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Biomedical subjects

S Y Tan

Publications and source records attributed to S Y Tan.

At least 145 records · Page 8Linked to original sources
PubMed1980

Prostaglandin stimulation of renin release: independence of beta-adrenergic receptor activity and possible mechanism of action.

Using a continuous superfusion system of rat kidney cortical slices, we investigated the renin-releasing effect of prostaglandin E2 (PGE2) and its possible mechanism of action. PGE2 caused significant stimulation of renin release in a dose-dependent fashion at concentrations of 3 x 10(-6) to 10(-4) M. Isoproterenol (8 x 10(-7) M) stimulated renin release significantly, and its effect was completely abolished by propranolol (2 x 10(-5) M). PGE2-stimulated renin release was not blocked by the same dose of propranolol. Dibutyryl cAMP caused a dose-dependent increase in renin release at concentrations of 10(-5) to 5 x 10(-3) M. Theophylline (4 x 10(-3) M) had no effect on renin release, but when added to subthreshold doses of PGE2 (10(-6) M), it stimulated renin release significantly. The simultaneous addition of maximal stimulating doses of PGE2 and dibutyryl cAMP had no additive or synergistic effects. These experiments show that PGE2 causes stimulation of renin release by a direct effect on the JG cell. The renin-releasing effect of PGE2 does not depend upon the beta-adrenergic receptors but may be mediated through cAMP.

Animals↗
PubMed1980

Inactive renin and prostaglandin E2 production in hyporeninemic hypoaldosteronism.

To ascertain whether inactive renin (IR) might predominate in the syndrome of hyporeninemic hypoaldosteronism (HH) and whether the production of prostaglandin E2 (PGE2), a potent stimulus for renin release, might be decreased, we measured PRA, active renin (AR), and IR by the acid activation method and urinary PGE2 in 10 patients with HH. In contrast to uniformly low levels of PRA (0.6 +/- 0.2 ng/ml . h) and AR (2.7 +/- 0.6), IR was either normal or elevated (14.7 +/- 2.2 in HH; 11.8 +/- 1.1 in 28 normal subjects) and the IR to AR ratio was markedly increased (8.5 +/- 2.0 vs. 3.4 +/- 0.5; P < 0.05). Urinary PGE2 was decreased in 4 patients but was in the normal range in 5 other patients with HH. In 16 human volunteers, PG inhibition with indomethacin led to a significant decrease in AR (P < 0.05) but not in IR, and the IR to AR ratio increased 2-fold (P < 0.02). The data suggest that HH is a disease involving the defective conversion of IR to AR rather than impaired total renin production. In some patients, PG deficiency may contribute to the development of HH.

Aldosterone↗
PubMed1979

Reversible acute renal failure induced by indomethacin.

Acute renal failure occurred during indomethacin therapy in a patient with chronic pyelonephritis. Urinary prostaglandin E2 levels were diminished but returned to normal after discontinuation of drug therapy and recovery of renal function. Prostaglandins may be critical for the integrity of renal function, and the use of prostaglandin inhibitors such as indomethacin and other nonsteroidal anti-inflammatory drugs may be deleterious in patients with underlying renal disease.

Acute Kidney Injury↗
PubMed1979

Influence of angiotensins (I, II, & III), bradykinin and arachidonic acid on renomedullary PGE production in vitro.

Renomedullary tissue from rabbit or rat was incubated with angiotensin I, II, III, arachidonic acid, bradykinin, indomethacin and meclofenamate to study their effect on PGE2 production. Arachidonic acid and bradykinin enhanced PGE2 production significantly. Indomethacin and meclofenamate inhibited PGE2 production by more than 70%. Angiotensin I, II and III did not influence PGE2 production. These results suggest that bradykinin and arachidonic acid stimulate PGE2 production by a direct cellular action whereas the angiotensins do not.

Angiotensin I↗
PubMed1979

Liddle syndrome.

Explore the source record for details and available documents.

Child, Preschool↗
PubMed1979

Low renin essential hypertension: failure to demonstrate excess 11-deoxycorticosterone production.

