title: Does whole body autoregulation mediate the hemodynamic responses to increased dietary salt in rats with clamped ANG II?
abstract: The present study was conducted to test the hypothesis that salt-dependent hypertension, in rats with an unresponsive renin-angiotensin system, is characterized by a "whole body autoregulation" hemodynamic profile. To test this hypothesis, rats were chronically instrumented to continuously measure cardiac output (CO) and arterial pressure (AP). A venous catheter was implanted for infusion of saline vehicle (Veh; n = 8) or treatment [enalapril (2 mg.kg-1.day-1) plus ANG II: ANG-NORM (5 ng.kg-1.min-1 ANG II, n = 8) or ANG-HI (10 ng.kg-1.min-1 ANG II, n = 9)] to pharmacologically clamp plasma ANG II. After a 10-day recovery period on a 0.1% NaCl diet, AP and CO were measured continuously for 5 days of control (0.1% NaCl), 7 days of high salt (4.0% NaCl), and 5 days of recovery (0.1% NaCl). Hemodynamics did not change in the Veh group at any time. AP increased by approximately 20 mmHg in the ANG-NORM and ANG-HI groups when NaCl was increased. Hypertension was mediated by an increase in CO of approximately 12% at steady state, with no change in total peripheral resistance (TPR) during the high salt period. AP returned to control levels when dietary sodium was decreased, mediated by a approximately 10% decrease in TPR, with CO remaining elevated. There was no difference in the hemodynamic responses to increased salt between the ANG-HI and ANG-NORM groups. We conclude that the whole body autoregulation hypothesis does not explain the hemodynamic profile of salt-dependent hypertension in rats with an unresponsive renin-angiotensin system.
authors.affiliation: Department of Physiology, University of Minnesota, Minneapolis, MN 55455, USA.
authors.forename: Deborah M
authors.initials: DM
authors.lastname: Fine
authors.forename: Pilar
authors.initials: P
authors.lastname: Ariza-Nieto
authors.forename: John W
authors.initials: JW
authors.lastname: Osborn
mesh_terms: D000804:Angiotensin II / Q000097:blood / Q000494:pharmacology*; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D004656:Enalapril / Q000494:pharmacology; D006706:Homeostasis / Q000502:physiology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000502:physiology; D017673:Sodium Chloride, Dietary / Q000494:pharmacology*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000097:blood / Q000494:pharmacology*
chemical_list: D000959:Antihypertensive Agents; D017673:Sodium Chloride, Dietary; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D004656:Enalapril