RESUMEN
Repeated sodium depletions produce a persistent, enhanced need-free salt intake in the rat, particularly in the female. The neurochemical mechanisms underlying the phenomenon are still unknown. The present studies evaluated the effect on the enhanced need-free salt intake of the female rat (1) of pharmacological interference with the natriorexigenic hormones angiotensin II and aldosterone and (2) of the central injection of the tachykinin peptides, which are endowed with antinatriorexic activity. The need-free salt intake of the female rat is not modified by treatment with the angiotensin-converting enzyme inhibitor captopril or by the aldosterone receptor antagonist RU-28318. On the other hand, the behavior is highly sensitive to the inhibitory effect of central tachykinins, suggesting the possibility that need-free salt intake might be linked to modification (down-regulation) of the inhibitory tachykininergic system.
Asunto(s)
Ingestión de Alimentos/efectos de los fármacos , Sodio en la Dieta , Taquicininas/farmacología , Aldosterona/farmacología , Angiotensina II/farmacología , Animales , Captopril/farmacología , Regulación hacia Abajo/efectos de los fármacos , Ingestión de Líquidos/efectos de los fármacos , Eledoisina/administración & dosificación , Eledoisina/farmacología , Femenino , Inyecciones Intraperitoneales , Inyecciones Intraventriculares , Kasinina/administración & dosificación , Kasinina/farmacología , Antagonistas de Receptores de Mineralocorticoides/farmacología , Ratas , Ratas Endogámicas , Receptores de Neurotransmisores/efectos de los fármacos , Receptores de Neurotransmisores/metabolismo , Receptores de Taquicininas , Espironolactona/análogos & derivados , Espironolactona/farmacología , Sacarosa , Taquicininas/administración & dosificaciónRESUMEN
The present study investigates the effect of the mammalian tachykinin neurokinin A on salt intake in the rat. Intracerebroventricular injection of neurokinin A inhibited salt intake elicited by sodium depletion, by subchronic deoxycorticosterone treatment and by adrenalectomy. It also inhibited the need-free salt intake of female rats that had been previously depleted of sodium. Since different brain mechanisms elicit salt intake in these experimental models, it is concluded that neurokinin A exerts a general antinatriorexic effect. Apparently, its inhibitory effect on salt intake is not due to malaise or competing behaviors, as shown by the fact that the doses of neurokinin A which suppress salt intake do not suppress milk intake. In comparison to the amphibian tachykinin kassinin, neurokinin A possesses a similar spectrum of antinatriorexic activities, but is markedly less potent and less effective in all the experimental models investigated. These findings suggest that activation of neurokinin A receptors cannot solely account for the potent antinatriorexic effect of kassinin and of other nonmammalian tachykinins.
Asunto(s)
Apetito/efectos de los fármacos , Ventrículos Cerebrales/fisiología , Kasinina/farmacología , Neuroquinina A/farmacología , Sodio en la Dieta , Adrenalectomía , Animales , Ventrículos Cerebrales/efectos de los fármacos , Desoxicorticosterona/farmacología , Femenino , Inyecciones Intraventriculares , Kasinina/administración & dosificación , Neuroquinina A/administración & dosificación , Ratas , Ratas Endogámicas , Valores de ReferenciaRESUMEN
In Wistar rats loaded with SC hypertonic NaCl solution kassinin produces an inhibition of cell-dehydration drinking which lasts several hours. The long duration of the effect does not depend on a renal excretion of sodium but, hypothetically, on a redistribution of electrolytes between the extra- and the intra-cellular compartments of body fluids.
