title: Hypertension and impaired renal angiotensin II response in rats after chronic neuronal nitric oxide synthase inhibition.
abstract: Nitric oxide (NO) produced by the macula densa cells is important for the control of tubuloglomerular feedback (TGF). Reduced production of NO by these cells activates TGF and could result in hypertension, although the TGF activity is then normalized in the hypertensive state. The normalization of TGF in this form of hypertension might be explained by an impaired ability of angiotensin II to constrict renal vessels or by up-regulation of some other vasodilator not affected by NO synthase inhibitors.
authors.affiliation: Department of Physiology and Biophysics, Uppsala University, Sweden.
authors.forename: A E
authors.initials: AE
authors.lastname: Persson
authors.forename: A
authors.initials: A
authors.lastname: Ollerstam
authors.forename: M
authors.initials: M
authors.lastname: Salomonsson
authors.forename: C
authors.initials: C
authors.lastname: Thorup
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D004791:Enzyme Inhibitors / Q000378:metabolism; D006977:Hypertension, Renal / Q000201:enzymology* / Q000503:physiopathology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D052248:Nitric Oxide Synthase Type I; D051381:Rats
chemical_list: D004791:Enzyme Inhibitors; D000804:Angiotensin II; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat