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Weisinger, R. S., J. R. Blair-West, P. Burns, D. A. Denton, and B. Purcell. Cerebral Na concentration, Na appetite and thirst of sheep: influence of somatostatin and losartan. Am J Physiol Regulatory Integrative Comp Physiol 280: R686-R694, 2001.--Na and water intakes of Na-depleted sheep are influenced by changes in cerebral Na concentration. The effect of intracerebroventricular infusion of somatostatin or losartan, the ANG II type 1 receptor antagonist, on the Na appetite and thirst of Na-depleted sheep during infusions that decrease (intracerebroventricular hypertonic mannitol) or increase (intracerebroventricular or systemic hypertonic NaCl) cerebral Na concentration was investigated. Na intake was increased but water intake was unchanged during intracerebroventricular infusion of hypertonic mannitol. The increased Na appetite caused by intracerebroventricular infusion of hypertonic mannitol was decreased by concurrent intracerebroventricular infusion of either somatostatin or losartan, with somatostatin being most effective. Water intake was increased during intracerebroventricular infusion of hypertonic mannitol and somatostatin. Na intake was decreased and water intake was increased during systemic or intracerebroventricular infusion of hypertonic NaCl. Intracerebroventricular infusion of losartan blocked both (Na and water intake), whereas somatostatin did not influence either of these changes in intake. The results further consolidate a role for somatostatin and ANG II in the central mechanisms controlling Na appetite and thirst of sheep. angiotensin II; sodium intake; water intake

Stress is a large stimulus of Na appetite in rabbits, rats, and mice. This study investigated the influence of some peptides implicated in stress, i.e., adrenocorticotropin (ACTH), corticotropin-releasing factor (CRF), and the recently discovered member of the CRF family, urocortin, on the ingestive behavior of sheep. Intracerebroventricular infusion of these peptides over 4 days decreased the need-free Na intake of Na-repleted sheep. Intracerebroventricular infusion of urocortin, however, did not alter Na intake of Na-depleted sheep. Systemic infusion of ACTH increased, whereas systemic infusion of either urocortin or CRF decreased, Na intake of Na-repleted sheep. The increase in Na intake caused by the peripheral infusion of ACTH was blocked by concurrent i.v. infusion of urocortin, substantiating the inhibitory role of this peptide on Na appetite. Central administration of all peptides and i.v. administration of urocortin or urocortin and ACTH combined decreased food intake. Water intake was not directly influenced by the peptides. Rather, decreased water intake, when observed, was secondary to decreased food intake, as determined by pair-feeding experiments. Whereas systemic infusion of ACTH mimics the increase in Na intake observed in several different stressful situations, CRF and urocortin actually inhibit Na intake, indicating a direct central action overriding any effect of these peptides on ACTH release. Indeed, the inhibition of Na intake by urocortin occurred despite its stimulation of ACTH release and the subsequent increase in peripheral level of cortisol. Thus it would appear that hormones associated with stress have both excitatory and inhibitory influences on Na intake. Presumably, other physiological processes entrained by stress also will be important in determining the quantitative outcome on Na appetite.

Denton, D. A., J. R. Blair-West, M. I. McBurnie, J. A. P. Miller, R. S. Weisinger, and R. M. Williams. Effect of adrenocorticotrophic hormone on sodium appetite in mice. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R1033-R1040, 1999.--A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 [micro]g/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion of ACTH (20 ng/ day) had no effect. Intracerebroventricular infusion of ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress. corticotrophin releasing factor; captopril; immobilization; stress; sodium intake; water intake

Cites a study conducted by researchers in Australia which examines the pressor effect of angiotensin II in pregnant sheep. Decrease of the pressor response to intravenous angiotensin; Factors that contributed to pregnancy and sodium deficiency; Measurement of the systolic blood pressure from a mercury manometer.

This article reports that several monovalent cations have been shown to influence aldosterone secretion by a direct action on the adrenal cortex. Adrenal arteroid infusion of KCI or a local reduction of sodium concentration in adrenal arterial plasma cause an increase of aldosterone secretion in the conscious sheep. Caesium and rubidium have been shown to increase aldosterone production in vivo and in vitro. Variation of dietary intake of magnesium or variation of plasma level of calcium due to disease, infusion of calcium or chelating agents affect renal excretion of sodium and potassium.

This article studies the effect of nephrectomy on aldosterone secretion in the conscious sodium-depleted hypophysectomized sheep. The possibility emerged that in these animals under acute experimental conditions some factor other than the pituitary, the kidney and plasma electrolytes was operative in sustaining aldosterone hyperseeretion. The studies reported in this article were designed to examine the effect of nephrectomy on aldosterone secretion when the animals were conscious and maintained under conditions as nearly normal as was feasible.

This article presents information regarding the role of circulating fluid volume and related physiological parameters in the control of aldosterone secretion. The precise role of the volume of the circulating blood in the control of aldosterone secretion remains obscure. Early studies, based on urinary aldosterone excretion, suggested existence of a definite relationship between these variables, but the subsequent observations that the hypersecretion of aldosterone due to hemorrhage and thoracic inferior caval constriction was not usually reversed by correction of the circulating blood volume, together with the presence of normal or increased blood volume in many clinical states of hyperaldosteronism, have led to a situation which is confused and in need of reappraisal.

The article presents information on the effect of angiotensin II on the sensitivity of the parotid gland of the sheep to aldosterone. The sensitivity of the parotid gland to DOCA or aldosterone is increased in sodium deficiency. Under these circumstances there is a reduction of the threshold dose for an effect upon sodium und potassium concentration of parotid saliva, and the magnitude of the change in concentration is greater for a given dose. It was postulated that the increase in sensitivity was due to ionic changes within the parotid cells or humoral factors acting on the parotid gland.

The pressor effect of intravenous infusion of antiotensin II in sheep was greatly reduced by sodium deficiency. There was a similar reduction in the pressor effect of Neosynephrine, Aramine and adrenaline. The significance of this finding is discussed in the light of the proposition that angiotensin His the aldosterone stimulating hormone. In sodium depletion catecholamines in low doses produced cardiac dysrhythmias. [ABSTRACT FROM AUTHOR]