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Biomedical subjects

D L Kaiser

Publications and source records attributed to D L Kaiser.

At least 109 records · Page 6Linked to original sources
PubMed1983

Effects of human pancreatic tumour growth hormone releasing factor on growth hormone and somatomedin C levels in patients with idiopathic growth hormone deficiency.

Human pancreatic tumour growth hormone releasing factor (hpGRF-40) 10 micrograms/kg was administered intravenously to 6 normal young men and 12 adult patients who had presented in childhood with growth hormone (GH) deficiency (7 patients had isolated GH deficiency, 4 had multiple anterior pituitary hormone deficiencies, and 1 had Hand-Schüller-Christian [HSC] disease). hpGRF-40 administration increased serum GH concentrations in all normal subjects and in 3 of 7 patients with isolated GH deficiency and in the 1 with HSC disease; however, the mean serum GH concentration in the patients who responded was less than that of the normal subjects. Somatomedin C concentrations were increased 24 h after a single dose of hpGRF-40 in 8 of 10 patients with GH deficiency. All subjects experienced flushing in response to hpGRF-40. A patient with isolated GH deficiency received 0.33 micrograms/kg hpGRF-40 every 3 h for 5 days. Despite the modest increase in GH in response to a subsequent dose of 10 micrograms/kg hpGRF-40, serum somatomedin C levels increased within 12 h from 0.06 to 0.1 U/ml and peaked at 0.36 U/ml at 72 h; in addition the patient with HSC disease, treated with hpGRF-40 daily for 5 days, demonstrated an increase in somatomedin C from 0.4 to 0.58 U/ml. The increase after hpGRF-40 in serum GH levels in this patient and the similar or greater responses in 3 of 7 patients suggest that at least some of these patients may have hypothalamic GH-releasing-hormone deficiency. hpGRF-40 may be useful in distinguishing pituitary disease from hypothalamic disease. After hpGRF-40 administration serum somatomedin C levels may increase without a change in serum immunoreactive GH concentrations. Further studies are needed to determine whether hpGRF-40 is useful in promoting linear growth in children with GH deficiency.

Adult↗
PubMed1983

Human pancreatic growth-hormone-releasing factor selectively stimulates growth-hormone secretion in man.

A growth-hormone-releasing factor has been characterised and sequenced from a pancreatic tumour removed from a patient with acromegaly. It is a 40-residue linear peptide. Synthetic human pancreatic growth-hormone-releasing factor (hpGRF-40), 1 microgram/kg bodyweight, was administered as an intravenous bolus to six healthy men. hpGRF-40 selectively stimulated growth-hormone secretion. Serum growth-hormone concentrations were increased within 5 min, reaching a peak between 30 and 60 min (20 . 4 +/- 6 . 5 ng/ml compared with 2 . 1 +/- 0 . 1 ng/ml after placebo). Serum levels of prolactin, thyrotropin, luteinising hormone, and corticotropin (measured indirectly through plasma cortisol) were not increased after administration of hpGRF-40. Similarly, the concentrations of blood glucose, plasma insulin, glucagon, pancreatic polypeptide, cholecystokinin, gastrin, gastric inhibitory peptide, motilin, and somatostatin were unaffected by hpGRF-40. There were no changes in blood pressure, pulse rate, or body temperature, and no side-effects were noted. The characteristics of this peptide fulfil many of the criteria required of the hypophysiotropic growth-hormone-releasing hormone. hpGRF holds promise for a new approach to the diagnosis and treatment of various disorders of growth-hormone secretion.

Acromegaly↗
PubMed1983

Acute effects of steroids on immune complex profile of patients with systemic lupus erythematosus. Correlation of profile with development of target organ involvement.

