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Central cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst) and are ineffective in inducing the intake of hypertonic saline solutions (i.e., the operational definition of sodium appetite). Recent studies have indicated that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic activation with carbachol (an experimental condition where only water is typically ingested) after the blockade of LPBN serotonergic mechanisms with methysergide treatment in rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4 nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of methysergide (4 microg), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by intracerebroventricular carbachol was not changed by LPBN methysergide injections. The results indicate that central cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the LPBN are attenuated.

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Glutamatergic mechanisms have been implicated in the control of fluid ingestion. In the present study, we investigated whether non-N-methyl-D-aspartate (NMDA) glutamatergic receptors in the lateral parabrachial nucleus (LPBN) are involved in the control of water and sodium intake. Male Sprague-Dawley rats had cannulas implanted bilaterally into the LPBN. They were acutely depleted of water and sodium by injections of the diuretic furosemide (Furo; 10 mg/kg, bw) and given a low dose of the angiotensin-converting enzyme inhibitor, captopril (Cap; 5 mg/kg, bw). Bilateral LPBN injections of the non-NMDA receptor antagonist DNQX (2 and 5 nmol/0.2 µl) increased the ingestion of 0.3 M NaCl and water of Furo/Cap treated rats. The increased ingestion produced by DNQX was abolished by pretreating the LPBN with α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), a non-NMDA receptor agonist. AMPA injected alone into the LPBN reduced water and 0.3 M NaCl intake. Injections of DNQX (5 nmol/0.2 µl) into the LPBN also produced ingestion of 0.3 M NaCl after sc injections of the β-adrenoceptor agonist, isoproterenol, a hypotensive drug that typically produces only water intake. Food intake, arterial blood pressure and heart rate were not altered by DNQX LPBN injections. We conclude that agonists acting on non-NMDA receptors in the LPBN exert an inhibitory influence on sodium intake during acute fluid depletion with hypotension and after isoproterenol treatment. A possible interaction of serotonin with glutamate within the LPBN is discussed. Keywordsglutamate; α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA); fluid and electrolyte balance; sodium appetite/intake; thirst

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The inflation of an intravascular balloon positioned at the superior vena cava and right atrial junction (SVC-RAJ) reduces sodium or water intake induced by various experimental procedures (e.g. sodium depletion; hypovolaemia). In the present study we investigated if the stretch induced by a balloon at this site inhibits a rapid onset salt appetite, and if this procedure modifies the pattern of immunohistochemical labelling for Fos protein (Fos-ir) in the brain. Male Sprague-Dawley rats with SVC-RAJ balloons received a combined treatment of furosemide (Furo; 10 mg (kg bw) −1 ) plus a low dose of the angiotensin-converting enzyme inhibitor captopril (Cap; 5 mg (kg bw) −1 ). Balloon inflation greatly decreased the intake of 0.3 m NaCl for as long as the balloon was inflated. Balloon inflation over a 3 h period following Furo-Cap treatment decreased Fos-ir in the organum vasculosum of the lamina terminalis and the subfornical organ and increased Fos-ir in the lateral parabrachial nucleus and caudal ventrolateral medulla. The effect of balloon inflation was specific for sodium intake because it did not affect the drinking of diluted sweetened condensed milk. Balloon inflation and deflation also did not acutely change mean arterial pressure. These results suggest that activity in forebrain circumventricular organs and in hindbrain putative body fluid/cardiovascular regulatory regions is affected by loading low pressure mechanoreceptors at the SVC-RAJ, a manipulation that also attenuates salt appetite.

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