J. R. Goding

THE EFFECT OF ALDOSTERONE, CORTISOL, AND CORTICOSTERONE UPON THE SODIUM AND POTASSIUM CONTENT OF SHEEP'S PAROTID SALIVA*

Sodium depletion in the sheep results in a fall in parotid salivary sodium/potassium concentration ratio (Na/K) from a normal 25 to 40 (Na, 170 to 185 and K, 4 to 6 mEqper L) to as low 0.3 (Na, 40 and K, 133 mEqper L) (1, 2). Earlier work in this laboratory suggested that this reciprocal alteration in the concentration of salivary sodium and potassium was due predominantly to the simultaneous operation of 1) a fall in the salivary secretion rate and 2) an increase in the secretion of electrolyte-active adrenal steroids. If suitable allowance were made for the effects of variation in the parotid salivary secretion rate and the latency of the response, it was proposed that the salivary Na/K ratio could be used as an index of the release of electrolyte-active steroid into the circulation (2-5). Cortisol (6), corticosterone (6), and aldosterone (7-9) have been identified in sheep adrenal venous blood. In order to obtain a basis for evaluating the contribution of each of these components of the adrenal secretion to the fall in parotid salivary Na/K ratio observed during different physiological states, the effects of these steroids upon salivary Na and K were studied in a series of experiments in normal and adrenalectomized sheep.

Control of Adrenal Secretion of Electrolyte-active Steroids—I

PART I Addison (1868) in his original report records the case of a tide waiter whose disease was exacerbated when living on salt provisions which would have been pickled with nitre-that is, potassium nitrate. Loeb, Atchley, Benedict, and Leland (1933) showed that adrenalectomy caused urinary loss of Na+ and a decrease of Na+ and increase of K± in the plasma. The demonstration of Na+-retaining action by deoxycortone acetate (D.C.A.) led to a search for this or a similarly active substance in the adrenals. The discovery of aldosterone, with 25 to 120 times the activity of D.C.A., not only in extracts but in the adrenal venous blood, has led to the acceptance of it as by far the most electrolyte-active steroid (Simpson, Tait, Wettstein, Neher, von Euw, and Reichstein, 1953). It is 500 to 1,000 times more active than cortisol, and 4,000 times more active than corticosterone in causing renal Na+ retention in rats (Swingle, Maxwell, Ben, Baker, LeBrie, and Eisler, 1954; Desaulles, 1958). It is also 100 times more active than these compounds in stimulating K+ excretion. The finding that there is increased urinary excretion of aldosterone in congestive cardiac failure (Deming and Luetscher, 1950; Singer and Wener, 1953) as in other oedematous states (Chart and Shipley, 1953) has raised the question whether increased adrenal cortical activity is a contributory cause of the development of oedema. Such an inference, however, like that proposing a causal relation between intravascular or extracellular volume and aldosterone secretion (Bartter, 1956; Bartter, Biglieri, Pronove, and Delea, 1958) depends on the assumption that the rate of urinary excretion of aldosterone is proportional to the rate of adrenal secretion in all conditions, and is not determined by other factors-for example, altered renal activity or liver metabolism (Wolff, Koczorek, and Buchborn, 1958). The amount of aldosterone excreted in the urine is about 5% of the amount secreted (Ayres, Garrod, Simpson, and Tait, 1957), but studies with labelled aldosterone by Ayres, Barlow, Garrod, Kellie, Tait, Tait, and Walker (1958) suggest that this small proportion may be a valid basis for inference in the instance of simple Na+ deprivation. The understanding of the role of the adrenal cortex in a complex situation like congestive heart failure would probably be simpler if the control of aldosterone

Effect of Variations of Plasma Sodium Concentration on the Adrenal Response to Angiotensin II

The secretion rate of aldosterone was increased by infusion of valine-5-angiotensin II into the adrenal arterial blood supply of sheep. The dimensions of the increase in aldosterone output were inversely related to the control plasma concentration. This high aldosterone secretion was reduced substantially by concurrent adrenal infusion of concentrated NaCl solution which increased plasma sodium concentration by approximately 10 meq/liter. The reduction of aldosterone secretion occurred within 20 minutes. Angiotensin II infusion did not increase the secretion rates of cortisol or corticosterone. The significance of the finding that environmental sodium concentration has different effects on the aldosterone-stimulating action and the pressor action of angiotensin II is discussed.

Release of Luteinizing Hormone by Oestradiol-17β and a Gonadotrophin-Releasing Hormone in Ewes Affected with Clover Disease

Sheep grazing the oestrogenic varieties of subterranean clover ( Trifolium subterraneum L.) exhibit an irreversible loss in fertility that has been associated with changes in the mec

Effect of Progesterone on the Release of Luteinizing Hormone Induced by a Synthetic Gonadotrophin-Releasing Factor in the Ewe

A synthetic decapeptide (Gn-RH) structurally identical to ‘ovine LH-releasing hormone’ was given by intra-carotid infusions (0, 0.5 and 1.5 µ g/h for 3 h) to two groups of ewes late

THE EFFECT OF ADRENAL CORTICAL STEROIDS ON PAROTID SALIVARY SECRETION

ABSTRACT This paper records detailed observations on the effect of administered corticosteroids, particularly aldosterone, on the Na and K content of the parotid saliva of the sheep. A dose response relation between intravenous administration of physiological amounts of aldosterone and salivary Na/K ratio was demonstrated in Na replete normal and in Na deficient adrenalectomized sheep. It has been shown that infused glucocorticoids at levels similar to those maximally secreted by the sheeps adrenals have little or no effect on the parotid salivary Na/K ratio, but infused aldosterone has equivalent effect of endogenous aldosterone. A striking difference was shown between the sensitivity to aldosterone of the parotid of Na replete and Na deficient sheep. Experiments on intravenous infusion of aldosterone show that the parotid of a 30 kg Na depleted sheep may respond to as little as 1–2 μg/hr. The relevance of these findings to the physiological problems of adaptation of ruminant animals to stringent ecological conditions involving changes in feeding habits is discussed.

Luteal function in sheep with ovarian autotransplants given concurrent infusions of prolactin and prostaglandin F2α into the ovarian artery

Abstract Four experimental sheep with ovarian autotransplants were infused with prolactin (10 or 100 μg/h), into the ovarian artery, for 6 hours and then prolactin together with prostaglandin F2α (PGF2α) (5 μg/h) for a further 6 hours. A control sheep received PGF2α alone, for 6 hours on two separate occasions. Prolactin failed to overcome the luteolytic action of PGF2α in 3 of the 4 experimental sheep.