title: Pursuit of roles for metabotropic glutamate receptors in the anteroventral third ventricular region in regulating vasopressin secretion and cardiovascular function in conscious rats.
abstract: This study aimed to evaluate the roles of metabotropic glutamate receptors (mGluRs) in the anteroventral third ventricular region (AV3V; a pivotal area for osmotic responses and PGE2 actions) in regulating AVP secretion and cardiovascular function. In conscious and unrestrained rats, we examined the effects of AV3V infusion of t-ACPD (an agonist for mGluRs) and 8-bromo (Br)-cAMP (an agonist for cAMP associated with mGluR action) on plasma and cardiovascular variables, and the effects of MCPG (an antagonist for mGluRs) on the responses to t-ACPD, PGE2, and hyperosmolality. AV3V infusion of t-ACPD or 8-Br-cAMP produced dose-dependent rises in plasma AVP, arterial pressure and heart rate after 5 or 15 min, without altering plasma osmolality, sodium, potassium or chloride. t-ACPD administration into the cerebral ventricle had no effects on the variables. The plasma AVP and arterial pressure responses to AV3V t-ACPD infusion were blocked by preadministration of MCPG 15 min before the infusion. MCPG treatment was also potent at inhibiting the augmentation of plasma AVP elicited by AV3V infusion of PGE2, although its pressor and tachycardiac actions were not influenced. MCPG application, however, had no effect on either the increases in plasma AVP or arterial pressure in response to the enhanced plasma osmolality induced by i.v. infusion of hypertonic saline or their stable levels during isotonic saline infusion. Histological analysis showed that the AV3V drug infusion sites were located in structures such as the median or medial preoptic nucleus and periventricular nucleus. These results suggest that AV3V mGluRs may act to potentiate AVP release and cardiovascular function when stimulated in the basal state, and may participate in the hormone secretion prompted by AV3V PGE2, despite probable negligible contributions to the mechanisms responsible for the PGE2 cardiovascular effects or the phenomenon provoked by osmotic load.
authors.affiliation: Department of Homeostatic Regulation and Development, Niigata University Graduate School of Medical and Dental Sciences, Asahimachi-Dori 1-757, Niigata City 951-8510, Japan. kenbo@med.niigata-u.ac.jp
authors.forename: Ken'ichi
authors.initials: K
authors.lastname: Yamaguchi
authors.forename: Kazuo
authors.initials: K
authors.lastname: Watanabe
mesh_terms: D000818:Animals; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D018690:Excitatory Amino Acid Agonists / Q000008:administration & dosage; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage; D007276:Injections, Intraventricular; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D018094:Receptors, Metabotropic Glutamate / Q000378:metabolism*; D020542:Third Ventricle / Q000378:metabolism*; D014667:Vasopressins / Q000378:metabolism*
chemical_list: D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018094:Receptors, Metabotropic Glutamate; D014667:Vasopressins