Biomedical subjects

D Horwitz

Publications and source records attributed to D Horwitz.

At least 37 records · Page 2Linked to original sources

PubMed1979

Relationship of human urinary and plasma kinins to sodium-retaining steroids and plasma renin activity.

In these studies we have shown that: 1. urinary kallikrein is an index of sodium-retaining steroid activity and may participate in the anti-natriuretic and kaliuretic effects of these hormones; 2. urinary kinin excretion is independent of changes in urinary kallikrein excretion; 3. levels of plasma bradykinin are highly correlated with levels of plasma renin activity probably because both respond to changes in extracellular fluid volume; and, 4. plasma bradykinin may act to antagonize angiotensin II to maintain normal blood pressure in hyper-reninemic states.

Adolescent↗

PubMed1979

Dietary fiber.

It is obvious that the effects of fiber on colonic functions are complex. The typical "Western diet" which is high in fat and protein and low in fiber may alter the bacterial flora and milieu interieur of the gastrointestinal tract, particularly the colon, to produce a high incidence of colonic cancer. However, the exact nature of the interrelationships between these dietary constituents remains elusive and will undoubtedly be the subject of intense investigation in years to come.

Animals↗

PubMed1978

Effect of orthostatic changes on urokinase excretion.

The effects of orthostatic changes on the excretion of urokinase were studied in healthy normal volunteers. Urokinase excretion rose (average +69%) significantly (p less than .005) while urine volume fell (average-59%) significantly (p less than .001) after the subjects had been standing. There was no difference between men and women nor was there an apparent diurnal variation in urokinase excretion of recumbent subjects. A relationship between urokinase excretion and sympathetic nervous system activity is suggested.

Adult↗

PubMed1978

Treatment of hypertension with biofeedback and relaxation techniques.

The present study describes a 16-week trial of the use of a combination of biofeedback and relaxation techniques for the treatment of hypertension. Twenty-two hypertensive patients were randomly allocated to one of three groups: (1) diastolic blood pressure feedback, electromyographic feedback, and verbal relaxation; (2) sham blood pressure feedback; and (3) no treatment. For the 14 patients completing active treatment during an initial or crossover period, the average changes in blood pressure as measured outside the laboratory were minimal (0/-1 and +1/0 mm Hg, supine and standing, respectively). Average blood pressure reduction in the laboratory was no greater with active than with sham blood pressure feedback (-3/-2 vs. -5/-2 mm Hg). One subject, however, after showing no change in blood pressure during sham feedback, achieved pronounced and prolonged improvement following active treatment. Overall results do not support the usefulness of these techniques as primary therapy in most hypertensives.

Adult↗

PubMed1978

Effects of dietary potassium and race on urinary excretion of kallikrein and aldosterone in man.

Urinary excretion of kallikrein by 16 normal and 8 hypertensive subjects was studied at three levels of dietary potassium: 85 meq/day for 5 days, 185 meq/day for 7 days, and 25 meq/day for 10 days. Excretion of kallikrein varied directly with potassium intake and paralleled excretion of aldosterone in both normotensive and hypertensive subjects. Mean levels of excretion of kallikrein at 85, 185, and 25 meq intake of potassium were 10.8, 19.1, and 5.8 esterase U/day (EU/day), respectively, for the normotensive subjects and 8.8, 13.9, and 6.1 EU/day for the hypertensive subjects. Mean levels of excretion of kallikrein were significantly higher in white that in black subjects among normals and hypertensives [13.0 vs. 5.9 EU/day for normals (P less than 0.05) and 13.7 vs. 4.0 EU/day for hypertensives (P less than 0.05) on the 85 meq/day diet]. The parallel changes in excretion of kallikrein and aldosterone support the hypothesis that changes in effective levels of aldosterone induce changes in the excretion of kallikrein. Because of racial differences in excretion of kallikrein, matched groups should be used for comparisons of the kallikrein system in disease states.

Adult↗

PubMed1977

The influence of allopurinol and size of dose on the metabolism of phenylbutazone in patients with gout.

Administration of allopurinol 300 mg/day produced minimal changes in the disappearance of phenylbutazone in each of five subjects following single doses (6 mg/kg) in clinical range and caused some prolongation (21%, 52%) of drug half-lives in two of six subjects after single small doses (0.5 mg/kg); mean half-life was not significantly altered by allopurinol at either dose level (means of 52 versus 48 at 0.5 mg/kg and 68 versus 70 h at 6 mg/kg). Size of dose altered half-life when phenylbutazone was used alone; three subjects showed considerably longer half-lives at the higher dose (86 versus 47, 91 versus 41, 65 versus 38 h). Allopurinol caused a greater than 50% prolongation of half-lives in two of five subjects who received single 0.5 g doses of probenecid. These preliminary data do not indicate a need to change the dose of phenylbutazone when subjects are receiving allopurinol.

Adult↗

PubMed1976

Relationships among urinary kallikrein, mineralocorticoids and human hypertensive disease.

Urinary kallikrein excretion is reduced in patients with hypertension of unknown etiology. In addition, the excretion of this renal, kinin-forming enzyme was found to be elevated in hypertensive patients with primary aldosteronism. Aldosterone regulates kallikrein excretion, as normal subjects show increased kallikrein excretion in response to a low sodium intake, high potassium intake, or the synthetic mineralocorticoid, fludrocortisone, whereas kallikrein excretion falls during treatment with spironolactone. The relationship between kallikrein excretion and aldosterone activity may directly reflect the intrarenal activity of the kallikrein-kinin system, as determined by studies of kallikrein levels from isolated renal cells or of plasma kinin levels in man in response to postural changes or saline loads. Some patients with essential hypertension do not show a normal increase in kallikrein excretion in response to low dietary sodium intake despite an apparently normal aldosterone response, suggesting that there may be a defect in the renal kallikrein-kinin system in these patients. Whether these findings are of pathogenetic significance in human hypertensive disease remains to be determined.

Fludrocortisone↗

PubMed1974