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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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Non-NMDA receptor antagonist-induced drinking in rat

Glutamate has been implicated in the central control of mechanisms that maintain body fluid homeostasis. The present studies demonstrate that intracerebroventricular (i.c.v.) injections of the non-N-methyl-d-aspartate (NMDA) receptor antagonists 6, 7-dinitroquinoxaline-2,3-dione (DNQX) and 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX) induce drinking in rats. The dipsogenic effect of i.c.v. DNQX was antagonized by the non-NMDA receptor agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). The water intake induced by DNQX was also blocked by pretreatment with a NMDA receptor antagonist, MK-801, but not by angiotensin type 1 (AT1) or acetylcholine muscarinic receptor antagonists (losartan and atropine). The results indicate that non-NMDA receptors may exert a tonic inhibitory effect within brain circuits that control dipsogenic activity and that functional integrity of NMDA receptors may be required for the non-NMDA receptor antagonists to induce water intake. Copyright 1998 Published by Elsevier Science B.V.

Non-NASA Center↗

Cholecystokinin actions in the parabrachial nucleus: effects on thirst and salt appetite

The present study investigated the effects of bilateral injections of the nonselective CCK receptor antagonist proglumide or CCK-8 into the lateral parabrachial nuclei (LPBN) on the ingestion of 0.3 M NaCl and water induced by intracerebroventricular injection of ANG II or by a combined treatment with subcutaneous furosemide (Furo) + captopril (Cap). Compared with the injection of saline (vehicle), bilateral LPBN injections of proglumide (50 micrograms . 200 nl-1 . site-1) increased the intake of 0.3 M NaCl induced by intracerebroventricular ANG II (50 ng/1 microliter). Bilateral injections of proglumide into the LPBN also increased ANG II-induced water intake when NaCl was simultaneously available, but not when only water was present. Similarly, the ingestion of 0.3 M NaCl and water induced by the treatment with Furo (10 mg/kg) + Cap (5 mg/kg) was increased by bilateral LPBN proglumide pretreatment. Bilateral CCK-8 (0.5 microgram . 200 nl-1 . site-1) injections into the LPBN did not change Furo + Cap-induced 0.3 M NaCl intake but reduced water consumption. When only water was available after intracerebroventricular ANG II, bilateral LPBN injections of proglumide or CCK-8 had no effect or significantly reduced water intake compared with LPBN vehicle-treated rats. Taken together, these results suggest that CCK actions in the LPBN play a modulatory role on the control of NaCl and water intake induced by experimental treatments that induce hypovolemia and/or hypotension or that mimic those states.

Non-NASA Center↗

Effects of angiotensin, vasopressin and atrial natriuretic peptide on intraocular pressure in anesthetized rats

The effects of atrial natriuretic peptide (ANP), vasopressin (AVP) and angiotensin (ANG) on blood and intraocular pressures of pentobarbital anesthetized rats were evaluated following intravenous, intracerebroventricular or anterior chamber routes of administration. Central injections did not affect intraocular pressure. Equipressor intravenous infusions of ANG raised, whereas AVP decreased, intraocular pressure. Direct infusions of a balanced salt solution (0.175 microliter/min) raised intraocular pressure between 30 and 60 min. Adding ANG or ANP slightly reduced this solvent effect but AVP was markedly inhibitory. An AVP-V1 receptor antagonist reversed the blunting of the solvent-induced rise by the peptide, indicating receptor specificity. Acetazolamide pretreatment lowered intraocular pressure, but the solvent-induced rise in intraocular pressure and inhibition by AVP still occurred without altering the temporal pattern. Thus, these effects appear unrelated to aqueous humor synthesis rate. The data support the possibility of intraocular pressure regulation by peptides acting from the blood and aqueous humor.

NASA Discipline Number 14-10↗