Eleven patients with active systemic lupus erythematosus, previously untreated, were studied to 1) determine the acute effect of corticosteroids on circulating immune complex (CIC) levels and 2) correlate the initial CIC profile with the development of organ system involvement. Using serial measurements of CIC as detected by assays for cryoglobulins and binding to C1q, Raji cells, and rheumatoid factor, we found that levels of CIC change little during the first month of high dose daily steroid therapy, but they uniformly decrease to near normal by 6 to 12 months. High levels of CIC detected by Raji cell assay early in the course of systemic lupus erythematosus and before steroid therapy appear to be predictive of the development of chronic lupus nephritis (P less than 0.005).

Adult↗
PubMed1983

Double-blind randomized study of prophylactic trimethoprim/sulfamethoxazole in granulocytopenic patients with hematologic malignancies.

In a double blind study, oral prophylactic trimethoprim/sulfamethoxazole was evaluated for its utility in preventing serious infections in patients with hematologic malignancy. Of 58 evaluated granulocytopenic episodes in 47 patients, acute leukemia was the underlying malignancy in 46 episodes. Trimethoprim/sulfamethoxazole prophylaxis resulted in fewer microbiologically documented infections (seven versus 15; p = 0.029). This was primarily the result of a reduction in episodes of bacteremia in the trimethoprim/sulfamethoxazole-treated group as compared with the placebo-treated group (three versus nine episodes; p = 0.05). The combined frequency of disseminated candidiasis, candidemia, and esophagitis of presumed fungal etiology was greater in the trimethoprim/sulfamethoxazole-treated group (six) than in the placebo-treated group (two) but not significantly so (p = 0.13). Similarly, there were no significant differences between groups in the overall incidence of infectious complications, number of febrile days, use of parenteral antibiotics, or number of days following randomization to first infectious episode. Throat and rectal surveillance cultures more frequently revealed trimethoprim/sulfamethoxazole-resistant gram-negative bacilli and yeasts in the trimethoprim/sulfamethoxazole-treated group. More frequent emergence of yeast isolates from previously culture-negative patients was documented (p = 0.033). Thus, in this study, trimethoprim/sulfamethoxazole prophylaxis during granulocytopenia reduced the incidence of microbiologically documented infections. However, the emergence of resistant bacteria and of fungi may limit the potential usefulness of this approach.

Adolescent↗
PubMed1983

Nosocomial urinary tract infections: secular trends, treatment and economics in a university hospital.

During a 71-month interval 3,024 nosocomial urinary tract infections were identified by prospective surveillance at our hospital. The annual attack rate varied between 2.0 and 3.1 per 100 admissions. Gram-negative bacilli caused 74 per cent of all urinary infections and recurrent infections in the hospital accounted for only 1 per cent. The most frequent pathogens were Escherichia coli (24 per cent), Pseudomonas aeruginosa (8 per cent), Streptococcus faecalis (7 per cent), Klebsiella pneumoniae (6 per cent) and Proteus mirabilis (6 per cent). Candida species caused 10 per cent of the infections and may represent a hospital-acquired pathogen of increasing importance. The burn unit had a significantly higher proportion of Enterobacter infections (21 per cent) than any other service (p less than 0.05). The plastic surgery service had more Serratia infections (24 per cent), whereas obstetrics and gynecology had more Escherichia coli infections (47 per cent) relative to other hospital services. More than 99 per cent of the patients with nosocomial urinary tract infections received antimicrobial drugs; in 63 per cent the chart documented that drug therapy was prescribed specifically for treatment of the urinary infections. Hospital-acquired urinary infections added approximately 1 million dollars to hospital expenses during the study interval. Estimates were made of the economic benefits of successful control programs.

Cross Infection↗
PubMed1983

Urinary tract etiology of bloodstream infections in hospitalized patients.

During a 23-month study, we identified 1,233 patients with nosocomial urinary tract infections (UTIs) among 40,718 consecutive admissions by using a standardized, prospective system of hospital-wide surveillance. Nosocomial bloodstream infections (BSIs) occurred in 565 patients, 32 of whom had BSIs originating from UTIs, for an attack rate of 2.7 per 100 patients with nosocomial bacteriuria. Patients with UTIs due to Serratia marcescens were most likely to develop secondary BSIs (rate, 16 per 100) compared to patients with nosocomial UTIs due to other organisms (rate, less than or equal to 4.3 per 100; P less than 0.05). Furthermore, the median interval between documentation of UTI and of secondary BSI was 24 days for patients with infections due to S marcescens compared to one day for the entire group (P less than 0.005). Risk factor analysis indicated that men with UTIs were more likely to develop secondary BSIs than were women (P less than 0.05). Intensified infection control efforts are particularly necessary with high-risk groups such as bacteriuric men--especially among those patients with UTIs due to S marcescens--to reduce the incidence of secondary, hospital-acquired BSIs.

Adult↗
PubMed1983

Acute hypoxemia and hypercapnia: increase in plasma catecholamines in conscious dogs.

To systemically evaluate the effects of acute hypoxemia and hypercapnic acidosis on the sympathetic nervous system, five unanesthetized mongrel dogs were studied during acute hypoxemia [arterial O2 tension (PaO2) 33 +/- 2 Torr], acute hypercapnic acidosis [arterial CO2 tension (PaCO2) 53 +/- 1 Torr; pH, 7.19 +/- 0.02], and combined acute hypoxemia and hypercapnic acidosis (PaO2, 36 +/- 1 Torr; PaCO2, 52 +/- 1 Torr; pH, 7.18 +/- 0.02). Combined acute hypoxemia and hypercapnic acidosis resulted in increased mean arterial pressure, cardiac output, and heart rate. Moreover, combining acute hypoxemia and hypercapnic acidosis acted synergistically to increase circulating norepinephrine and epinephrine. Acute hypoxemia alone and acute hypercapnic acidosis alone resulted in reversible increases in mean arterial pressure, cardiac output, heart rate, and circulating norepinephrine. Although plasma epinephrine concentrations increased during acute hypoxemia, circulating epinephrine was unchanged during acute hypercapnic acidosis. These data indicate that acute hypoxemia and hypercapnic acidosis result in synergistic increase in circulating catecholamines.

Acidosis↗
PubMed1983

Autoregulation of renal blood flow in the rat: effects of growth and uninephrectomy.

As a result of normal maturation or after reduction in renal mass, renal blood flow (RBF) progressively increases. However, the effects of renal growth on the relationship of RBF to renal perfusion pressure (RPP) have not been systematically investigated. We examined RBF as a function of RPP in anesthetized young and adult rats that had been subjected to uninephrectomy or sham operation 3-4 wk previously. As a result of normal growth, mean arterial blood pressure increased from 94.1 +/- 2.7 (SE) to 118.9 +/- 4.2 mmHg. The calculated autoregulation factor, in which a value less than 1 indicates the presence of autoregulation, was 0.44 +/- 0.10 over RPP 70-100 mmHg and 1.74 +/- 0.25 over RPP 40-70 mmHg in sham-operated young animals. In adult sham-operated rats, the factor was 0.38 +/- 0.07 over RPP 100-130 mmHg and 1.03 +/- 0.07 over RPP 70-100 mmHg. Uninephrectomy in adults resulted in a 30% rise in RBF over RPP 100-130 mmHg, and there was no change in the autoregulation factor. Uninephrectomy in young rats, however, resulted in a 35% rise in RBF at RPP = 100 mmHg with only a 17% rise at RPP = 70 mmHg, and the autoregulation factor increased to 0.91 +/- 0.10 over this range of RPP. We conclude that the autoregulatory range shifts with increasing blood pressure during normal growth and that autoregulation is "reset" to higher RBF in the uninephrectomized adult rat. Although autoregulation takes place in the young animal, uninephrectomy alters the relationship of RBF to RPP such that autoregulation is impaired.

Aging↗
PubMed1983

Prediction of cardiac events after uncomplicated myocardial infarction: a prospective study comparing predischarge exercise thallium-201 scintigraphy and coronary angiography.

