title: Renal mechanisms of angiotensin II-induced hypertension.
abstract: The kidneys play a central role in the long-term control of arterial pressure by regulating sodium balance and extracellular fluid volume. The renin-angiotensin system is important in the regulation of the arterial pressure through its chronic effects on the pressure natriuresis relationship. Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. An inability to suppress Ang II formation in response to increases in sodium intake can lead to salt-sensitive hypertension. Excess formation of Ang II, such as in renovascular hypertension, causes the pressure natriuresis relationship to be shifted to higher arterial pressures so that higher arterial pressures are necessary to maintain sodium balance. Ang II decreases pressure natriuresis by enhancing tubular reabsorption and/or reducing glomerular filtration. Because Ang II does not decrease glomerular filtration in most circumstances, the sodium retaining actions of Ang II are usually caused by increased tubular reabsorption. However, there are a number of pathophysiologic conditions where Ang II interacts with various local autocrine and paracrine factors (such as nitric oxide [NO], eicosanoids, adenosine, and superoxide) to influence glomerular filtration rate. Ang II enhances tubular reabsorption either indirectly, through aldosterone stimulation, via alterations in renal hemodynamics (physical factors or medullary blood flow), or by directly enhancing tubular sodium transport. Converting enzyme inhibitors or Ang II receptor antagonists improve pressure natriuresis and are very effective in the treatment of various forms of hypertension associated with normal or enhanced activity of the renin-angiotensin system.
authors.affiliation: Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson 39216-4505, USA.
authors.forename: J P
authors.initials: JP
authors.lastname: Granger
authors.forename: C G
authors.initials: CG
authors.lastname: Schnackenberg
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D019898:Autocrine Communication / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009318:Natriuresis / Q000502:physiology; D019899:Paracrine Communication / Q000502:physiology; D011945:Receptors, Angiotensin / Q000502:physiology; D012079:Renal Circulation / Q000502:physiology; D012084:Renin-Angiotensin System / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D011945:Receptors, Angiotensin; D000804:Angiotensin II