Intrarenal renin-angiotensin system and counteracting protective mechanisms in angiotensin II-dependent hypertension.
It is now well accepted that alterations in kidney function, due either to primary renal disease or to inappropriate hormonal influences on the kidney, are a cardinal characteristic in all forms of hypertension, and lead to a reduced ability of the kidneys to excrete sodium and the consequent development of elevated arterial pressures. However, it is also apparent that many extrarenal factors are important contributors to altered kidney function and hypertension. Central to many hypertensinogenic processes is the inappropriate activation of the renin-angiotensin system (RAS) and its downstream consequences by various pathophysiologic mechanisms. There may also be derangements in arachidonic acid metabolites, endothelium derived factors such as nitric oxide and carbon monoxide, and various paracrine and neural systems that normally interact with or provide a counteracting balance to the actions of the RAS. Thus, when the capacity of the kidneys to maintain sodium balance and extracellular fluid volume within appropriate ranges is compromised, increases in arterial pressure become necessary to re-establish normal balance.
Mitchell
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Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, 1430 Tulane Ave, SL 39, New Orleans, Louisiana, LA 70112, USA. kdmitch@tulane.edu
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D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002248:Carbon Monoxide / Q000502:physiology; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015777:Eicosanoids / Q000096:biosynthesis; D006418:Heme / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology*; D006977:Hypertension, Renal / Q000209:etiology; D012084:Renin-Angiotensin System / Q000502:physiology*
D016861:Cyclooxygenase Inhibitors; D015777:Eicosanoids; D000804:Angiotensin II; D006418:Heme; D002248:Carbon Monoxide; D009320:Atrial Natriuretic Factor; D006419:Heme Oxygenase (Decyclizing)