Biomedical subjects

F W Beck

Publications and source records attributed to F W Beck.

At least 37 records · Page 2Linked to original sources

PubMed1996

Zinc status and serum testosterone levels of healthy adults.

Zinc deficiency is prevalent throughout the world, including the USA. Severe and moderate deficiency of zinc is associated with hypogonadism in men. However, the effect of marginal zinc deficiency on serum testosterone concentration is not known. We studied the relationship between cellular zinc concentrations and serum testosterone cross-sectionally in 40 normal men, 20 to 80 y of age. In four normal young men (27.5 +/- 0.5 y), we measured serum testosterone before and during marginal zinc deficiency induced by restricting dietary zinc intake. We also measured serum testosterone in nine elderly men (64 +/- 9 y) who were marginally zinc deficient before and after 3 to 6 mo of supplementation with 459 mumol/ d oral zinc administered as zinc gluconate. Serum testosterone concentrations were significantly correlated with cellular zinc concentrations in the cross-sectional study (lymphocyte zinc versus serum testosterone, r = 0.43, p = 0.006; granulocyte zinc versus serum testosterone, r = 0.30, p = 0.03). Dietary zinc restriction in normal young men was associated with a significant decrease in serum testosterone concentrations after 20 weeks of zinc restriction (baseline versus post-zinc restriction mean +/- SD, 39.9 +/- 7.1 versus 10.6 +/- 3.6 nmol/L, respectively; p = 0.005). Zinc supplementation of marginally zinc-deficient normal elderly men for six months resulted in an increase in serum testosterone from 8.3 +/- 6.3 to 16.0 +/- 4.4 nmol/L (p = 0.02). We conclude that zinc may play an important role in modulating serum testosterone levels in normal men.

Adult↗

PubMed1988

Salt sensitivity in blacks. Salt intake and natriuretic substances.

Accumulating evidence suggests that hypertension in blacks is manifested in part by impaired renal excretion of salt. Consequently, this study was performed to determine if hypertensive and normotensive black subjects differ in their ability to generate known natriuretic substances. Fourteen normotensive and 11 hypertensive blacks were maintained on constant metabolic diets containing either 40 or 180 mmol of salt per day for 14 days each. During the last 4 days of each salt intake period, urine was collected for measurement of sodium, dopamine, and norepinephrine. On the last day of each 14-day dietary period, blood pressures were measured, blood was collected for measurement of plasma atrial natriuretic factor (ANF) and aldosterone, and urine was collected over 2 hours for measurement of prostaglandin E2 (PGE2). Both the normotensive and the hypertensive groups manifested salt sensitivity; their mean arterial pressure rose by 7 +/- 0.2 and 6 +/- 0.2%, respectively, when salt intake was increased from 40 to 180 mmol/day. The hypertensive group exhibited decreased (p less than 0.05) dopamine excretion as compared with the normotensive group for both dietary salt intakes. Plasma ANF levels increased (p less than 0.05) in the hypertensive group, but not in the normotensive group, with increasing dietary salt. Plasma aldosterone and urinary norepinephrine and PGE2 were comparable in the two groups for both dietary salt intakes. These data suggest that salt sensitivity is not unique to hypertensive blacks but occurs in normotensive blacks as well. Decreased renal production of dopamine may be a pathogenic factor in the development and maintenance of hypertension in blacks.

Adult↗

PubMed1988

The WISC-R and the Woodcock-Johnson Tests of Achievement: correlations for exceptional children.

The present study concerns correlations of scores on the Woodcock-Johnson Tests of Achievement with those on the Wechsler Intelligence Scale for Children--Revised (WISC--R). Correlations between WISC--R Full Scale, Verbal, and Performance IQ and the Reading Aptitude Cluster, the Mathematics Aptitude Cluster, and the Written Language Aptitude Cluster of the Woodcock-Johnson were expected to be high and support the contention that conventional measures of ability do predict achievement for children. Results confirm the hypothesis. The Verbal IQ was the best one-variable predictor of each aptitude cluster, with R s ranging from .32 to .78.

Achievement↗

PubMed1986

Myocardial norepinephrine, epinephrine and dopamine concentrations after cardiac autotransplantation in dogs.

Myocardial norepinephrine is markedly reduced after cardiac transplantation because of interruption of postganglionic cardiac sympathetic nerves. There are also substantial stores of dopamine in the myocardium, but the influence of cardiac denervation on dopamine remains unknown. The effect of cardiac transplantation was determined and, thus, the effect of denervation on myocardial norepinephrine, dopamine and epinephrine. Myocardial catecholamines were measured with high-performance liquid chromatography with electrochemical detection in five dogs 6 to 8 weeks and in four dogs 8 to 12 years after cardiac autotransplantation and in six sham-operated dogs with intact cardiac innervation. Norepinephrine, dopamine and epinephrine levels were determined from samples obtained from the right and left atria and ventricles. Samples from the left ventricular apex and base were analyzed separately. There was a striking depletion of norepinephrine in all cardiac chambers after short-term autotransplantation. The norepinephrine content of the left atrium in sham-operated dogs (1,659 +/- 219 ng/g) was significantly higher than that of dogs with long-term autotransplanted hearts (754 +/- 372 ng/g). Sham-operated dogs and dogs with long-term autotransplanted hearts had statistically significant (p less than 0.05) differences in norepinephrine content in the left ventricular apex (480 +/- 197 versus 294 +/- 198 ng/g), left ventricular base (876 +/- 2204 versus 654 +/- 156 ng/g) and right ventricle (766 +/- 133 versus 247 +/- 29 ng/g). In contrast to norepinephrine, dopamine concentrations were relatively preserved in the short-term group despite the virtual depletion of myocardial norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Oxide↗

PubMed1986

Comparison of PPVT-R and WISC-R in a mild/moderate handicapped sample.

The Peabody Picture Vocabulary Test-Revised, Form L was compared with the Wechsler Intelligence Scale for Children--Revised with a sample of 32 mild/moderate handicapped students (24 boys, 8 girls). Significant correlations were found between the WISC-R Full Scale IQ (.46) and the WISC-R Verbal IQ (.50) and the PPVT-R, but no significant correlation was found between the WISC-R Performance IQ and the PPVT-R (.34). Mean scores on the PPVT-R and WISC-R were significantly different.

Adolescent↗

PubMed1985

Absent aldosterone response to metoclopramide in patients with high spinal cord transection: evidence that metoclopramide stimulates aldosterone secretion through central pathways.

This study evaluates dopaminergic regulation of aldosterone secretion in 6 patients with high spinal cord transections. Administration of the dopamine antagonist metoclopramide resulted in a marked rise in plasma aldosterone and 18-hydroxycorticosterone levels in 12 normal individuals, but no change in plasma levels of these zona glomerulosa corticosteroid products in spinal cord patients. Spinal cord transected patients also did not have the rise in plasma renin activity that was observed in normals following metoclopramide administration. Basal levels of aldosterone, 18 hydroxycorticosterone, corticosterone and renin activity as well as the aldosterone responses to graded dose infusion of adrenocorticotropin were similar in the spinal cord patients and the normals. These data suggest that dopaminergic regulation of adrenal zona glomerulosa corticosteroid and renal renin secretion is absent in patients with high spinal cord transections, suggesting that intact neural pathways from the central nervous system are necessary for metoclopramide stimulation of aldosterone and renin secretion in men. Since basal plasma aldosterone levels were normal in spinal cord transected patients, it appears that the absence of dopaminergic control does not result in elevated secretion.

18-Hydroxycorticosterone↗

PubMed1985

Dopaminergic regulation of natriuretic response to acute volume expansion in dogs.

Effects of carbidopa, a dopa (3,4-dihydroxyphenylamine) decarboxylase inhibitor, on the renal, haemodynamic and hormonal responses to acute volume expansion were examined in six healthy mongrel dogs which were infused intravenously with 0.9% sodium chloride solution (saline; 30 ml h-1 kg-1) over 2 h. Saline infusion studies were performed in the absence (control) and in the presence of carbidopa given by nasogastric tube in a dose of 1 mg/kg every 8 h beginning 24 h before the infusion. Saline infusion resulted in an increase in renal excretion of dopamine (3,4-dihydroxyphenylethylamine) and a decrease in renal excretion of noradrenaline. Carbidopa treatment decreased urinary sodium excretion and eliminated the increase in renal production of dopamine in response to saline infusion without affecting renal or haemodynamic response to acute vascular volume expansion with saline. Carbidopa treatment obliterated the suppression of aldosterone produced by saline infusion. Thus, dopamine appears to play a significant role in mediating both the natriuretic and aldosterone response to acute volume expansion.

Aldosterone↗

PubMed1985

Studies of renin activation and regulation of aldosterone and 18-hydroxycorticosterone biosynthesis in hyporeninemic hypoaldosteronism.

In an attempt to evaluate deficiencies of renin activation and adrenal zona glomerulosa biosynthesis in hyporeninemic hypoaldosteronism (HH), we studied active and inactive renin (AR and IR, respectively) responses to the dopamine antagonist metoclopramide, furosemide, and graded dose infusion of ACTH in 10 HH patients and 6 normal subjects. In HH patients, AR levels, but not IR levels, were decreased relative to normal values. While normal subjects had an AR response to metoclopramide, the HH patients did not. The AR response to furosemide in HH patients was markedly diminished compared to that in normal subjects. Plasma cortisol and corticosterone levels were in the normal range, but the zona glomerulosa products 18-hydroxycorticosterone (18-OHB) and aldosterone (Aldo) were low in HH patients. Plasma 18-OHB and Aldo responses to metoclopramide and furosemide were diminished, but cortisol and 18-OHB responses to ACTH were normal in the HH patients. Our observation that 18-OHB and Aldo responses to metoclopramide were diminished refutes the possibility that excessive adrenal zona glomerulosa dopaminergic activity could account for reduced biosynthesis of 18-OHB and Aldo in HH patients. Our results appear most consistent with the concept that the primary etiological factor in the HH syndrome is impairment of renal activation of renin.

18-Hydroxycorticosterone↗

PubMed1985

Dopaminergic mediation of the natriuretic response to volume expansion.

Previous studies have shown a direct relationship between urinary sodium excretion and both urinary dopamine excretion and plasma dopamine levels. The significance of this relationship is unclear. We therefore studied the effect of dopaminergic blockade on the renal response to volume expansion produced by the infusion of 2 L 0.9% saline solution intravenously over 4 hours in a group of six healthy adult volunteers previously shown to have appropriate sodium balance. The dopamine receptor antagonist metoclopramide was administered intravenously at a dose of 10 mg/hr throughout the study period; a separate group of control subjects received saline infusion without metoclopramide. During saline infusion urinary sodium excretion increased steadily in controls, from a basal level of 127 +/- 25 mu Eq/min to a peak value of 451 +/- 83 mu Eq/min (p less than 0.005) during the fourth hour of infusion. The study group receiving saline solution along with metoclopramide failed to show any significant increase in urinary sodium excretion over the basal levels. Cumulative sodium excretion during saline loading was significantly less in those receiving saline solution with metoclopramide (55 +/- 14 mEq) than in controls (101 +/- 15 mEq)(p less than 0.05). The plasma aldosterone levels in the control group receiving saline solution alone fell steadily from a preinfusion level of 11.0 +/- 0.9 ng/dl to the nadir of 6.5 +/- 0.9 ng/dl (p less than 0.02), reached during the third hour of infusion. In contrast, in the study group receiving saline solution with metoclopramide, the plasma aldosterone levels remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Evidence for direct inhibitory effects of dopamine on zona glomerulosa secretion of 18-hydroxycorticosterone in rhesus monkeys.

