[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.