title: Influence of angiotensin II on pressure natriuresis and renal hemodynamics in volume-expanded rats.
abstract: This study examined whether angiotensin II (ANG II) influences the pressure-natriuretic (PN) response by altering renal cortical or medullary hemodynamics. Studies were performed in Inactin-anesthetized rats that were acutely volume expanded to maintain plasma renin activity and ANG II levels in the physiological range. Neural influences on the kidney were eliminated by renal denervation, and plasma levels of norepinephrine, vasopressin, cortisol, and aldosterone were fixed by intravenous infusion. In control rats (n = 8), sodium excretion increased from 3 to 17 microeq.min-1.g kidney wt-1 as renal perfusion pressure (RPP) was elevated from 96 to 141 mmHg (n = 8). Captopril (2 mg/kg, n = 9) reduced plasma levels of ANG II from 48 +/- 5 to 18 +/- 2 pg/ml, but it did not alter the PN relationship. Infusion of ANG II (20 ng.kg-1.min-1, n = 9) increased plasma levels of ANG II to 232 +/- 42 pg/ml and shifted the PN relationship to the right by 14 mmHg. Captopril increased renal blood flow, and infusion of ANG II returned it to control. Captopril had no effect on glomerular filtration rate (GFR) or glomerular capillary pressure (Pglom); however, subsequent ANG II infusion decreased Pglom from 56 +/- 2 to 48 +/- 2 mmHg and reduced GFR by 30%. Neither captopril nor ANG II altered papillary bloodflow or vasa recta capillary pressure at normal levels of RPP. These results indicate that the shift of the PN relationship during infusion of ANG II is due to a decrease in filtered load and enhanced tubular reabsorption of sodium. Acute blockade of the renin-angiotensin system had little effect on the PN response in volume-expanded rats despite affecting renal hemodynamics, because either the plasma and/or intrarenal levels of ANG II were already suppressed below those needed to influence tubular function or volume expansion inhibits tubular reabsorption in the nephron segments normally influenced by ANG II.
authors.affiliation: Department of Physiology, Medical College of Wisconsin 53226.
authors.forename: D L
authors.initials: DL
authors.lastname: Mattson
authors.forename: H
authors.initials: H
authors.lastname: Raff
authors.forename: R J
authors.initials: RJ
authors.lastname: Roman
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000494:pharmacology* / Q000502:physiology; D000818:Animals; D002216:Captopril / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D006854:Hydrocortisone / Q000097:blood; D006874:Hydrostatic Pressure; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D007672:Kidney Cortex / Q000187:drug effects / Q000502:physiology; D007679:Kidney Medulla / Q000187:drug effects / Q000502:physiology; D008297:Male; D009318:Natriuresis / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects; D014667:Vasopressins / Q000097:blood
chemical_list: D014667:Vasopressins; D000804:Angiotensin II; D000450:Aldosterone; D002216:Captopril; D006854:Hydrocortisone; D009638:Norepinephrine