Pathophysiology of experimental renovascular hypertension.
The genesis of renovascular hypertension follows a continuum from an acute to a chronic phase. Reduction in renal perfusion initiates renin release and angiotensin-mediated systemic vasoconstriction. Aldosterone secretion, sodium and water retention, and expansion of the extracellular volume ensue. Sustained hypertension is further maintained by interacting physiologic mechanisms including increased angiotensin II sensitivity, vasopressin, ouabain-like substance, the sympathetic nervous system, CNS mechanisms, autoregulation, and structural changes.
D000208:Acute Disease; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology; D002490:Central Nervous System / Q000503:physiopathology; D002908:Chronic Disease; D004195:Disease Models, Animal; D004285:Dogs; D006439:Hemodynamics; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply; D010042:Ouabain / Q000502:physiology; D010477:Perfusion; D051381:Rats; D012084:Renin-Angiotensin System; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014661:Vasoconstriction; D014667:Vasopressins / Q000502:physiology
D014667:Vasopressins; D000804:Angiotensin II; D010042:Ouabain