The Effect of Aldosterone, Cortisol, and Corticosterone Upon the Sodium and Potassium Content of Sheep's Parotid Saliva*

Abstract

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 mEq per L) to as low 0.3 (Na, 40 and K, 133 mEq per 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. METHODSAnimals. Eighteen crossbred Merino wethers were used in this study. All had unilateral parotid fistulae (1) and carotid loops, and 11 were bilaterally adrenalectomized (5). Of the nonadrenalectomized sheep, two * This work was supported by U. S. Public Health Service research grant H-6284 from the National Heart Institute and by the National Health and Medical Research Council of Australia, the Wool Research Trust Fund, the Anti-Cancer Council of Victoria, and the Rural Credits Fund of the Reserve Bank. A preliminary report was presented to the International Conference on Salivary Glands and Their Secretions, University of Washington, Seattle, Wash., August 27-29, 1962. had adrenal transplants (10, 11) and two had inflatable cuffs placed on the thoracic inferior vena cava (12).Diet. The animals were allowed 0.4 kg oaten chaff and 0.4 kg lucerne chaff per day with a Na content of approximately 100 mEq per day. All animals were housed in metabolism cages, and had free access to water and sodium bicarbonate solution except during Na depletion (13). Voluntary Na intake and volumes of saliva and urine were recorded daily.Initial experimental conditions. The salivary response to corticosteroids was examined in Na-replete normal and adrenalectomized animals and in adrenalectomized sheep with known Na deficit.Normal sodium balance. In this instance, the animal's voluntary Na intake was recorded daily for the 3 to 4 days before the experiment (13); 3 to 4 hours before the experiment, 200 to 300 mEq NaHCO3 was given into the rumen to ensure that the animal was Na-replete. In the adrenalectomized animals, the daily maintenance dose of 5 mg desoxycorticosterone and 25 mg cortisone acetate was last given 24 to 48 hours before the experiment. Sodium deficiency was produced by loss of parotid sa...

Transport of cations and anions across forestomach epithelia: conclusions from in vitro studies

“…When animals are Na 1 -depleted (Scott, 1966) and under stimulation by aldosterone (Blair-West et al, 1963), both the salivary and the ruminal concentration of K 1 may rise to 100 mmol/l (Kay, 1960;Blair-West et al, 1963;Scott, 1966 and1967) Under these conditions, K 1 replaces (scarce) Na 1 in saliva, and not surprisingly, perhaps, a sizable reabsorption of K 1 from the rumen can be observed. Provided that ruminal K 1 is sufficiently high, a number of in vivo and in vitro studies have shown that preintestinal regions can contribute substantially to total recirculation of K 1 in the gastrointestinal tract of ruminants.…”

Muzzle Secretion Electrolytes as a Possible Indicator of Sodium Status in Buffalo (Bubalus bubalis) Calves: Effects of Sodium Depletion and Aldosterone Administration

“…Clear evidence has now accumulated that a major factor causing a decrease in salivary Na: K ratio during salt depletion in sheep is increased secretion of aldosterone (Blair-West et al 1963, 1970a. In the present investigation, intravenous aldosterone administration in normal animals simulated the effect of sodium depletion as far as changes in saliva were concerned.…”

The Effect of Bilateral Nephrectomy and Midcollicular Decerebration with Pinealectomy and Hypophysectomy on the Corticosteroid Secretion of Sodium-deficient Sheep *

“…Furthermore, the control sodium-replete sheep submitted to the same series of ablations without exception had very low final outputs of aldosterone. In those sodiumdeficient sheep where the ablation caused a significant decrease of aldosterone secretion (e.g., Roland, Horst, and Archibald) the parotid salivary Na/K ratio rose, indicating a fall of aldosterone level in peripheral blood, whereas in those animals where the aldosterone remained high, the salivary Na/K ratio remained low, i.e., the chemical assay was consistent with this biological index of aldosterone secretion (29). \Ve are satisfied that radiochemical purity was achieved and that in the sodium-deficient animal the large aldosterone secretion assessed after these ablations was valid and not observed in the sodium-replete controls.…”

“…With Croesus (Figure 1) and Ambrose (Figure 2), aldosterone remained high after all ablations, and correspondingly salivary Na/K ratio remained low throughout. With Ambrose the ratio was very low (0.02) and near the asymptote of the dose response curve relating aldosterone infusion rate to parotid salivary Na/K ratio (29). The fall of aldosterone secretion rate observed 2 hours after decerebration was followed 2 hours later by a rise of Na/K ratio.…”

“…In these experiments there was a close correlation between the salivary Na/K ratio reflecting peripheral aldosterone level and the adrenal aldosterone secretion rate as measured directly by, the double isotope dilution method. This is provided due allowance is made for the time delay of 90 to 120 minutes for effect on the parotid, a delay attributed to the half-life of aldosterone and the 60-to 90-minute delay time of the direct response of the parotid to change of peripheral blood aldosterone concentration (20,29). Figures 1 to 6, in which salivary Na/K ratio is graphed on a logarithmic coordinate, show this relation.…”