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Biomedical subjects

H D Itskovitz

Publications and source records attributed to H D Itskovitz.

At least 37 records · Page 2Linked to original sources
PubMed1983

Hemodynamic effects of antihypertensive drugs.

Elevated total peripheral resistance and normal cardiac output are the hemodynamic characteristics of chronic essential hypertension. One approach to treating hypertension matches the individual pathophysiology with the hemodynamic effects of antihypertensive drugs. Antiadrenergic drugs are appropriate second-step therapy in many cases of established hypertension; by reducing total peripheral resistance, these agents can reduce blood pressure while sparing cardiac output and renal blood flow. The physician should treat elderly hypertensive patients cautiously and consider using drug with a favorable hemodynamic profile.

Adrenergic beta-Antagonists↗
PubMed1982

Bilateral pheochromocytoma and islet cell adenoma of the pancreas.

An 18-year-old woman with bilateral pheochromocytomas and an asymptomatic islet cell adenoma of the pancreas represents the 11th patient to be described with this combination of endocrine tumors. No other components of any multiple endocrine adenomatosis (MEA) syndromes were present. Because of this "overlap syndrome," in which tumors that have traditionally been considered to be components of separate and mutually exclusive MEA syndromes have occurred concomitantly in the same patient, a question is raised regarding the validity of a rigid classification of these various MEA syndromes. The possibility of a pancreatic tumor should be kept in mind in any patient with a pheochromocytoma, especially if it is bilateral of multicentric in origin.

Adenoma, Islet Cell↗
PubMed1982

Sites of action of loop diuretics.

Isolated canine kidneys were perfused at a constant systolic pressure of 140 mm Hg with autologous blood. Infusion of maximally effective amounts of furosemide (F) increased the fractional excretion of Cl (FEcl) from 0.03 to 0.18. Parallel changes in FENa and FEH2O were observed and, at maximal response, urine/plasma osmolality was 0.91. Ethacrynic acid (EA) was then added to the infusion fluid and produced a further increase in FECl to 0.28. Urine/plasma osmolality returned to unity. When the order of administration of the two diuretics was reversed, the response to EA alone was greater than after F (from FECl 0.05 control to 0.30 after EA) and the urine became isosmotic (urine/plasma osmolality = 1.0). After F was added, FECl increased further to 0.39. K secretion induced by F or by EA was demonstrable in all experiments. These data indicate that: 1) EA is more effective than F; 2) both drugs can completely inhibit Cl- transport in the thick ascending limb; 3) EA is more effective than F in blocking NaCl transport at sites distal to the loop of Henle; and 4) the proximal tubule is a site of action of F and possibly of EA. Whether the two drugs act entirely on membranal transport systems or, in part, by modifying the production of release of intrarenal substances and/or by diverting blood from one region to another cannot be ascertained from this work.

Animals↗
PubMed1981

Long-term treatment of hypertension with methyldopa. VIII. Overview.

A multiclinic retrospective study in patients who received methyldopa, some for up to 10 years, has provided a large body of long-term data on the efficacy and tolerability of the drug as part of an antihypertensive regimen. Blood pressure and dosage data were analyzed over the first 4.5 years. The results of this survey are summarized here.

Adolescent↗
PubMed1981

Long-term treatment of hypertension with methyldopa. I. Study objectives and design.

In this retrospective study, a group of 435 patients provided meaningful analyses of blood pressure and dosage data for treatment periods of up to 4.5 years. The protocol, study objectives, and pretreatment demographic characteristics of the group are summarized in this report, which is the first in a series in this issue describing the results of this survey.

Adolescent↗
PubMed1980

Plasma dopamine-beta-hydroxylase in uremia--increase in enzyme activity after renal transplantation.

Plasma dopamine-beta-hydroxylase in uremia. Plasma dopamine-beta-hydroxylase (DBH) activity was found to be low in 26 uremic patients when compared with 56 normal individuals (p less than 0.001). Hemodialysis caused only a slight increase in plasma DBH levels in the uremic group. In contrast, a group of kidney transplanted patients with a return of good renal function had DBH values similar to the normal group (p greater than 0.1). The mean plasma DBH activity in eight patients measured pre- and post-transplantation increased from 4.5 to 28 International Units/l (p less than 0.01). No evidence was found to indicate that the depressed levels of plasma DBH in uremia were secondary to genetic or enzyme inhibiting factors. It is suggested that low levels of DBH activity in patients with renal failure may be a consequence of altered sympathetic nervous activity which is known to occur in the uremic state.

