title: Cholesterol feeding does not alter renal hemodynamic response to acetylcholine and angiotensin II in rabbits.
abstract: Aortic ring studies have demonstrated a decrease in endothelium-dependent relaxation or an enhanced response to vasoconstrictors in rabbits fed a high-cholesterol diet. Whether such abnormalities exist in the renal circulation is unclear. The purpose of this study was to determine functional renal responses to acetylcholine (ACh) or angiotensin II (ANG II) infusion in anesthetized rabbits after 8-10 wk of either a control diet (ACh, n = 6; ANG II, n = 6) or a 1% cholesterol diet (ACh, n = 7; ANG II, n = 7). Mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR) were measured. Renal vascular resistance (RVR) was calculated as MAP/RBF. For ANG II experiments, captopril (15 microg x kg(-1) x min(-1)) was infused to suppress endogenous ANG II production. After two control clearance periods, either ACh (1 microg x kg(-1) x min(-1)) or ANG II (0.5 ng x kg(-1) x min(-1)) was infused into the renal artery; RBF was allowed to stabilize before experimental clearances. RBF increased with ACh (control: 25 +/- 2 to 39 +/- 2 ml/min; cholesterol: 26 +/- 2 to 40 +/- 3 ml/min) and decreased with ANG II infusions (control: 40 +/- 4 to 25 +/- 3 ml/min; cholesterol: 36 +/- 3 to 24 +/- 2 ml/min). Nitrate/nitrite excretion also increased with ACh infusion (control: 2.3 +/- 1.0 to 5.2 +/- 1.8 nmol x kg(-1) x min(-1); cholesterol: 2.3 +/- 0.3 to 6.0 +/- 1.3 nmol x kg(-1) x min(-1)). However, there were no significant differences between control and cholesterol groups in either response. GFR was unaltered during ACh and ANG II infusions. MAP, RVR, and urinary sodium and potassium excretion did not differ between groups in response to either drug. These results suggest that, despite significant hypercholesterolemia and large-vessel atherosclerosis, both nitric oxideinduced vasodilation and endothelium-dependent modulation of ANG II vasoconstriction in the renal circulation are unaffected by cholesterol feeding.
authors.affiliation: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
authors.forename: J F
authors.initials: JF
authors.lastname: Carroll
authors.forename: H L
authors.initials: HL
authors.lastname: Mizelle
authors.forename: K
authors.initials: K
authors.lastname: Cockrell
authors.forename: J F
authors.initials: JF
authors.lastname: Reckelhoff
authors.forename: B R
authors.initials: BR
authors.lastname: Clower
authors.forename: J P
authors.initials: JP
authors.lastname: Granger
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology / Q000187:drug effects / Q000473:pathology; D001794:Blood Pressure / Q000187:drug effects; D002791:Cholesterol, Dietary / Q000494:pharmacology*; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D006439:Hemodynamics / Q000187:drug effects*; D007668:Kidney / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D011188:Potassium / Q000652:urine; D011817:Rabbits; D012039:Regional Blood Flow / Q000187:drug effects; D012077:Renal Artery / Q000187:drug effects / Q000502:physiology*; D012079:Renal Circulation / Q000187:drug effects*; D012964:Sodium / Q000652:urine; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D002791:Cholesterol, Dietary; D000804:Angiotensin II; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium