Search PubMed⌕ Search

Biomedical subjects

R G Dluhy

Publications and source records attributed to R G Dluhy.

119 records · Page 7Linked to original sources
PubMedDate not supplied

Interrelationships among thiazide diuretics and calcium, magnesium, sodium, and potassium balance in normal and hypertensive man.

The benzothiadiazide diuretics are known to cause magnesium and potassium wasting and retention of calcium and uric acid. The effect of magnesium replacement on diuretic-induced changes in sodium, potassium, calcium, and magnesium balance, weight, and blood pressure was studied in 12 normal subjects and 13 hypertensive patients to determine whether oral magnesium would reduce thiazide-induced kaliuresis. The groups differed in their response to diuresis in that the normotensive subjects did not show a fall in blood pressure (despite an equivalent weight loss), returned to a state of sodium balance earlier, and developed a greater net negative potassium balance over 12 days of diuretic therapy. Both groups displayed calcium and uric acid retention and magnesium wasting during diuretic therapy. The addition of oral magnesium replacement during diuretic therapy had no effect on any measured values beyond that seen in subjects who took diuretics without magnesium replacement. Thus, magnesium replacement did not reduce urinary potassium loss. However, urinary calcium losses increased when magnesium was given to subjects who were not receiving diuretics. The data provide the first report that small doses of oral magnesium enhance calcium excretion in hypertensive subjects.

Adult↗
PubMedDate not supplied

Glucocorticoid-remediable aldosteronism.

GRA is an inherited disorder of aldosterone biosynthesis. To date, all cases have been the result of chimeric gene duplications in which the regulatory region of the 11-beta hydroxylase gene is fused to more distal coding sequences of the aldosterone synthase gene. This results in ectopic expression of aldosterone synthase in fasciculata cells. Genetic testing has been remarkably precise in identifying these individuals with 100% concordance of the presence of the chimeric gene with increases in 18-oxygenated cortisol products. Several implications follow from these findings. First, GRA may be more common in the hypertensive population than had been previously estimated, and second, genetic testing of subsets of the essential hypertensive population (e.g., those who have low plasma renin activity) may allow the identification of GRA patients who could then be treated specifically. We recommend that hypertensive patients with signs of aldosteronism and no radiologic evidence of an aldosteronoma, especially young hypertensive subjects with low renin activity, be genetically screened for GRA. To track the success of this approach and to identify responses to various therapeutic programs, a central international registry for GRA has been established. This registry not only provides access to screening for GRA, but also informational resources for patients and physicians.

Aldosterone↗
PubMedDate not supplied

Converting enzyme inhibition in essential hypertension: the hypotensive response does not reflect only reduced angiotensin II formation.

To determine the relative importance of hormonal factors in mediating the hypotensive response to converting enzyme inhibition (CEI), plasma renin activity (PRA), angiotensin II, and bradykinin responses to SQ20,881 were measured in 20 supine patients with essential hypertension in balance on a 10 mEq sodium diet. Patients were divided into two groups according to their diastolic blood pressure response: responders had a decrement in diastolic pressure which exceeded 9 mm Hg, the upper value of the 95% confidence limits for normotensive patients studied under similar conditions; nonresponders did not. Compared to the nonresponders, responders not only had a higher control PRA (8.7 +/- 1.7 ng/ml/hr vs 4.8 +/- 2.1, p < 0.05) and larger decrement in plasma angiotensin II (18.7 +/- 4.9 pg/ml vs 3.2 +/- 1.7, p < 0.01), but also had a higher control bradykinin (3.2 +/- 0.7 ng/ml vs 1.1 +/- 0.2, p < 0.05) and larger increment in bradykinin (4.5 +/- 1.3 ng/ml vs 1.0 +/- 0.4, p < 0.05) following SQ20,881. Because SQ20,881 altered both angiotensin II and bradykinin concentrations, we assessed the contribution of blockade of angiotensin II formation by administering angiotensin II infusions to seven responders during coverting enzyme blockade, with the angiotensin II dose adjusted to restore diastolic pressure to control levels. The plasma angiotensin II level required to return blood pressure to control was 45 +/- 15 pg/ml higher than the control plasma angiotensin II level (p < 0.01), suggesting that some other factor(s), perhaps bradykinin, are also responsible for the hypotensive response to converting enzyme inhibition.