This study was designed to more selectively investigate the dopaminergic regulation of 18-hydroxycorticosterone (18-OHB) and aldosterone production by the adrenal zona glomerulosa. Mature rhesus monkeys received either an infusion of dopamine (2 micrograms/kg/min) or 5% dextrose (0.2 ml/min) over a 60 min period (N=6). Dopamine had no effect on plasma levels of renin activity, cortisol, corticosterone, aldosterone or blood pressure. However, dopamine suppressed (p less than 0.05) plasma 18-OHB levels from a baseline of 31.6 +/- 3.5 ng/dl to 23.6 +/- 2.1 ng/dl at 60 min after onset of infusion. This observation is in agreement with some studies in humans but differs from others in which no depression in 18-OHB was observed following dopamine infusion. Dopamine infusion markedly (p less than 0.001) suppressed plasma PRL levels by 30 min after onset of infusion. Corticosteroid responses to metoclopramide (200 micrograms/kg) after dexamethasone 1 mg im every 6 h X 5 days or placebo treatment (vehicle im every 6 h X 5 days) was then evaluated. Dexamethasone significantly suppressed basal cortisol, corticosterone, 18-OHB and aldosterone. Although dexamethasone blunted the prolactin response, it did not inhibit the aldosterone response to metoclopramide. The 18-OHB response to metoclopramide was increased (p less than 0.01) following dexamethasone treatment. Following dexamethasone suppression, 18-OHB levels were still lowered (p less than 0.05) by dopamine infusion. These results suggest that dopamine selectively inhibits zona glomerulosa production of 18-OHB and aldosterone in rhesus monkeys.

18-Hydroxycorticosterone↗

PubMed1984

Role of dopamine in the regulation of aldosterone and 18-hydroxycorticosterone secretion in man.

This study was designed to investigate dopaminergic mechanisms involved in the control of corticosteroid secretion. Administration of the dopamine agonist bromocriptine (2.5 mg three times a day for 4 days) to 10 normal males suppressed (p less than 0.01) plasma 18-hydroxycorticosterone (18-OHB) responses to upright posture, isometric handgrip exercise, furosemide administration and angiotensin II infusion without altering supine blood pressure, electrolytes or plasma cortisol. Plasma 18-OHB responses to adrenocorticotropic hormone infusion were not altered by bromocriptine treatment. These observations suggest that angiotensin-mediated 18-OHB and aldosterone secretion is selectively inhibited by dopaminergic mechanisms. Thus, dopamine and angiotensin II may operate as opposing factors in the control of aldosterone biosynthesis.

18-Hydroxycorticosterone↗

PubMed1984

The role of corticosteroids in the regulation of myocardial Na, K-ATPase in normotensive and spontaneously hypertensive rats.

Sodium, potassium-dependent adenosine triphosphatase (ATPase) of the renal tubule is known to be dependent on both gluco- and mineralocorticoids. Recent evidence suggests that corticosteroids may modulate ATPase activity at extrarenal sites. The myocardium contains glucocorticoid receptors to which mineralocorticoids can also bind. Thus, the possibility that myocardial ATPase is corticosteroid dependent was examined in the Wistar-Kyoto (WKY) normotensive rat and also in the spontaneously hypertensive (SH) rat, a strain previously shown to exhibit reduced myocardial ATPase activity. WKY and SH rats (in groups of 10) were either sham operated or adrenalectomized and placed on 1% NaCl solution as drinking water. Adrenalectomized rats subsequently received daily intraperitoneal injections of either vehicle (1% NaCl, 0.5 ml), aldosterone (30 micrograms/kg) or dexamethasone (60 micrograms/kg). Renal cortical and myocardial ATPase activities were determined 21 days later in all groups. Adrenalectomized WKY rats had reduced myocardial ATPase activity (5.15 +/- 0.88 vs 8.18 +/- 0.93 mumol of phosphate h-1 mg-1 of protein in controls; P less than 0.01). This observed decrease in ATPase in adrenalectomized rats could be at least partly prevented by selective aldosterone or dexamethasone replacement. Parallel changes were observed with renal cortical ATPase. SH rat myocardial ATPase was lower than in WKY rats (P less than 0.05, 5.88 +/- 0.99 mumol of phosphate h-1 mg-1 of protein) and was unaffected by adrenalectomy (5.47 +/- 0.68 mumol of phosphate h-1 mg-1 of protein) whether accompanied by aldosterone (6.08 +/- 0.68 mumol of phosphate h-1 mg-1 of protein) or dexamethasone (6.47 +/- 0.84 mumol of phosphate h-1 mg-1 of protein) therapy or not.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗

PubMed1984

Sodium-potassium ATPase in deoxycorticosterone-salt hypertension: opposing effects of sodium load and mineralocorticoids.

