[NO-synthase inhibition induces a resistant pressor reaction during the 10-minute intravenous infusion of angiotensin-2 to narcotized rats].
With intact NO-synthase, the 10-minute intravenous infusion of angiotensin-2 evoked the escape phenomenon from its pressor action. The intravenous infusion of the same dose of angiotensin-2 with the NO-synthase blocker (NG-monomethyl-arginine) led to a stable pressor response, i.e. no escape phenomenon was observed. L-arginine restored the escape phenomenon from the pressor action of angiotensin-2 almost completely. The findings show that normal functioning of the endothelium relaxing factor (nitric oxide) generation system is significant for reduction of angiotensin-2 pressure action.
Shebeko
V I
VI
Rodionov
Iu Ia
IuIa
D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors*; D000804:Angiotensin II / Q000008:administration & dosage*; D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000031:analogs & derivatives; D001794:Blood Pressure / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D005260:Female; D007262:Infusions, Intravenous; D019001:Nitric Oxide Synthase; D010424:Pentobarbital; D051381:Rats; D013997:Time Factors; D019323:omega-N-Methylarginine
D000804:Angiotensin II; D019323:omega-N-Methylarginine; D001120:Arginine; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases; D010424:Pentobarbital