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Biomedical subjects

J Lowenstein

Publications and source records attributed to J Lowenstein.

At least 37 records · Page 2Linked to original sources
PubMed1986

Effects of prazosin, atenolol, and thiazide diuretic on plasma lipids in patients with essential hypertension.

The effects of prazosin and atenolol monotherapy on plasma lipid concentrations were compared in 51 patients with mild to moderate essential hypertension. Prazosin monotherapy (mean dose 5.4 +/- 5.3 mg per day) resulted in a significant decrease in total and low-density lipoprotein cholesterol concentrations; these changes were evident at three months and at six to 12 months. Atenolol monotherapy (mean dose 66 +/- 23 mg per day) resulted in a significant increase in plasma triglyceride concentration that persisted during one year of treatment. The deletion of thiazide from the regimen of prazosin plus thiazide resulted in a small stepwise decrease in plasma triglyceride concentration over 12 months of observation. The addition of polythiazide (0.5 mg two to three times weekly) to the regimen of patients in whom acceptable blood pressure was not attained with prazosin or atenolol monotherapy resulted in a decrease in blood pressure, averaging 18.8 mm Hg for systolic and 10.3 mm Hg for diastolic, and a small, though significant, increase in the concentration of low-density lipoprotein cholesterol. It is suggested that the effects of prazosin on plasma lipid composition may be mediated, at least in part, by blocking an action of either the sympathetic nervous system or circulating catecholamines that normally modulate lipoprotein metabolism and might mediate the lipid alterations induced by thiazide diuretics.

Atenolol↗
PubMed1984

Effects of prazosin and propranolol on serum lipids in patients with essential hypertension.

The effects of prazosin and propranolol on total serum cholesterol concentration, low-density lipoprotein and high-density lipoprotein cholesterol fractions, and serum triglyceride concentration were compared in a crossover study in 29 patients with mild to moderate essential hypertension. All patients received polythiazide at a constant dose throughout control and drug treatment periods. Comparable blood pressure reduction was achieved with prazosin (9.3 +/- 7.1 mg per day) and propranolol (183.6 +/- 154.5 mg per day). Prazosin administration was associated with a significant reduction in the concentrations of total serum cholesterol (-5.5 percent), triglyceride (-20.0 percent), and low-density lipoprotein cholesterol (-10.1 percent). High-density lipoprotein cholesterol concentration increased (+8.0 percent) as did the ratio high-density lipoprotein: total cholesterol (+14.1 percent). No significant changes in any of the serum lipid fractions were observed during propranolol administration.

Blood Pressure↗
PubMed1984

Effects of prazosin on serum lipids in patients with essential hypertension: a review of the findings presented at the Satellite Symposium on coronary heart disease: hypertension and other risk factors, Milan, 1983.

Accumulated evidence has indicated that the failure of blood pressure control with antihypertensive therapy to reduce the incidence of myocardial infarction may be due to unfavorable effects of drug therapy on other cardiovascular risk factors, particularly lipid concentrations. Several studies have demonstrated that beta-blocking drugs increase serum triglyceride concentration and reduce high-density lipoprotein cholesterol concentration, both of which are risk factors for coronary artery disease. However, several investigators have reported that prazosin, an alpha-adrenergic blocking agent, does not cause adverse changes in those lipid parameters or in the cholesterol ratio. If one considers the net effect of antihypertensive therapy to be the reduction of blood pressure plus the alterations in lipid metabolism, the metabolic response to a drug may be an important determinant of the overall effectiveness of treatment and a deciding factor in the choice among available antihypertensive agents.

Adrenergic beta-Antagonists↗
PubMed1981

Renal failure in minimal change nephrotic syndrome.

Renal insufficiency, with serum creatinines ranging from 2.3 to 13.4 mg/dl, was observed in 15 patients with the minimal change nephrotic syndrome. Recovery of renal function occurred in association with diuretic therapy in 13, eight of whom subsequently underwent steroid-induced remission of the nephrotic syndrome. Two patients failed to undergo diuresis or to have a remission of the nephrotic syndrome and died with persistent renal failure. Glomerular filtration rate (Cinulin) was reduced out of proportion to renal plasma flow (CPAH) as evidenced by remarkably low filtration fractions ranging from 0.03 to 0.095. The invariable association between diuresis and recovery of renal function, the recurrence of renal failure when fluid reaccumulated and the finding of markedly depressed filtration fractions lead us to postulate that renal failure in minimal change nephrotic syndrome may be due to a reversible alteration in glomerular hemodynamics which is related to fluid retention and associated intrarenal edema.

Adolescent↗
PubMed1980

Propranolol: an unrecognized cause of central nervous system dysfunction in patients undergoing cardiopulmonary bypass.

An organic mental syndrome developed in a patient soon after he underwent repair of a dissecting thoracic aortic aneurysm. The operation was accomplished with cardiopulmonary bypass. Initially, the mental changes were thought to be related to the operation. However, they subsequently were shown to be associated with propranolol. The potential role of propranolol in inducing central nervous system disturbances is emphasized, and the literature on the subject is reviewed.