Adolescent↗
PubMed1980

Angiotensin II and norepinephrine after indomethacin in isolated perfused canine kidneys. Tachyphylaxis vs. modulator effect of prostaglandins.

High levels of radioimmunoassayable PGE2 were measured in the perfusate of isolated kidneys. Indomethacin inhibited PGE2 release in this system. Small reductions in the pressor effects of norepinephrine (NE) were associated with increasing perfusate levels of PGE2; a large increase in the pressor effect of NE followed additions of indomethacin and reductions in perfusate PGE2 levels. A marked reduction in pressor responsiveness to angiotensin II (AII) was measured in the isolated kidney which could not be prevented or reversed by indomethacin. It is believed that tachyphylaxis was responsible for the marked reduction in pressor responsiveness to AII and that this is independent of alterations in prostaglandin metabolism. However prostaglandins appeared to modulate the pressor effects of AII as they did NE in the isolated perfused kidney.

Angiotensin II↗
PubMed1980

Clonidine and the kidney.

The effects of clonidine on renal hemodynamics and renal function make it a particularly useful antihypertensive agent. During treatment of hypertensive patients with clonidine, renal blood flow and glomerular filtration rate are well maintained, and renin secretion is reduced. Early in therapy, a slight tendency to retain salt and water may be seen as blood pressure is lowered. This effect on salt and water excretion is usually transient and may be avoided if a diuretic is used concomitantly. No deterioration of renal function was noted in patients with primary hypertension who were treated with clonidine for periods from 6 months to at least 5 years. The drug is effective in patients with renal hypertension with or without renal failure and well tolerated. Clonidine is also effective in hypertensive patients undergoing chronic hemodialysis, but doses may have to be reduced because the drug is excreted chiefly by the kidney.

Adrenal Gland Neoplasms↗
PubMed1979

Prazosin in hypertension with and without methyldopa.

The efficacy of prazosin was assessed in 21 patients with essential hypertension who failed to respond adequately to a combination of methyldopa and hydrochlorothiazide. The patients were divided randomly into two groups; in the first group prazosin was substituted for methyldopa and in the second group prazosin was added to the combination. In group 1, the average blood pressure (BP) fell from 144/102 mmHg (sitting) and 142/105 mmHg (standing) to 136/91 mmHg (sitting) and 129/91 mmHg (standing) after prazosin (17 mg) was substituted for methyldopa. The fall in the diastolic BP was statistically significant (p less than 0.01). In group 2, BP fell from 146/101 mmHg (sitting) and 143/103 mmHg (standing) to 126/87 mmHg (sitting) and 118/86 mmHg (standing) when prazosin 14 mg was added to methyldopa and hydrochlorothiazide. The reductions in systolic and diastolic pressures were statistically significant (p less than 0.001).

Adult↗
PubMed1979

Attenuation of angiotensin II- and III-induced aldosterone release by prostaglandin synthesis inhibitors.