The ability of predischarge quantitative exercise thallium-201 (201T1) scintigraphy to predict future cardiac events was evaluated prospectively in 140 consecutive patients with uncomplicated acute myocardial infarction; the results were compared with those of submaximal exercise treadmill testing and coronary angiography. High risk was assigned if scintigraphy detected 201T1 defects in more than one discrete vascular region, redistribution, or increased lung uptake, if exercise testing caused ST segment depression greater than or equal to 1 mm or angina or if angiography revealed multivessel disease. Low risk was designated if scintigraphy detected a single-region defect, no redistribution, or no increase in lung uptake, if exercise testing caused no ST segment depression or angina, or if angiography revealed single-vessel disease or no disease. By 15 +/- 12 months, 50 patients had experienced a cardiac event; seven died (five suddenly), nine suffered recurrent myocardial infarction, and 34 developed severe class III or IV angina pectoris. Compared with that of patients at low risk, the cumulative probability of a cardiac event was greater in high-risk patients identified by scintigraphy (p less than .001), exercise testing (p = .011), or angiography (p = .007). Scintigraphy predicted low-risk status better than exercise testing (p = .01) or angiography (p = .05). Each predicted mortality with equal accuracy. However, scintigraphy was more sensitive in detecting patients who experienced reinfarction or who developed class III or IV angina. When all 50 patients with events were combined, scintigraphy identified 47 high-risk patients (94%), whereas exercise-induced ST segment depression or angina detected only 28 (56%) (p less than .001). The presence of multivessel disease as assessed by angiography identified nine more patients with events than exercise testing (p = .06). However, the overall sensitivity of angiography was lower than that of scintigraphy (71% vs 94%; p less than .01) because three patients who experienced reinfarction and 10 who developed class III or IV angina had single-vessel disease. Importantly, 12 (92%) of these 13 patients with single-vessel disease who had an event exhibited redistribution on scintigraphy. These results indicate that (1) submaximal exercise 201T1 scintigraphy can distinguish high- and low-risk groups after uncomplicated acute myocardial infarction before hospital discharge; (2) 201T1 defects in more than one discrete vascular region, presence of delayed redistribution, or increased lung thallium uptake are more sensitive predictors of subsequent cardiac events than ST segment depression, angina, or extent of angiographic disease; and (3) low-risk patients are best identified by a single-region 201T1 defect without redistribution and no increased lung uptake.

Adult↗
PubMed1983

Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs.

Since heart failure may occur in the setting of lung dysfunction and CO2 retention with only modest increases in cardiac work load, we questioned whether myocardial function is impaired by hypercapnic acidosis. To determine the influence of hypercapnic acidosis on right ventricular function, we measured the effects of acute (2 hours) and chronic (2 weeks) hypercapnic acidosis on right ventricular performance during normal and increased right ventricular afterload in five conscious dogs. Systemic hemodynamic and right ventricular functions were unaltered during normal right ventricular afterload by acute hypercapnic acidosis (PaCO2 = 49 +/- 3 mm Hg, pH = 7.27 +/- 0.003). As right ventricular afterload was increased by progressive balloon occlusion of the right ventricular outflow tract during acute hypercapnic acidosis, the rise (slope) in right ventricular end-diastolic pressure was increased 4-fold (P less than 0.01) over that observed in normocapnic control. Maximum isovolumic right ventricular dP/dt rose (P less than 0.05) comparably with increasing right ventricular afterload during normocapnic control and acute hypercapnic acidosis. Chronic hypercapnic acidosis (PaCO2 = 55 +/- 2 mm Hg, pH = 7.28 +/- 0.01) resulted in systemic vasodilation and increased (P less than 0.05) heart rate and cardiac output during normal right ventricular afterload. As right ventricular afterload was increased during chronic hypercapnic acidosis, the rate of rise in right ventricular end-diastolic pressure was 2-fold (P less than 0.01) above normocapnic control but maximum isovolumic right ventricular dP/dt was unchanged in contrast to normocapnic control and acute hypercapnic acidosis. Moreover, cardiac output fell and stroke work was unchanged with increasing afterload during chronic hypercapnic acidosis. beta-Adrenergic blockade resulted in an increased (P less than 0.01) rate of rise in right ventricular end-diastolic pressure with afterload during normocapnic control and chronic hypercapnic acidosis. We conclude that hypercapnic acidosis results in diminished right ventricular performance during increased right ventricular afterload, evidenced by accentuated rise in right ventricular end-diastolic pressure, and may contribute to the congestive heart failure and edema observed in patients with pulmonary hypertension and CO2 retention.