Aortic Dissection↗
PubMed1980

Rebound hypertension after sodium nitroprusside-induced hypotension.

Patients undergoing surgical procedures using sodium nitroprusside-induced hypotension were studied to determine the role of the renin-angiotensin system in the pathogenesis of rebound hypertension (RH) after discontinuing sodium nitroprusside (SNP) infusion. Retrospective observations documented RH in 9 of 12 patients (group I) with a systolic blood pressure (SBP) increase from 112 +/- 3.92 before SNP to 144 +/- 5.60 torr 10 min after SNP (p less than 0.001). In 12 patients (group II), plasma renin activity (PRA) rose from 950 +/- 432 to 3,611 +/- 1.874 pg/ml/hr (p less than 0.0005) during SNP and remained elevated (2,504 +/- 792 pg/ml/hr) 30 min after cessation of SNP. SBP rose from a control (pre-SNP) value of 112 +/- 5.24 to 129 +/- 8.52 torr after discontinuation of SNP (p less than 0.05). Significant PRA and SBP changes did not occur in a matched group of patients (group III) who did not receive SNP. That RH after cessation of SNP infusion was associated with persistent elevation of PRA leads us to suggest that RH may be attributable to the unopposed effects of the renin-angiotensin system after the rapid plasma disappearance of SNP.

Anesthesia, General↗
PubMed1980

Effect of a heptapeptide angiotensin analog on aldosterone secretion in the rabbit.

We examined the effects of an angiotensin III (AIII) analog, isoleucine-7 AIII (Ile7-AIII), on the steroidogenic and pressor responses to angiotensin II (AII) and AIII. AII or AIII (25 ng/kg/min) were infused alone or superimposed on an infusion of Ile7-AIII (100 ng/kg/min) in conscious male New Zealand rabbits. AII and AIII induced comparable increases in plasma aldosterone concentration, but AII exhibited significantly greater pressor effect. Ile7-AIII infusion resulted in significant inhibition of AII- but not AIII-induced steroidogenesis. Despite inhibition of aldosterone production, Ile7-AIII failed to block the pressor or renin-suppressing effect of AII. Inhibition of the steroidogenic effect of AII, but not of AII, by Ile7-AIII may be taken as evidence that adrenal stimulation by AII is direct and is not mediated by in vivo conversion to the heptapeptide. The ability of the heptapeptide analog to block aldosterone stimulation by the octapeptide AII suggests that adrenal receptors may, however, have a greater affinity for the heptapeptide.

Adrenal Glands↗
PubMed1980

Drugs five years later: clonidine.

Clonidine represents the prototype of a new class of centrally acting antihypertensive agents, classed as partial alpha-adrenergic antagonists. Blood pressure reduction is characterized, hemodynamically, by reduced cardiac output with unchanged peripheral vascular resistance at rest. Reflex control of blood pressure during orthostasis and exercise appears to be unimpaired, and orthostatic hypotension is uncommon. As with most other antihypertensive agents, satisfactory reduction of blood pressure with clonidine given as a sole agent is limited to patients with relatively mild hypertension; an additive or synergistic effect of diuretic administration has been well documented. Abrupt withdrawal of clinidine has been reported to be followed, within 24 to 36 h, by rebound hypertension, tachycardia, cardiac arrhythmias, and other changes suggestive of sympathetic overactivity. The incidence and clinical significance of rebound hypertension after abrupt cessation of clonidine therapy, and indeed the profile of blood pressure responses to varying physical activity during therapy, remain to be evaluated.

Animals↗
PubMed1979

Unimpaired beta adrenergic responses during prazosin administration.

We have examined insulin-induced hypoglycemia to determine whether prazosin inhibits the response to sympathetic stimulation, either centrally or at beta adrenergic receptors. Nine patients with essential hypertension were studied during administration of prazosin, hydralazine or placebo. Plasma renin activity increased significantly with hydralazine and was unchanged during prazosin administration. In response to insulin, blood glucose decreased equally with both drugs and placebo, and small increases in dopamine beta-hydroxylase occurred. Plasma renin activity and heart rate increased during hypoglycemia; the increases were greater in patients taking prazosin or hydralazine. The unimpaired responses of plasma dopamine beta-hydroxylase, renin activity and heart rate to insulin-induced hypoglycemia provide evidence that prazosin does not block either the sympathetic discharge elicited by central stimulation (hypoglycemia) or the responses mediated through beta adrenergic receptors.

Blood Glucose↗
PubMed1978

Plasma renin and serum dopamine-beta-hydroxylase during orthostatic hypotension in quadriplegic man.

