG.D., M.D. Mayo Clinic Proceedings Volume 72, Issue 3, Pages 251-260 (March 1997) DOI: 10.4065/72.3.251 Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 1 Changes in renal plasma flow (RPF), glomerular filtration rate (GFR), and urine sodium excretion (U Na) induced by alterations in renal arterial pressure. Expression n normal indicates that normal sodium excretion is increased by the factor n-numbers given in ordinate. (From Romero and associates.2 By permission.) Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 2 Laser-Doppler flowmeter signal recorded from renal cortex and papillary blood flow in Sprague-Dawley rat as renal perfusion pressure varied from 150 to 50 mm Hg. (From Roman.20 By permission.) Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 3 Sequence of reactions triggered in kidney by alterations in arterial pressure. Putative reciprocal changes in release of renin were not considered. BP = blood pressure; NO = nitric oxide; PG = prostaglandins. Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 4 Main adaptive mechanisms in one-kidney, one-clip Goldblatt hypertension. Ang II = angiotensin II; CO = cardiac output; PRA = plasma renin activity; TP = total peripheral. Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 5 Adaptive mechanisms in two-kidney, one-clip Goldblatt hypertension. Cont = contralateral; Kd = kidney; PRA = plasma renin activity. Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 6 Effect of intravenous infusion of [Sar1, Il8]angiotcnsin II (ang. ant.) in normotensive rabbits and after development of renovascular hypertension during normal and high intake of salt. HBP =high blood pressure. Vertical bars represent mean ± SEM. (From Romero and associates.49 By pennission.) Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 7 Phosphoinositide-calcium-protein kinase C effector system. Ang Il = angiotensin II; ATP = adenosine triphosphate; DAG = diacylglycerol; IP3 = inositol trisphosphate; PIP2 = phosphatidylinositol bisphosphate; PKC = protein kinase C; PLC = phospholipase C; R = receptor; SR = sarcoplasmic reticulum. Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions

Fig. 8 Postulated prostanoid-mediated mechanism of vascular contraction in rats with angiotensin-dependent hypertension due to aortic coarctation. AA = arachidonic acid; HETES =hydroxyeicosatetraenoic acids; PGs =prostaglandins; TX =thromboxane. Mayo Clinic Proceedings 1997 72, 251-260DOI: (10.4065/72.3.251) Copyright © 1997 Mayo Foundation for Medical Education and Research Terms and Conditions