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Biomedical subjects

J E Sealey

Publications and source records attributed to J E Sealey.

At least 163 records · Page 9Linked to original sources
PubMed1972

Angiotensin II vascular receptors: their avidity in relationship to sodium balance, the autonomic nervous system, and hypertension.

During intravenous administration of varying doses of angiotensin II antibody to anesthetized rats, apparently specific vascular receptors were characterized. These receptors compete with administered antibody to bind circulating angiotensin. This competitive phenomenon was used to evaluate the affinity of these receptors for angiotensin. Apparent vascular receptor affinity was defined by the amount of antibody required to block the blood pressure response to exogenous angiotensin. It was found that this receptor affinity varies directly with sodium intake so that the amount of antibody required to block was eightfold greater in normal animals on a high sodium intake, as compared with those on a low sodium intake. Sodium dependence of receptors was also demonstrated in nephrectomized animals, in desoxycorticosterone (DOC)-treated rats, and in chronic renal hypertension. Thus the observed changes in receptor affinity were usually inversely related to measured endogenous angiotensin II levels. Ganglionic blockade increased antibody requirement eightfold. All of these changes were consistent, with no overlap observed in response of individual animals from different groups. These results may explain the variation in pressor activity of angiotensin associated with changes in salt balance and ganglionic blockade. In general, when sufficient antibody was injected to block the effect of exogenous angiotensin a blood pressure lowering effect was also observed. Two exceptions were the nephrectomized and the one-kidney renal hypertensive animals, in both of which antibody administration had no effect on blood pressure. Additional results suggest that changes in receptor affinity are involved in the pathogenesis of various types of experimental hypertensions because the amount of antibody required to block angiotensin was enhanced in renal (twofold), DOC (fourfold), and genetic (fourfold) hypertension. Accordingly, changes in the affinity of these receptors could be critically involved in normal blood pressure control and in various forms of experimental and clinical hypertension, even when circulating angiotensin II levels are normal.

Angiotensin II↗
PubMed1971

Hypertension of renal origin: evidence for two different mechanisms.

Antibody to angiotensin 11, or a specific peptide competitive inhibitor of angiolensin II, was used to investigate the role of the renin-angiotensin system in two types of renal hypertension in rats. The data indicate that angiotensin II is in fact critically involved in the pathogenesis of the form of renal hypertension in which one renal artery is clamped and the contralateral kidney is left in place, but that it probably plays no significant role in the maintenance of experimental renal hypertension in which the opposite kidney has been removed.

Angiotensin II↗
PubMed1970

Potassium balance and the control of renin secretion.

Plasma renin activity and renin substrate were measured in nine groups of rats which were maintained for 7 wk on diets in which the proportions of sodium and potassium were varied. Balance data indicated that the highest dietary intake of potassium employed (92 mEq K(+)/100 g food) consistently induced sodium depletion. With less consistency, the highest sodium intake employed (52 mEq Na(+)/100 g food) tended to induce potassium depletion.In accordance with previous reports, sodium deprivation induced significant increases in plasma renin activity. But the present results indicated that changes in potassium intake exerted a highly significant modulating influence on this characteristic response. The results describe an inverse relationship between potassium administration and the concurrent level of plasma renin activity. The highest serum renin levels of all occurred in the potassium-depleted animals and the usual renin response to sodium deprivation was virtually abolished in the presence of a high potassium diet. Neither the suppressing effect of K(+) administration nor the stimulating effect of K(+) depletion on plasma renin activity could be explained in terms of any predicted changes in aldosterone secretion or observed changes in sodium balance. Therefore, the effect seems to be mediated by a direct influence of potassium ions on renal renin secretion, perhaps via induced changes in sodium load to the macula densa.These studies point to an important role for potassium in the regulation of renin secretion. The results in turn raise the possibility that renin secretion per se may be importantly involved in effecting potassium conservation and potassium elimination. The means by which these interactions are finally mediated remain to be clarified.

Aldosterone↗
PubMed1970

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects.

The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen. Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion. The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis. In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure. The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance. These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an intrarenal action of potassium ions to modify renin release. Potassium might modify renin secretion directly by acting on the juxtaglomerular cells or by a change in its tubular reabsorption or secretion. The effects of potassium ions on renin secretion might also be mediated indirectly via an induced change in tubular sodium transport.

Adult↗
PubMed1969

Natriuretic activity in plasma and urine of salt-loaded man and sheep.

The present study was designed to examine the question of whether or not there is a natriuretic hormonal substance involved in the renal regulation of sodium balance. For this purpose, procedures for concentration and fractionation of plasma and urine samples and a sensitive bioassay for demonstrating changes in renal sodium excretion were developed. The natriuretic assay utilized rats with mild diabetes insipidus which were maintained in salt and water balance. Using these approaches a natriuretic humoral substance was demonstrated in plasma and urine from normal man and sheep, and in patients with primary aldosteronism or essential hypertension. It seems likely that this substance participates in day to day regulation of sodium balance because it was not detectable in sodium-depleted subjects and it consistently appeared in the sodium-loaded subjects. The hormonal agent may not act immediately and its activity can be apparent for up to 3 hr. Full expression of its activity requires that the assay animals be appropriately volume expanded. This suggests that the increases in sodium excretion mediated by this hormonal substance depend in part on the coparticipation of other physical and perhaps humoral factors. This natriuretic substance appears to be of large molecular weight or carried by a large molecule. The data suggest that it acts, at least in part, to block sodium reabsorption in a more distal portion of the tubule.

Adult↗