Adolescent↗
PubMedDate not supplied

Differences in response to the peptidyldipeptide hydrolase inhibitors SQ 20,881 and SQ 14,225 in normal-renin essential hypertension.

We compared vascular and hormonal responses to teprotide (SQ 20,881) and captopril (SQ 14,225) in patients with normal renin essential hypertension given a 10 mEq sodium diet. In 10 patients receiving SQ 20,881, significant changes occurred in diastolic blood pressure (DBP, -13 +/- 2.5 mm Hg), angiotensin II (-7.1 +/- 2.1 pg/ml), and plasma renin activity (PRA, +6.6 +/- 1.9 ng/ml/hr) (p < 0.01 in all cases). Twenty-one patients receiving SQ 14,225 had significant changes in mean DBP (-18 +/- 1.5 mm Hg), angiotensin II (-6.6 +/- 1.5 pg/ml), and PRA (+7.8 +/- 2.4 ng/ml/hr) (all p values < 0.01). In spite of a significantly greater hypotensive response (p < 0.02), patients receiving SQ 14,225 showed increments in PRA and decrements in angiotensin II that did not differ significantly from those seen after SQ 20,881. Moreover, there was a significant change in plasma kinins in patients receiving SQ 20,881 (+2.0 +/- 0.9 ng/ml, p < 0.01) but no change in kinins in patients receiving SQ 14,225 (0.0 +/- 0.1, ns). We conclude that there are important differences in the mechanism mediating the hypotensive response to SQ 20,881 and SQ 14,225 in normal renin essential hypertension.

Adult↗
PubMedDate not supplied

Contribution of prostaglandins to the antihypertensive action of captopril in essential hypertension.

To determine whether prostaglandins contribute to the depressor response to the converting enzyme inhibitor, captopril, we measured the plasma prostaglandin levels by radioimmunoassy before and after captopril administration, and then examined the effect of prostaglandin synthetase inhibition on captopril's antihypertensive effect. When a single oral captopril dose (25-100 mg) was given to 31 sodium-restricted patients with essential hypertension, the levels of the stable transformation product of prostacyclin remained unmeasurable and that of thromboxane A2 did not change, while the metabolite of PGE2 (PGE-M) increased by 53% (34 +/- 4pg/ml pre-captopril, 52 +/- 5 pg/ml after; p less than 0.001). As expected, blood pressure (BP) and angiotension II (AII levels fell, and kinin levels rose (all changes p less than 0.001). We then blocked prostaglandin synthesis in 18 of these subjects for 24 hours with either indomethacin (n = 10) or aspirin (n = 8) before repeating the captopril dose, to assess the importance of these PGE-M increments. The PGE-M responses to captopril were effectively blocked in nine of 10 subjects receiving indomethacin and four of eight receiving aspirin. In these 13 patients, the depressor response to captopril was significantly blunted (-20 +/- 3mm Hg pre-synthetase inhibition vs - 13 +/- 2 mm Hg post; p less than 0.05). When these agents did not block the PGE-M response to captopril, the BP response was also unchanged (-15 +/- 4mm Hg pre, -18 +/- 5mm Hg post). Neither indomethacin nor aspirin changed the AII or kinin responses to captopril. We conclude that the prostaglandins may be important mediators of captopril's antihypertensive effect in the sodium-restricted state.

Adult↗
PubMedDate not supplied

Pheochromocytoma.

Explore the source record for details and available documents.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

The biology and clinical relevance of somatostatin receptor scintigraphy in adrenal tumor management.

Somatostatin receptors are present in the normal adrenal cortex and medulla. These receptors are also expressed by tumors that cause Cushing's syndrome and by pheochromocytomas. Somatostatin analogues such as octreotide have been developed to target somatostatin receptors for diagnostic and therapeutic purposes. This article reviews the current knowledge of the biology of somatostatin receptors in the normal adrenal gland and in adrenal tumors and defines the current role of the somatostatin receptor in the diagnosis, staging and management of Cushing's syndrome and pheochromocytomas.

Adrenal Gland Neoplasms↗