title: Interactive nitric oxide-angiotensin II influences on renal microcirculation in angiotensin II-induced hypertension.
abstract: The present study was conducted to determine the contribution of nitric oxide to angiotensin II (Ang II) reactivity of afferent and efferent arterioles from Ang II-infused hypertensive rats. Experiments were performed in vitro with the blood-perfused juxtamedullary nephron technique in kidneys harvested from hypertensive Sprague-Dawley rats (181+/-1 mm Hg) that had received 60 ng/min Ang II subcutaneously for 13 days. Superfusion with 0.1, 1, and 10 nmol/L Ang II reduced afferent arteriolar diameter (18.1+/-0.6 microm; n=12) by 10.0+/-0.7%, 28.1+/-1.7%, and 52.8+/-1.9%, respectively, and efferent arteriolar diameter (17.2+/-1.4 microm; n=8) decreased by 9.3+/-0.7%, 27.0+/-1.2%, and 50.4+/-1.6%, respectively. Nitric oxide synthase inhibition with 100 micromol/L N(omega)-nitro-L-arginine (NLA) reduced resting afferent and efferent arteriolar diameters to 14.7+/-0.4 and 14.3+/-1.2 microm, respectively, and enhanced afferent but not efferent arteriolar reactivity to Ang II. The enhanced afferent arteriolar reactivity to Ang II was eliminated by addition of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP, 10 micromol/L), which reversed the NLA-induced decrease in diameter. Addition of 10 micromol/L SNAP, without NLA, blunted efferent but not afferent arteriolar reactivity to Ang II. Afferent (n=7) and efferent arteriolar diameters (n=6) decreased by 48.5+/-2.2% and 41.0+/-1.9%, respectively, in response to 10 nmol/L Ang II. These results suggest that in this model of hypertension, maintained nitric oxide production in afferent arterioles counteracts the enhanced afferent arteriolar reactivity that occurs in Ang II-induced hypertension.
authors.affiliation: Department of Physiology, Tulane University School of Medicine, New Orleans, LA 70112, USA. ichihara@mailhost.tcs.tulane.edu
authors.forename: A
authors.initials: A
authors.lastname: Ichihara
authors.forename: J D
authors.initials: JD
authors.lastname: Imig
authors.forename: E W
authors.initials: EW
authors.lastname: Inscho
authors.forename: L G
authors.initials: LG
authors.lastname: Navar
mesh_terms: D000804:Angiotensin II / Q000008:administration & dosage; D000818:Animals; D001160:Arterioles / Q000187:drug effects* / Q000502:physiology; D003627:Data Interpretation, Statistical; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D066298:In Vitro Techniques; D007668:Kidney / Q000098:blood supply*; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D010396:Penicillamine / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; C110881:S-nitro-N-acetylpenicillamine; D000804:Angiotensin II; D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D010396:Penicillamine