11-Deoxycorticosterone (DOC) was determined by specific RIA in 27 normal subjects and in 25 normal renin and 23 low renin hypertensives. None of the patients exhibited unprovoked hypokalemia. Strict criteria were employed for renin profiling the hypertensive patients, including age matching, exclusion of diabetics, and the use of medications known to interfere with the renin response or with DOC measurements. In all 3 groups, comparable DOC levels were found in plasma and urine. In contrast, DOC was elevated in 7 of 19 patients with primary aldosteronism. These results do not support a DOC excess hypothesis for the syndrome of low renin essential hypertension.

Adult↗
PubMed1979

Indomethacin-induced prostaglandin inhibition with hyperkalemia. A reversible cause of hyporeninemic hypoaldosteronism.

Hyporeninemic hypoaldosteronism was diagnosed in a young woman with glomerulonephritis who was receiving indomethacin therapy. Despite only mildly abnormal renal function, serum K+ was elevated to 6.2 meq/L, and plasma renin activity (0.12 ng/mL h) and aldosterone (4.4 ng/dL) failed to respond to the combined stimuli of furosemide and posture. Urinary prostaglandin E2 (PGE2) was suppressed (70 ng/24 h). When indomethacin was withdrawn, significant kaliuresis occurred, accompanied by normalization of serum K+ and PGE2 and a supranormal rebound in renin and aldosterone levels. Challenge with indomethacin resulted in antikaliuresis and resuppression of PGE2, renin, and aldosterone. This case study documents for the first time that indomethacin can cause the syndrome of hyporeninemic hypoaldosteronism, probably by inhibiting prostaglandin biosynthesis.

Adult↗
PubMed1978

Deoxycorticosterone and 17-ketosteroids. Elevated levels in adult hypertensive patients.

Plasma 11-deoxycorticosterone levels were manyfold elevated in three adult patients with hypertension and elevated urinary excretion levels of 17-ketosteroids but without Cushing's syndrome. Dexamethasone therapy resulted in suppression of these steroids and in improvement of blood pressure in two of the patients. A partial adrenal 11beta-hydroxylase deficiency appears to best explain these findings.

17-Ketosteroids↗
PubMed1978

Impaired renal prostaglandin E2 biosynthesis in human hypertensive states.

Urinary Prostaglandin E2 (PGE2), a known indicator of renal production, was measured by specific radioimmunoassay in 111 normal volunteers, 85 patients with essential hypertension, 6 with renovascular hypertension, and 23 patients with primary aldosteronism. Women excreted less PGE2 than men in both normotensive and hypertensive groups. When compared to normals, essential hypertensives demonstrated significantly lower PGE2 levels, with one third excreting less than 100 ng/24 hr, values usually seen only in subjects receiving the prostaglandin synthetase inhibitor, indomethacin. Normal PGE2 was seen in patients with renovascular hypertension, and levels were uninfluenced by treatment with the converting enzyme inhibitor SQ14225, Despite normalization of blood pressure and increased plasma renin activity. Normal PGE2 was also encountered in primary aldosteronism. These data indicate that impaired renal PGE2 biosynthesis is specific for human essential hypertension, and is not secondary to the elevated blood pressure. Although PGE2 excretion tends to be lower in low-renin hypertension, a constant relationship between PGE2 and renin is not always apparent.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1978

Impaired renal production of prostaglandin E2: a newly identified lesion in human essential hypertension.

To test the hypothesis that impaired renal prostaglandin production may accompany the hypertensive state, we have measured urinary PGE2 by radioimmunoassay in 52 normotensive and 50 hypertensive subjects. PGE2 levels were lower in females, and were not affected by Na+ intake or age. Patients with essential hypertension had significantly lower PGE2, particularly those with low-renin hypertension. Forty percent of the hypertensives excreted less than 70 ng/24 hr, values never observed in normotensives except after receiving indomethacin, a well-known prostaglandin synthetase inhibitor. It appears that impaired renal prostaglandin production is commonly encountered in patients with essential hypertension, perhaps contributing to their increased renal resistance. The data further suggest a role for renal prostaglandins in the pathogenesis of low-renin hypertension.

