Role of Nitric Oxide in Short-term and Prolonged Effects of Angiotensin II on Renal Hemodynamics

• DOI: 10.1161/01.hyp.27.5.1173
• Publication Date: 2012-06-12T00:53:46Z
• Authors: Xiaolin Deng; William J. Welch; Christopher S. Wi...
• Keywords: Male; Time Factors; Angiotensin II; Hemodynamics; Arginine; Nitric Oxide; Acetylcholine; Rats; Renal Circulation; 3. Good health; Rats, Sprague-Dawley; Vasodilation; 03 medical and health sciences; NG-Nitroarginine Methyl Ester; 0302 clinical medicine; Animals; Vascular Resistance; Nitric Oxide Synthase

Abstract Short-term infusions of angiotensin II (Ang II) increase renal vascular resistance and thereby endothelial shear stress nitric oxide (NO) release. Prolonged stimulation Ang can decrease the expression NO synthase isoforms in macula densa, but prolonged increases transcription synthase. Therefore, we designed these studies to test hypothesis that exerts time-dependent effects on generation as assessed from excretion nitrate nitrite, percent during inhibition with intravenous N G -nitro- l -arginine methyl ester (L-NAME), or decreases acetylcholine. Rats were tested graded short-term (30 90 minutes intravenous) (5 6 days subcutaneous) led dose-dependent blood pressure reductions flow. Captopril was administered for 3 4 suppress generation. The nitrite increased (from 205±22 331±58 pmol·min −1 , P <.05) unchanged infusion (control group, 197±33 versus II, 245±42 =NS). L-NAME potentiated dose dependently by not long-term infusions. control rats without +150±13%. At an 200 ng·kg ·min L-NAME–induced significantly ( <.01) compared controls II–infused (+369±70%) different infused (+190±33%). Intravenous acetylcholine caused vasodilation changed receiving <.005) those (change at 10 μg·kg control, −21.5±5.0%; −24.9±4.5%; −52.1±7.2%). In conclusion, short- equivalent changes flow hence presumably stress. However, only dependence circulation NO, whereas acetylcholine-induced release enhanced selectively This suggests may become uncoupled yet remains highly responsive receptor-mediated stimulation.