Acidosis, Respiratory↗
PubMed1983

Synergistic effects of acute hypoxemia and hypercapnic acidosis in conscious dogs. Renal dysfunction and activation of the renin-angiotensin system.

The effects of acute hypoxemia and hypercapnic acidosis were examined in five unanesthetized dogs in which sodium intake was controlled at 80 mEq/24 hours for 4 days prior to study. Each animal was studied during combined acute hypoxemia and hypercapnic acidosis (Pao2 = 36 +/- 1 mm Hg, Paco2 = 52 +/- 1 mm Hg, pH = 7.18 +/- 0.02), acute hypoxemia alone (Pao2 = 32 +/- 1 mm Hg, Paco2 = 32 +/- 1mm Hg, pH = 7.34 +/- 0.01), and acute hypercapnic acidosis alone (Pao2 = 82 +/- 2 mm Hg, Paco2 = 51 +/- 1 mm Hg, pH = 7.18 +/- 0.02). Although mean arterial pressure, cardiac output, and heart rate increased during combined hypoxemia and hypercapnic acidosis, effective renal plasma flow and glomerular filtration rate decreased. In addition, filtered sodium load and urinary sodium excretion decreased during combined hypoxemia and hypercapnic acidosis. Either acute hypoxemia or hypercapnic acidosis alone resulted in increased mean arterial pressure, cardiac output, and heart rate. However, in contrast to their combined effects, renal hemodynamic function was unchanged and natriuresis was observed. Measurement of plasma renin activity and angiotensin II concentrations indicated that hypoxemia or hypercapnic acidosis alone resulted in moderate activation of the renin-angiotensin system. Moreover, combined hypoxemia and hypercapnic acidosis acted synergistically resulting in major renin-angiotensin activation. Systemic angiotensin II blockade using 1-sarcosine, 8-alanine, angiotensin II (2 micrograms/kg per min) during combined acute hypoxemia and hypercapnic acidosis resulted in decreased renal hemodynamic function. We conclude that acute hypoxemia and hypercapnic acidosis act synergistically to increase mean arterial pressure, diminish renal hemodynamic function and activate the renin-angiotensin system. Systemic angiotensin inhibition studies suggest activation of the renin-angiotensin system maintains renal hemodynamic function during combined hypoxemia and hypercapnic acidosis, instead of mediating the renal vasoconstriction.

Acidosis, Respiratory↗
PubMed1983

Ca+2 dependence of gonadotropin-releasing hormone-stimulated luteinizing hormone secretion: in vitro studies using continuously perifused dispersed rat anterior pituitary cells.

A continuously perifused dispersed rat anterior pituitary cell system was used to determine the importance of calcium (Ca+2) on the release of LH by GnRH. In response to continuous exposure to 10 nM GnRH, LH was released in a biphasic fashion; arbitrarily, phase I was defined as being the LH released during the initial 40 min and phase II as the subsequent release. Withdrawal of Ca+2 from the perifusion medium during phases I or II of LH release led to a rapid inhibition of the LH secretion. Cells were exposed to GnRH for 2.5 min, washed with medium for 30 min, and then reexposed to GnRH for 30 min. This sequence was repeated 1 h later under identical conditions in the presence of a Ca+2 blocking agent; D600 (20 or 100 microM). D600 inhibited both the 2.5- and the 30-min GnRH-stimulated LH release. The results were expressed as the ratio obtained by dividing the total LH released during the second GnRH exposure (either 2.5 or 30 min) by the total LH released during the respective initial GnRH exposure of same duration. For the cells perifused with 20 microM D600 the ratios +/- SE (D600 vs. control) were 0.48 +/- 0.06 vs. 1.28 +/- 0.13 (P = 0.0001) and 0.29 +/- 0.05 vs. 1.01 +/- 0.08 (P less than or equal to 0.0001) for the 2.5- and 30-min exposures, respectively. For the cells perifused with 100 microM D600 the ratios +/- SE (D600 vs. control) were 0.18 +/- 0.05 vs. 1.28 +/- 0.13 (P less than or equal to 0.00001) and 0.12 +/- 0.03 vs. 1.01 +/- 0.08 (P = 0.002) for the 2.5- and 30-min exposures, respectively, revealing an even more profound inhibitory effect of D600 on GnRH stimulated LH secretion. Our data both confirm previous reports that Ca+2 is involved in LH release and demonstrate that Ca+2 is an essential requirement during both phases of GnRH-stimulated LH release in perifused dispersed rat anterior pituitary cells.

