Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats.
OBJECTIVE
To examine local actions of nitric oxide (NO) on the neural mechanisms controlling the release of vasopressin (AVP) and the cardiovascular system in the anteroventral third ventricular region (AV3V), a pivotal area for autonomic functions, and to pursue the problem of whether it may have any role in the AVP and cardiovascular responses evoked by plasma hypertonicity or by increased prostaglandin E(2) (PGE(2)) in the AV3V - one possible factor implicated in osmotic responses.


METHODS
We infused NO-related agents into the AV3V, its adjacent area, the nucleus of the vertical limb of the diagonal band (VDB), or into the lateral cerebral ventricle of conscious rats, monitoring effects on plasma AVP, osmolality, sodium, potassium and chloride, arterial pressure and heart rate in the presence or absence of an osmotic or PGE(2) stimulus. The infusion sites were determined histologically.


RESULTS
Infusion of L-arginine, the substrate of NO synthase (NOS), into the AV3V structures such as the median preoptic nucleus and periventricular nucleus produced dose-related increases in plasma AVP, arterial pressure and heart rate 5 or 15 min later, whereas infusion of D-arginine (which is not a substrate for NO synthesis) was without significant effect on these variables. Plasma osmolality or electrolytes were not changed by these treatments. The AV3V infusion of sodium nitroprusside (SNP), a spontaneous releaser of NO, also induced dose-dependent augmentations of plasma AVP, without evoking remarkable alteration in the cardiovascular parameters. The infusion of L- or D-arginine into the VDB affected none of the variables significantly. When applied intracerebroventricularly, L-arginine caused only increases in plasma AVP, whereas SNP caused only reductions in arterial pressure, leaving other variables at stable values. The effects of AV3V L-arginine on plasma AVP and the cardiovascular variables were abolished by N(G)-nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NOS, applied 15 min before. In contrast, infusion of L-NAME to the AV3V did not exert a significant effect on the responses of plasma AVP or cardiovascular variables to AV3V application of PGE(2) or i.v. infusion of hypertonic NaCl. The infusion of L-NAME alone did not affect plasma variables including AVP, although it tended to increase basal arterial pressure and heart rate.


CONCLUSIONS
These results suggest that NO generated in or near the AV3V may act to enhance AVP release, arterial pressure and heart rate, but it may not play an essential role in eliciting the responses of these variables to osmotic or PGE(2) stimuli.
Yamaguchi
K
K
Department of Physiology, Niigata University School of Medicine, Niigata, Japan.
Watanabe
K
K
Yamaya
K
K
D000818:Animals; D001120:Arginine / Q000008:administration & dosage / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002552:Cerebral Ventricles / Q000378:metabolism*; D015232:Dinoprostone / Q000097:blood; D004573:Electrolytes / Q000097:blood; D004791:Enzyme Inhibitors / Q000008:administration & dosage / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000502:physiology; D007276:Injections, Intraventricular; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000008:administration & dosage / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052248:Nitric Oxide Synthase Type I; D051381:Rats; D017208:Rats, Wistar; D014667:Vasopressins / Q000378:metabolism*; D014882:Water-Electrolyte Balance / Q000502:physiology
D004573:Electrolytes; D004791:Enzyme Inhibitors; D014667:Vasopressins; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496322:Nos1 protein, rat; D015232:Dinoprostone; D019331:NG-Nitroarginine Methyl Ester