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Biomedical subjects

J I Drayer

Publications and source records attributed to J I Drayer.

At least 91 records · Page 5Linked to original sources
PubMed1979

Echocardiographic assessment of cardiac anatomy and function in hypertensive subjects.

Cardiovascular complications are a major source of morbidity and mortality in hypertensive patients. To assess the prevalence of anatomic and functional abnormalities of the heart in such patients, we studied 234 asymptomatic subjects with mild-to-moderate systemic hypertension by echocardiography. After adjusting the echocardiographic values for age and body surface area, we found abnormally increased ventricular septal and/or posterobasal free-wall thickness in 61% of the hypertensive subjects. We found increased left atrial, aortic root, and left ventricular internal dimension (at end-diastole) in 5-7%, and decreased mitral valve closing velocity (E-F slope) and left ventricular ejection fraction were noted in six and 15% of the subjects, respectively. Four percent of the patients had disproportionate septal thickening (i.e., ventricular septal-to-left ventricular free-wall thickness ratio greater than or equal to 1.3). In contrast to the high prevalence of cardiac abnormalities detected by echocardiography, less than 10% of the hypertensive subjects had abnormal 12-lead ECGs or abnormal chest x-rays. These findings demonstrate a high prevalence of cardiac abnormalities in a population of asymptomatic hypertensive subjects. These abnormalities can be detected by echocardiography before they are otherwise apparent.

Adult↗
PubMed1979

The immediate pressor response to saralasin in man: a test of angiotensin II receptor vacancy.

Saralasin, 10 microgram/kg per min, caused an immediate rise in blood pressure in 52 of 57 (91.2%) hypertensive patients. The increase in diastolic pressure averaged 18.8 +/- 1.83 mm Hg (mean +/- SE) in normal renin patients on a normal salt intake. This immediate pressor response was absent in only five high renin patients and, conversely, was very large in three low renin patients. Direct arterial recordings are necessary to define the response accurately; it begins in 60--90 seconds, peaks in amplitude at 2.05 +/- 0.38 minutes, and subsides over the next 5 minutes in normal renin and high renin patients. The blood pressure elevation is inversely related to background plasma renin activity (r = -0.66, P less than 0.001), and also is directly, but weakly, related to 24-hour urinary sodium excretion (r = + 0.29). Therefore, the amplitude of the elevation is predictably diminished by the rise in plasma renin consequent to prior sodium restriction, and also by preliminary receptor exposure to low dose nonpressor infusions of saralasin itself (0.01-0.1 microgram/kg per min). Phentolamine had no effect on the response in two patients. We propose that the immediate pressor response to saralasin is related directly to the preexisting degree of vacancy of angiotensin II vascular receptors and that the initial agonistic action of the drug may prove useful in defining the angiotensin II receptor status in hypertensive diseases.

Angiotensin II↗
PubMed1979

Leydig cell responsiveness to single and repeated human chorionic gonadotropin administration.

A single im injection of 1500 IU hCG significantly increased plasma testosterone levels for at least 96--120 h in normal men (n = 7), patients with isolated gonadotropin deficiency (n = 6), and boys with delayed puberty (n = 7); the maximum values [1315 +/- 309, 370 +/- 177, and 963 +/- 249 ng/100 ml (mean +/- SD), respectively] were achieved after 72 h in each group. Repeated daily injections of 1500 IU hCG for 3 days increased plasma testosterone levels in the same subjects at 72 h after the start to levels (1342 +/- 412, 407 +/- 199, and 1052 +/- 449 ng/100 ml, respectively) similar to those found in the single dose experiment. The levels achieved at 24 and 48 h also did not differ significantly in the two experiments. The data indicate the lack of additional leydig cell stimulation by repeated hCG injections given within 48 h after a single dose.

Adolescent↗
PubMed1979

Pituitary-thyroid function in spironolactone treated hypertensive women.

Four weeks high dose spironolactone treatment (Aldactone Searle, 100 mg q. i. d.) significantly enhanced the TSH (delta max. 8.5 +/- 4.1 vs. 4.6 +/- 3.1 microunits/ml, P less than 0.05) and T3 (delta max. 32 +/- 27 vs. 11 +/- 16 ng/100 ml, P less than 0.05) responses to an intravenous TRH/LH-RH bolus injection in 6 eumenorrhoeic euthyroid hypertensive women, without affecting basal serum TSH, T3 or T4 levels or the basal and stimulated LH, FSH and prolactin values (P greater than 0.10). The mean serum testosterone, 17-hydroxyprogesterone and oestradiol levels were also similar before and during therapy. Spironolactone, possibly by virtue of its antiandrogenic action, may exert its enhancing effect on pituitary-thyroid function by modulating the levels of receptors for TRH in the thyrotrophs or by altering the T3 receptor in the pituitary permitting a greater response to TRH.