Animals↗
PubMed1983

Possible mechanism of action of metoclopramide-induced aldosterone secretion: in vivo and in vitro studies in the sheep.

To define further the mechanism by which metoclopramide, a dopamine antagonist, stimulates aldosterone secretion, seven lambs were injected iv with metoclopramide during a constant infusion of 5% dextrose in water and again during a constant infusion of trimethapan, a ganglionic blocker. In addition, suspensions of adrenal zona glomerulosa cells from the lambs were incubated in vitro in the presence of various concentrations of metoclopramide and known secretagogues. Plasma aldosterone concentrations increased in response to both metoclopramide and trimethaphan. However, during the trimethaphan infusion, no further increase in plasma aldosterone concentrations occurred after metaclopramide injection. In vitro, aldosterone concentrations in the zona glomerulosa cell suspensions increased in the presence of ACTH, potassium, and angiotensin II, but no increase in aldosterone concentration occurred in the presence of metoclopramide. These results suggest that in the sheep, metoclopramide stimulates aldosterone secretion by an indirect mechanism. This mechanism may involve the autonomic nervous system, since ganglionic blockade appeared to abolish the aldosterone response to metoclopramide.

Adrenal Glands↗
PubMed1983

Human pancreatic growth hormone-releasing factor-40 (hpGRF-40) allows stimulation of GH release by TRH.

The effects of synthetic hpGRF-40 on GH release from continuously perifused male rat anterior pituitary cells were studied. Pulses (2.5 min) of hpGRF-40 stimulated GH release in a log-linear dose response relationship: concentrations of 0.03, 0.1, 0.3, 1, 3, 10, 30 and 100 nM given in a random order elicited a GH response above baseline of 1.2 +/- 0.3, 2.4 +/- 0.4, 2.8 +/- 0.2, 4.3 +/- 0.2, 6.2 +/- 0.7, 7.0 +/- 1.0, 8.7 +/- 1.7, and 10.8 +/- 0.8 micrograms/10(7) cells (mean +/- SEM; n = 3; r = 0.93), respectively. During a 5-h hpGRF-40 infusion, GH stimulation peaked within 5 min and waned to near baseline by the end of the fifth h. The integrated GH responses to 0.03, 0.1 and 0.3 nM hpGRF-40 were 37.6 +/- 7.4, 52.9 +/- 8.5, and 66.15 +/- 8.2 micrograms/10(7) (mean +/- SEM; n = 3; r = 0.72), respectively. The interaction of TRH and hpGRF-40 in the control of GH secretion was studied to investigate the mechanism of the "paradoxical" TRH stimulation of GH release associated with GH excess states in humans. Dispersed cells were perifused with either 100 nM TRH for 0.5 h, 5 nM hpGRF-40 for 4 h, or 5 nM hpGRF-40 for 4 h, to which a 0.5 h pulse of TRH was added at 2 h. GH levels did not change significantly in the presence of TRH alone. When TRH was added to the ongoing hpGRF-40 perifusion, GH release increased from 1.4 +/- 0.06 to 4.0 +/- 1.0 micrograms/min.10(7) cells (n = 4; P = 0.03). Thus, dispersed pituitary cells are highly sensitive to very low concentrations of hpGRF-40 administered as both an acute pulse and as a tonic infusion. When the cells are exposed to a maximal concentration of hpGRF-40 (i.e. 5 nM), TRH becomes a secretagogue at the pituitary level, thus suggesting the site and mechanism of the "paradoxical" GH response to TRH observed in some acromegalics.