To determine whether orthostatic hypotension in patients with cervical spinal cord lesions is the result of impaired sympathetic nerve response and/or impaired renin release, serum dopamine-beta-hydroxylase (DbetaH) activity and plasma renin activity (PRA) were examined during passive tilting in 6 quadriplegic patients and in 6 able-bodied control subjects. Serum DbetaH was measured by an isotopic enzymatic method and PRA by radioimmunoassay. Following head-up tilting, quadriplegic subjects demonstrated a prompt, significant decrease in mean arterial pressure (MAP) and increase in heart rate (HR). DbetaH and PRA both increased significantly 15 minutes after tilt. In normal subjects, although HR increased, MAP was unchanged; DbetaH and PRA did not increase significantly during head-up tilt. The finding of increased DbetaH during tilt hypotension in quadriplegic patients provides evidence that reflex sympathetic nerve stimulation persists despite cervical cord transection. Increased PRA may be attributed to decreased renal perfusion pressure and increased sympathetic stimulation during tilt hypotension. These data suggest that orthostatic hypotension in quadriplegia patients cannot be attributed solely to failure of the sympathetic nervous system or the renin-angiotensin system to respond to the stimulus of orthostasis.

Adolescent↗
PubMed1977

Hyperthyroidism after propranolol withdrawal.

Classic features of thyrotoxicosis developed in three patients with no prior history of thyroid disease shortly after the discontinuation of therapy with or decrease in doseage of propranolol hydrochloride. Graves' disease probably developed fortuitously after propranolol therapy was instituted, but the beta-adrenergic blockade masked the clinical features of hyperthyroidism. On discontinuation of propranolol therapy or decrease in propranolol dosage, previously latent thyrotoxicosis became manifest. If hyperthyroidism masked by beta-blockade is not recognized before withdrawal of propranolol therapy in patients with ischemic heart disease, the sudden appearance of thyrotoxicosis may lead to symptoms of increased myocardial ischemia.

Adult↗
PubMed1977

Lupus nephritis. Clinical course as related to morphologic forms and their transitions.

An intensive study of the course of lupus nephritis has been undertaken in 88 patients in whom strict morphologic criteria were utilized in classification. All were treated with steroid, and 17 received cytotoxic drugs in addition. Focal proliferative lupus nephritis generally follows a benign course except in the occasional instances when transition to the diffuse proliferative or membranous forms occurs. Membranous lupus nephritis, when characterized by persistent nephrotic syndrome, leads slowly to renal failure, but this progression is aborted in the one-third in whom remission of the nephrotic syndrome can be achieved. A fatal outcome occurs within five years in the majority of those with diffuse proliferative lupus nephritis and the nephrotic syndrome, often in association with necrotizing renal vasculitis, severe hypertension and accelerated renal failure. A small number with the diffuse proliferative form have a remission and then show only mesangial abnormalities, usually, however, with the appearance of glomerular sclerosis. Progressive glomerular sclerosis is observed in some patients and may be a sequel of the remission of the diffuse or focal proliferative lesions, or it may represent still another form of lupus nephritis. Mesangial immune deposits with or without proliferation, at times in the absence of clinical renal disease, are observed early in the course of systemic lupus erythematosus (SLE) and may proceed to the diffuse proliferative or membranous forms. The present observations serve to emphasize the importance of strict morphologic classification in the comparison of different treatment regimens for lupus nephritis. In view of the grave prognosis of established diffuse proliferative lupus nephritis, which probably evolves from a mesangial involvement common to all patients with SLE from its onset, early therapy may be the key to the management of lupus nephritis.

Adolescent↗
PubMed1977

Aldosterone production during dietary sodium restriction and beta-adrenergic blockade.

The role of the renin-angiotensin system in mediating the aldosterone response to sodium depletion was examined by administration of propranolol during dietary sodium restriction. The beta-adrenergic antagonist prevented the expected increase of plasma renin activity in response to sodium restriction in six of twelve studies. Plasma angiotensin II concentration failed to increase in four of five subjects in whom the renin response was abolished. Despite unchanged or decreased plasma renin activity and plasma angiotensin II concentration, plasma aldosterone concentration increased significantly in response to dietary sodium restriction. The increase in aldosterone production could not be attributed to changes in plasma sodium or potassium concentration or increased ACTH secretion. It is suggested that the aldosterone response to sodium restriction is mediated not only by increased plasma renin activity and angiotensin II concentration, but also another mechanism, possibly related to increased adrenal sensitivity to angiotensin during sodium depletion.

Aldosterone↗
PubMed1977

Failure of sodium restriction to abolish exaggerated natriuresis in poststreptococcal glomerulonephritis.

Exaggerated natriuresis in response to hypertonic saline infusion occurs with great regularity in patients with documented previous attacks of poststreptococcal glomerulonephritis. Five patients were studied before and after 1 week of dietary sodium restriction in order to examine the possibility that increased extracellular fluid volume might play a role in the response to acute saline infusion. Plasma renin activity (PRA) and PRA responsiveness to sodium depletion were normal, suggesting that extracellular fluid volume was not increased. In all patients, extracellular fluid volume decreased during sodium restriction, as judged by weight loss, cumulative negative sodium balance, small decreases in measured plasma volume, and appropriate increases of PRA and plasma aldosterone concentration. Hypertonic saline infusion provoked exaggerated natriuresis in all patients equally as well after dietary sodium restriction as before. Exaggerated natriuresis in poststreptococcal glomerulonephritis occurs without evidence of chronic expansion of extracellular fluid volume and is not affected by reduction of extracellular fluid volume.

Adolescent↗