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

Effect of inhibition of nitric oxide synthesis on vasopressin secretio n 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 pit uitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chr onically prepared rabbits to determine the effect of NO synthesis inhi bition with N-G-nitro-L-arginine methyl ester hydrochloride (L-NAME) o n basal vasopressin secretion and vasopressin responses to increased p lasma osmolality (hypertonic saline infusion; P-osm) and decreased blo od pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg(-1).m in(-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 mo smol/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 altere d by pretreatment with L-NAME. Nitroprusside infusion decreased MAP [8 3.9 +/- 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 p rovide evidence that NO participates in regulation of basal vasopressi n release but not in vasopressin responses to hyperosmolality and hypo tension.