Adult↗
PubMed1979

Echocardiographic comparison of black and white hypertensive subjects.

Echocardiography was used to compare cardiac structure and function in 35 pairs of hypertensive blacks and hypertensive whites matched for age, sex, level and known duration of hypertension, treatment status, and renin level.Echocardiographic abnormalities were common in both groups and included increased ventricular septal thickness and/or left ventricular free-wall thickness in 51 percent of black hypertensives and 69 percent of white hypertensives. Paired analysis indicated no significant difference between black and white hypertensive subjects in any of the echocardiographic parameters including ventricular transverse dimensions (at end diastole and at end systole), left atrial and aortic root dimensions, left ventricular ejection fraction, and mitral valve E-F slope. Thus echocardiographic evaluation of black and white hypertensive subjects, matched for clinical characteristics, suggests a similar prevalence of cardiac abnormalities in the two groups.

Adult↗
PubMed1978

Dexamethasone-responsive hypertension in young women with suppressed renin and aldosterone.

Pronounced hypoaldosteronism was found in three young women with hypertension and symptoms of mineralocorticoid overproduction--i.e., hyporeninaemia, hypokalaemia, and a fall in blood-pressure after diuretic therapy. Plasma 11-deoxycorticosterone and 18-hydroxy-11-dooxycorticosterone concentrations were normal Treatment with dexamethasone induced a return to normal of blood-pressure and plasma-potassium and an increase in plasma-renin activity and urinary aldosterone excretion. The data suggest that hypertension in these patients is maintained by overproduction of an unknown adrenocorticotropindependent mineralocortocoid.

Adrenocorticotropic Hormone↗
PubMed1978

Effects of indomethacin alone and during diuretic or beta-adrenoreceptor-blockade therapy on blood pressure and the renin system in essential hypertension.

1. Indomethacin was administered alone or in addition to either diuretic or propranolol therapy to three groups of patients with essential hypertension on a free sodium diet. 2. Indomethacin administration reduced renin secretion by about 30% in untreated uncomplicated hypertensive patients and by about 75% in those whose renin secretion had either been stimulated or suppressed by maintained diuretic or beta-adrenoreceptor-blockade therapy. 3. Indomethacin administration produced no net effect on blood pressure in untreated patients with uncomplicated hypertension but it blunted or reversed the antihypertensive effect of either diuretic or propranolol therapy. 4. Salt and water retention may be an important factor in the blood pressure-raising effect of indomethacin during diuretic or propranolol therapy: In addition, prostaglandin synthesis may be important in counteracting increased alpha-adrenergic tone, which may limit the blood pressure-lowering effect of beta-adrenoreceptor-blockade. 5. Because of these interactions and their pressor potential indomethacin should be used with caution when combined with either diuretics or beta-adrenoreceptor blockers.

Adult↗
PubMed1978

Evidence for an unidentified, adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in young women with hypoaldosteronism.

1. Pronounced hypoaldosteronism was found in five young women with low-renin hypertension and characteristic features of the mineralocorticoid hypertensive syndrome. 2. There was no overproduction of the mineralocorticoids 11-deoxycorticosterone and 18-OH-11-deoxycorticosterone. 3. Dexamethasone restored blood pressure to normal, decreased body weight, increased plasma potassium, and increased plasma renin activity and aldosterone excretion in all patients. 4. The data suggest overproduction of an unknown adrenocorticotrophic hormone-dependent mineralocorticoid maintaining hypertension in these patients.

Adult↗
PubMed1977

Disparate patterns of aldosterone response during diuretic treatment of hypertension.

