Involvement of anteroventral third ventricular AMPA/kainate receptors in both hyperosmotic and hypovolemic AVP secretion in conscious rats.
The area of the brain called the anteroventral third ventricular region (AV3V) includes three different subtypes of glutamate receptor, as well as neural circuits controlling fluid balance and cardiovascular and neuroendocrine functions. Although our previous data indicate the ability of AV3V N-methyl-d-aspartate (NMDA) and metabotropic receptors to provoke vasopressin (AVP)-releasing, pressor and hyperglycemic responses, the roles of non-NMDA receptors selective for alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainate have not been elucidated to date. To address this question, the effects of intracerebral infusion with FWD or NBQX (specific agonist and antagonist for non-NMDA receptors, respectively) on plasma AVP, glucose, osmolality, electrolytes and cardiovascular parameters were examined in conscious rats in the absence or presence of an osmotic or volemic stimulus. When applied topically to AV3V structures such as the median preoptic nucleus, FWD augmented plasma AVP, osmolality, glucose and arterial pressure in a dose-associated fashion. All responses of the variables were abolished by pre-administering NBQX, which exerted no conspicuous effect on any variable except arterial pressure. It was revealed that NBQX administration in AV3V structures such as the median preoptic nucleus and the periventricular nucleus inhibited the rise of plasma AVP in response to intravenous infusion with hypertonic saline or removal of systemic blood through the femoral artery. Elevation of plasma osmolality and sodium evoked by osmotic load, and elevation of plasma osmolality, glucose and angiotensin II and decrease of arterial pressure caused by bleeding, were not significantly affected by NBQX treatment. These results suggest that AV3V non-NMDA receptors, as well as NMDA receptors, may elicit AVP-releasing, pressor and hyperglycemic actions when stimulated in the basal state, and may facilitate AVP secretion under both hyperosmotic and hypovolemic conditions, without contributing to cardiovascular, blood glucose or other responses.
Yamaguchi
Ken'ichi
K
Department of Homeostatic Regulation and Development, Niigata University Graduate School of Medical and Dental Sciences, Asahimachi-Dori 1-757, Niigata City, Niigata Prefecture 951-8510, Japan. kenbo@med.niigata-u.ac.jp
Yamada
Takaho
T
D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood* / Q000378:metabolism; D001786:Blood Glucose / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D006943:Hyperglycemia / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D007031:Hypothalamus / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D020896:Hypovolemia / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009994:Osmolar Concentration; D011301:Preoptic Area / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D012462:Saline Solution, Hypertonic / Q000494:pharmacology; D020542:Third Ventricle / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology*
D001786:Blood Glucose; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D012462:Saline Solution, Hypertonic; D001127:Arginine Vasopressin