The effect of two prostaglandin synthesis inhibitors, indomethacin and meclofenamate, on angiotensin II (AII)- and III (AIII)-induced aldosterone release was studied in normal and sodium-depleted conscious rats and in adrenal capsular cell suspensions obtained from normal rats. In normal rats, in vivo AII and AIII were equipotent in causing dose-related increases in serum aldosterone concentrations. Indomethacin decreased the basal serum aldosterone levels by 50% and serum renin levels by 43%. In addition, the steroidogenic effects of AII and AIII were reduced by 45 and 63% with 3 mg/kg of indomethacin and 63 and 73% with 10 mg/kg, respectively. In contrast, meclofenamate failed to alter basal serum levels of aldosterone or AII-stimulated aldosterone release but inhibited serum renin levels by 27% and the aldosterone-stimulating effect of AIII by 99%. Indomethacin (3 mg/kg) and meclofenamate (2 mg/kg) inhibited urinary prostaglandin (PG)E(2) and PGF(2alpha) excretion by 63 and 52% and 37 and 31%, respectively. Both inhibitors significantly decreased the adrenal capsular PGE(2) and PGF(2alpha) content and the conversion of [(14)C]arachidonate to [(14)C]PGE(2) and [(14)C]PGF(2alpha). In sodium-depleted rats, indomethacin produced similar effects reducing the control serum aldosterone levels by 29%, AII-stimulated aldosterone by 47%, and completely suppressing the aldosterone response to AIII without altering serum renin activity. In adrenal cell suspensions, similar results were observed with indomethacin inhibiting basal and AII- and AIII-stimulated aldosterone release by 29, 81, and 93%, respectively. Meclofenamate failed to alter basal and AII-stimulated aldosterone release but inhibited that stimulated by AIII by 86%. The present findings suggest that prostaglandins modulate the effects of the renin-angiotensin system by stimulating the release of renin from the kidney and augmenting the steroidogenic effects of AII and AIII in the adrenal cortex.

Adrenal Cortex↗
PubMed1979

Production of maximally acid urine by the isolated dog kidney.

The isolated kidney has not been reported to acidify urine maximally. To study this defect, kidneys from dogs fed NH4Cl were perfused with autologous blood. Perfusate pH was 7.20 +/- 0.03 [HCO3] was 14 +/- 1 mEq/L, and urine pH was abnormally high, 6.60 +/- 0.08. When corrected for difference in GFR, UNH4+V was similar to that seen in vivo, but UTAV and UNet H+V were low. FEHCO3- was 2.3% +/- 0.8% and HCO3- excretion persisted to a small degree at perfusate [HCO3-] of 8 to 9 mEq/L. In response to HCO3- infusions, large increases in excretion were not seen until perfusate values were over 24 to 26 mEq/L. HCO3- Tmax was 2.94 +/- 0.07 mEq/dl of glomerular filtrate. The isolated kidney failed to raise U-B PCO2 with HCO3- infusion secondary to low urine [HCO3-] and [Pi]. During perfusion in another group of kidneys from dogs fed NH4Cl and given DOC, perfusate pH and [HCO3-] were similar to those in the first group. Urine pH was also inappropriately high, 7.12 +/- 0.09, and there was no UNet H+V. In response to Na2SO4 infusion, urinary pH fell to 5.00 +/- 0.27. Log10UUAV was correlated to urine pH during the control perfusions in both groups and after Na2SO4 in the NH4Cl + DOC group. Thus production of a low urine pH in the isolated kidney may be mediated by changes in transtubular potential difference resulting from increased distal nephron delivery of Na+ and nonabsorbable anion. The defect in acidification is similar to that observed in incomplete forms of clinical type 1 (distal) renal tubular acidosis.

Ammonium Chloride↗
PubMed1978

Treatment of idiopathic orthostatic hypotension (Shy-Drager syndrome) with indomethacin.

Four patients with idiopathic orthostatic hypotension (I.O.H.) and one with postural hypotension and diabetes were studied. Plasma-renin activity (P.R.A.) was low and did not rise appropriately with salt restriction and diuretic stimulation. Aldosterone levels were normal and rose with diuretic therapy. Plasma-volume, plasma dopamine beta-hydroxylase, urinary catecholamines, metanephrines, and vanillyl mandelic acid (V.M.A) were normal. Treatment with indomethacin (75-150 mg/day) raised the upright blood-pressure (B.P.) by an average of 20-30 mm Hg diastolic and allowed the four patients with I.O.H. to walk about without orthostatic symptoms but it had no effect in the fifth patient. When indomethacin was discontinued in one patient who had been taking it for 9 months with symptomatic relief, the B.P. fell to pretreatment levels within 48 h. When indomethacin was reinstituted the B.P. rose again. Indomethacin was more effective in these patients than either propranolol or fludrocortisone. There may be an absolute or relative excess of certain vasodepressor prostaglandins in the peripheral vessels which results in pooling of blood and orthostatic hypotension. If this is the case indomethacin might improve the orthostatic symptoms of I.O.H. by its inhibitory effect on prostaglandin synthesis, but its mechanism of action remains to be determined.

Administration, Oral↗