In 50 patients with essential hypertension treated with chlorthalidone, 100 mg daily for 6 weeks, treatment responders (fall in mean pressure, greater than or equal to 10%) and nonresponders experienced similar weight and electrolyte changes. Although induced increments and post-treatment values of plasma renin were higher in nonresponders than responders, there was a far more striking difference in aldosterone reactivity. Aldosterone excretion rose by less than 10% in the responders but almost doubled in the nonresponders. Again, within the normal renin subgroup alone (n = 28), nonresponders exhibited control renin values and treatment-induced changes in plasma renin closely similar to those in responders, but experienced a significantly greater increase in aldosterone excretion. Possibly this increase in aldosterone produced subtle volume retention or a direct pressor effect in nonresponding patients. Although changes in aldosterone and in renin correlated with each other in both responders and nonresponders, the slopes of the regression lines in the two groups differed significantly. Thus, cofactors governing sensitivity of the aldosterone response to renin stimulation ultimately may determine the antihypertensive effectiveness of diuretics.

Adult↗
PubMed1977

The immediate pressor response to saralasin: a measure of the degree of angiotensin II vascular receptor vacancy.

(1) An immediate pressor response so saralasin, 10 microgram/kg/min, occurred in 52 of 57 (91%) hypertensive patients. (2) We propose that the amplitude of the immediate pressor response functions as an in vivo measure of the number of initially vacan angiotensin II vascular receptors. (3) The immediate pressor response to saralasin forecasts the subsequent sustained response, both of which are related to the renin-sodium profile. (4) The dual blood pressure responses to saralasin, immediate and sustained, make this drug useful for the pharmacological identification of high, normal, and low renin hypertensive patients as they are presently classified. (5) The ability of saralasin to elevate the BP immediately in most hypertensive patients shows the need for caution in its use. It is a safe drug from this standpoint if very small infusions (0.01-0.10 microgram/kg/min) are first tried in hypertensive patients whose PRA is unknown.

Angiotensin II↗
PubMed1977

Renin reactivity as a determinant of responsiveness to antihypertensive treatment.

In 79 patients with essential hypertension, treatment with propranolol hydrochloride and chlorthalidone together produced significantly greater falls in both systolic and diastolic blood pressures than were obtained with either drug alone. There were no differences between patients in the high, normal, and low renin subgroups in their responsiveness to this combination. Although plasma renin level during combined treatment was twice as high as it was in the untreated control, aldosterone excretion actually decreased. These divergent changes may have been influenced by the renin-raising and aldosterone-lowering effects of the marked hypokalemia observed during combined treatment. By comparison with patients whose blood pressures fell, treatment in nonresponding patients produced even greater body weight reductions and significantly higher renin and aldosterone values. It is possible that increased activity of the renin axis, triggered by excessive volume depletion and perhaps by changes in potassium balance, were responsible for sustaining the high levels of blood pressure in those patients failing to respond to treatment.

Adult↗
PubMed1976

Renin and aldosterone suppression in the antihypertensive action of clonidine.

In 18 hypertensive patients receiving a constant (100 mEq/day) sodium diet, treatment with clonidine (0.3 mg/day for 5 days) decreased blood pressure in 11 patients with high and normal renin levels and 7 with low renin levels. The high and normal renin group had early and rapid reductions in blood pressure and plasma renin activity. In contrast, the low renin group had a more gradual hypotensive response and only a small absolute decrease in plasma renin. For all patients, pretreatment renin levels were related to the initial decrease in blood pressure but not to the reductions measured after 5 days. Thus, two mechanisms of action of clonidine are possible, one related to acute inhibition of the renin-angiotensin system in patients with high and normal renin levels and another that is independent of renin mechanisms and occurs in all hypertensive patients. In six additional patients with high renin levels induced by prior sodium depletion (10 mEq/day sodium diet), clonidine did not reduce blood pressure or renin, thus indicating that the suppressive action of this agent on renin pressor mechanisms occurs only in patients whose elevated renin levels are intrinsic to hypertension and unrelated to sodium depletion. Of the 18 patients receiving a normal sodium diet, 13 were classified as responding to treatment (decrease in both systolic and diastolic pressures of at least 10%). The five nonresponders had greater weight gain and higher values for aldosterone excretion. For all patients, there was a significant correlation between decrements in blood pressure and in aldosterone, suggesting that the countervailing effects of fluid accumulation on blood pressure in nonresponding patients resulted from a failure of aldosterone to be suppressed. Changes in aldosterone, in turn, correlated significantly with changes in renin. Thus, the antirenin effect of clonidine enhances its antihypertensive action not only by acutely ablating renin-angiotensin pressor mechanisms, but also by inhibiting aldosterone production and thereby minimizing longer-term reactive volume retention during treatment.

Adult↗