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NO and Angiotensin II Effects on Blood Pressure andFluid Homeostasis
Author(s) -
Liu Hanwu,
Terrell Mary Lee,
Bui Vuong,
SummyLong Joan Y.,
Kadekaro Massako
Publication year - 1997
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1997.00606.x
Subject(s) - angiotensin ii , endocrinology , vasopressin , medicine , oxytocin , renin–angiotensin system , blood pressure , basal (medicine) , homeostasis , stimulation , chemistry , peptide hormone , hormone , insulin
Angiotensin II (50 ng/5 μl) and L‐NAME (250 μg/5 μl), an inhibitor of NO synthase (NOS), were administered intracerebroventricularly alone or in combination to conscious rats. Mean arterial blood pressure (MABP) increased reaching a peak within 5 min in all groups compared to controls treated with the vehicle, artificial CSF (5 μl). MABP returned to basal levels at 30 min after angiotensin II and remained stable for the following 90 min. In animals treated with L‐NAME alone, after the initial pressor response, MABP declined but began to increase progressively from 30 min until the end of the experiment at 120 min. When administered with angiotensin II, however, the initial pressor response was prolonged. Angiotensin II‐induced drinking was significantly attenuated by L‐NAME. In control rats, inhibiting NOS elevated plasma levels of oxytocin and vasopressin but in angiotensin II‐stimulated animals, only oxytocin was further elevated after L‐NAME. Thus, NO formed centrally inhibits basal secretion of oxytocin and vasopressin as well as the resting blood pressure. During stimulation with angiotensin II, NO facilitates drinking, limits the pressor response and selectively inhibits oxytocin release.