Previous studies of the sodium-potassium pump in the deoxycorticosterone (DOC)-salt (DS) model of hypertension yielded contrasting results, some investigators reporting increased and others finding decreased pump activity. To test the possibility that the net pump activity in the DS rats results from separate effects of sodium overload and mineralocorticoid activity, we compared the Na+-K+-ATPase pump in DS rats with that in other experimental models in which these potential determinants do not coincide. Renocortical and myocardial ATPase activities were measured in control rats; adrenalectomized-saline-repleted rats; adrenalectomized aldosterone- or dexamethasone-repleted rats; uninephrectomized, saline-drinking rats; and uninephrectomized, saline-drinking, DOC- and salt-treated rats. DOC- and salt-treated rats had higher (P less than 0.001) blood pressures and lower (P less than 0.05) serum potassium levels than control rats. Renocortical and myocardial ATPase activities were considerably (P less than 0.01) decreased in adrenalectomized, saline-repleted rats, but could be at least partially restituted by either aldosterone or dexamethasone therapy. Uninephrectomized, saline-drinking rats had reduced (P less than 0.01) renocortical and myocardial ATPase activities compared with control rats. In uninephrectomized, saline-drinking rats treated with DOC, renocortical and myocardial ATPase activities were not different from control values. The results of this study suggest that the Na+-K+-ATPase pump in DOC- and salt-treated rats is modulated by the opposing effects of sodium overload-associated suppression and DOC-mediated stimulation.

Adrenalectomy↗

PubMed1984

Relationship between urinary dopamine production and natriuresis after acute intravascular volume expansion with sodium chloride in dogs.

The role of renal production of dopamine in mediating the natriuretic response to acute vascular volume expansion was investigated. The effect of infusion of 0.9% saline (30 ml/kg X h) over 2 h on urine excretion of sodium and catecholamines, as well as other hemodynamic and renal function parameters, was examined in seven dogs during control and carbidopa (1 mg/kg every 8 h for 24 h before saline infusion) treatment periods. Acute vascular volume expansion with saline resulted in a rise (P less than 0.01) in the renal excretion of dopamine and a depression (P less than 0.01) in renal excretion of norepinephrine which paralleled the natriuretic response to saline infusion. Epinephrine excretion was not altered by saline infusion. Carbidopa treatment was not associated with changes in left ventricular filling pressure, arterial blood pressure, glomerular filtration rate, renal blood flow, renal excretion of norepinephrine or epinephrine. However, carbidopa eliminated the increase in renal production of dopamine and markedly attenuated the natriuretic response to saline infusion. Since carbidopa blocks tissue conversion of dopa to dopamine, it appears that renal production of dopamine is an important mechanism mediating the natriuretic response to acute volume expansion.

Animals↗

PubMed1984

Effect of ganglionic blockade with trimethaphan on corticosteroid responses to metoclopramide in rhesus monkeys.

In order to investigate whether metoclopramide stimulates 18-hydroxycorticosterone and aldosterone production directly by way of the autonomic nervous system, we have examined the effects of ganglionic blockade with trimethaphan on the responses to metoclopramide (200 micrograms/kg) in rhesus monkeys. Trimethaphan, infused at a rate (200 micrograms/kg/min) which significantly decreased mean arterial pressure from 122 +/- 7 to 62 +/- 4 mmHg, did not alter the peak plasma 18-OHB and aldosterone responses to metoclopramide. These results suggest that 18-hydroxycorticosterone and aldosterone responses to metoclopramide occur independently of adrenergic neuronal input.

