EFFECT OF INHIBITION OF NITRIC-OXIDE SYNTHESIS ON VASOPRESSIN SECRETION IN CONSCIOUS RABBITS

Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits. Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H822-H828, 1994. - NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with N-G-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P-osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg(-1).min(-1) iv) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml(-).2 h(-1) (P < 0.001)], and increased plasma vasopressin-concentration [P-AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P-osm did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml(-1).2 h(-1) (P < 0.01)], increased P-osm [284 +/- 1 to 305 +/- 2 mosmol/kgH(2)O (P < 0.001)], and increased P-AVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)]. These responses were not significantly altered by pretreatment with L-NAME. Nitroprusside infusion decreased MAP [83.9 +/- 2.2 to 57.4 +/- 2.5 mmHg (P < 0.01)], increased HR [216 +/- 9 to 323 +/- 11 beats/min (P < 0.01)], increased PRA [4.9 +/- 1.1 to 26.7 +/- 2.9 ng.ml(-1) 2 h(-1) (P < 0.01)], and increased P-AVP [2.9 +/- 0.4 to 16.4 +/- 4.9 pg/ml (P < 0.05)]. Again, none of these responses was significantly altered by pretreatment with L-NAME. These results provide evidence that NO participates in regulation of basal vasopressin release but not in vasopressin responses to hyperosmolality and hypotension.