Female↗
PubMed1978

Regulation of 18-hydroxydeoxycorticosterone in the rat.

Simultaneous measurements of plasma 18-hydroxydeoxycorticosterone (18 OH-DOC), corticosterone, and aldosterone were performed in the rat by using RIA. Under basal conditions, 18 OH-DOC levels averaged 11.3 +/- 3.7 (SE) ng/ml. Plasma concentrations were increased 8-fold (86.8 +/- 8.0 ng/ml) 1 h after 1 U sc ACTH. Dexamethasone suppressed 18 OH-DOC to less than 1.5 ng/ml, irrespective of Na+ intake. Neither Na+ depletion nor Na+ loading had any influence on 18 OH-DOC levels. Excellent correlation between 18 OH-DOC and corticosterone (r = 0.90, P less than 0.001) was observed, whereas there was none between 18 OH-DOC and aldosterone (r = 0.061, P greater than 0.6). In the rat, 18 OH-DOC is an ACTH-dependent steroid which does not appear to be under the influence of the renin-angiotensin system.

18-Hydroxydesoxycorticosterone↗
PubMed1978

Plasma mineralocorticoids, plasma renin, and urinary kallikrein in salt-sensitive and salt-resistant rats.

Plasma aldosterone, deoxycorticosterone (DOC), 18-hydroxy-deoxycorticosterone (18OH-DOC), and corticosterone were measured in Dahl salt-sensitive (S) and salt-resistant (R) rats. Plasma corticosterone and DOC were not different between strains but plasma aldosterone was decreased and plasma 18OH-DOC increased in S compared to R. Plasma renin activity and urinary kallikrein excretion were both lower in S than R. Urinary kallikrein is known to vary directly with mineralocorticoid activity and 18OH-DOC is a weak mineralocorticoid. The lower urinary kallikrein in the presence of elevated 18OH-DOC could mean that urinary kallikrein differences between S and R are under independent genetic control from 18OH-DOC.

18-Hydroxydesoxycorticosterone↗
PubMed1978

Is low-renin hypertension an overdiagnosed syndrome?

The controversy surrounding low-renin hypertension ranges from the concept that it carries a favorable prognosis to the therory that it a form of nephrosclerosis. At least a part of the debate may result from the use of different methods of classifying patients with this condition. The study presented here clearly shows that age and sex have an important influence on plasma renin activity. Women had lower values than age-matched men, and studies in normal volunteers showed that plasma renin activity decreases with age. Other factors also affect renin profiling. Diabetes is associated with renin suppression, and blacks have lower values of plasma renin activity than whites. In addition, use of anti-inflammatory drugs such as aspirin significantly lowers renin levels. Since some of these variables have not been considered in published studies to date, it would seem that the true incidence of low-renin hypertension among hypertensives is lower than the accepted figure of 25%.

Adult↗
PubMed1977

Steroid profile in a case of adrenal carcinoma with severe hypertension.

The case of a young boy who had Cushing's syndrome and severe hypertension in association with metastatic adrenal carcinoma is described. Marked elevation of the mineralocorticoid 11-deoxycorticosterone was demonstrated in the plasma. 11-Deoxycortisol, 17alpha-hydroxyprogesterone, and urinary tetrahydro-11-deoxycortisol and pregnanetriol were also elevated. Aldosterone excretion was low. The data implicate defective 11beta hydroxylation and suggest that excessive 11-deoxycorticosterone production may have been responsible for the hypertension.

17-Hydroxycorticosteroids↗
PubMed1977

Plasma 17alpha-hydroxyprogesterone in spironolactone-treated hypertensives.

When measured by a specific radio-assay method which excludes drug interference, plasma 17alpha-hydroxyprogesterone levels were found to be similar in spironolactone treated hypertensives, in untreated hypertensives, and in normotensive volunteers. No in vivo evidence for a significant inhibitory effect of spironolactone on adrenal 11beta, 17alpha and 21 hydroxylases was uncovered.

Humans↗