18-Hydroxycorticosterone↗

PubMed1984

A simplified hyperbaric oxygen technique for leg ulcers.

A modified technique for administering hyperbaric oxygen with the use of disposable polyethylene bags was evaluated for the treatment of arterial leg ulcers. The potential advantages of the method include fairly low expense, lack of cross-infection, and simplicity in the administration of oxygen. Six men with 27 chronic arterial ulcers were treated with this technique, and five men (ten ulcers) served as controls. In the treated group, 18 of 27 ulcers (5/6 patients) were healed within six to 21 days, with 50% to 90% reduction in size of seven of nine of the remaining ulcers after a three-week period. None were healed in the control group. The treated ulcers healed by 7.8% +/- 1.15% per day compared with -0.5% +/- 0.37% in the control patients. The results indicate that our technique of administering hyperbaric oxygen for the treatment of leg ulcers is simple and effective. It can be adapted for either inpatient or outpatient treatment.

Adult↗

PubMed1983

Glucocorticoid suppression enhances the 18-hydroxycorticosterone and aldosterone response to metoclopramide in man.

18-Hydroxycorticosterone (18-OHB) is a precursor of aldosterone and is the only corticosteroid, other than aldosterone, that is synthesized predominantly in the zona glomerulosa. Administration of the dopamine antagonist, metoclopramide results in parallel rises in plasma 18-OHB and aldosterone levels without affecting the plasma levels of other aldosterone precursors. However, 18-OHB is a product of the zona fasciculata as well as the glomerulosa. Thus, it is possible that metoclopramide may stimulate zona fasciculata secretion of 18-OHB. In order to more selectively examine dopaminergic regulation of zona glomerulosa secretion of 18-OHB we have examined the effect of glucocorticoid suppression of the fasciculata on the 18-OHB and aldosterone responses to metoclopramide, 10 mg iv in 6 normal volunteers. Dexamethasone, 2 mg every 6 hours for 5 days, suppressed basal levels of cortisol, corticosterone, 18-OHB and aldosterone. Dexamethasone treatment had no effect on basal levels of PRA or PRA responses to metoclopramide. The 18-OHB and aldosterone responses to metoclopramide were enhanced (p less than .05) by dexamethasone suppression. The results suggest that dopaminergic mechanisms selectively suppress glomerulosa production of 18-OHB. Endogenous ACTH may inhibit zona glomerulosa production of 18-OHB and aldosterone in response to the dopamine antagonist, metoclopramide.

18-Hydroxycorticosterone↗

PubMed1983

Effects of dietary sodium on circadian rhythm and physiological responses of 18-hydroxycorticosterone.

1. The effects of dietary sodium intake on plasma 18-hydroxycorticosterone (18-OHB) responses to physiological stimuli and recumbent 24-h-plasma 18-OHB levels have been examined in nine normal male subjects. 2. Basal supine levels of 18-OHB during a 40 mmol of sodium intake period (62.5 +/- 6.0 ng/dl) were considerably greater (P less than 0.0001) than the levels during a 200 mmol of sodium intake period (9.8 +/- 1.2 ng/dl). Further incremental and percentage changes of 18-OHB in response to graded dose infusions of angiotensin II and adrenocorticotropic hormone (ACTH) were greater during the 40 mmol of sodium intake period. 3. Although the mean 24 h levels of plasma 18-OHB during the 40 mmol of sodium intake period (43.9 +/- 4.0 ng/dl) were greater (P less than 0.001) than those during the 200 mmol of sodium intake period (9.4 +/- 1.2 ng/dl), the circadian rhythm of 18-OHB secretion was similar under the two extremes of sodium intake. 4. Factors which increase angiotensin II levels, such as sodium restriction, isometric exercise and angiotensin infusion, selectively increase 18-OHB and aldosterone, suggesting that angiotensin II increases 18-OHB and aldosterone secretion, in part, by modulation of the 18-hydroxylation reaction involved in conversion of corticosterone into 18-OHB.

18-Hydroxycorticosterone↗