Animals↗
PubMed1983

Suppression of basal and stimulated noradrenergic activities by the dopamine agonist bromocriptine in man.

This study was designed to determine the effects of dopaminergic receptor stimulation on basal and stimulated catecholamine release in man. Five normal white male volunteer subjects were studied in metabolic balance at constant 150-meq sodium, 60-meq potassium intake and then daily for 8 days on an isocaloric constant diet of 10 meq sodium and 60 meq potassium/day in each of two separate protocols. In one protocol, the subjects received the dopamine agonist bromocriptine for 14 days before and during the study; in the other protocol, placebo was substituted for bromocriptine. During normal sodium intake, bromocriptine suppressed supine plasma norepinephrine concentrations from 193 +/- 10 to 159 +/- 9 pg/ml (P = 0.01). Dietary sodium depletion increased supine plasma norepinephrine concentrations in subjects taking placebo from 193 +/- 10 to 229 +/- 10 pg/ml (P less than 0.001). Bromocriptine prevented the supine plasma norepinephrine response to sodium depletion. After discontinuation of bromocriptine treatment, supine plasma norepinephrine concentrations returned to placebo control values. Upright posture stimulated an increase in plasma norepinephrine concentrations from 193 +/- 10 to 419 +/- 30 pg/ml (P = 0.0001) during normal sodium intake, and bromocriptine suppressed this response from 419 +/- 30 to 286 +/- 29 pg/ml (P = 0.004). Dietary sodium depletion enhanced the plasma norepinephrine response to upright posture, and bromocriptine markedly suppressed this enhancement. After discontinuation of bromocriptine treatment, supine and upright plasma norepinephrine concentrations returned to placebo control values. Bromocriptine induced a parallel downward shift in the inverse hyperbolic relationship between the plasma norepinephrine concentration and urinary sodium excretion in erect subjects, and decreased overnight urinary norepinephrine excretion in supine subjects from 1.1 +/- 0.1 to 0.6 +/- 0.1 ng/h (P = 0.0002). No consistent effects of bromocriptine on plasma epinephrine or dopamine concentrations were observed. The results of this study strongly suggest an inhibitory action of dopamine receptor stimulation by bromocriptine on basal and stimulated norepinephrine output at noradrenergic nerve terminals in the central nervous system and/or the periphery.

Adult↗
PubMed1983

Dopaminergic inhibition of aldosterone secretion in man is independent of the autonomic nervous system.

To determine whether the plasma aldosterone response to metoclopramide, a dopamine antagonist, is mediated by the autonomic nervous system in man, five healthy male volunteers were injected with metoclopramide during an infusion of either 5% dextrose in water or trimethaphan, a ganglionic blocker. Despite evidence of ganglionic blockade during the trimethaphan infusion, the aldosterone response to metoclopramide remained intact. This suggests that the aldosterone response to metoclopramide is not mediated by the autonomic nervous system in man as it appears to be in the sheep, and suggests species variation in the mechanism of this this mineralocorticoid response.

Adult↗
PubMed1983

Naloxone attenuates recovery from insulin-induced hypoglycemia in normal man.

The effect of the opioid antagonist, naloxone, on recovery of serum glucose concentrations from insulin-induced (0.1 U/kg) hypoglycemia was determined in five normal adult men. Each subject was studied on 2 separate days, at least 2 weeks apart, during an infusion of either normal saline (6.5 ml/h) or naloxone (0.8 mg/h). The order of the infusions was randomized and double blinded. Although glucose recovery was complete by 120 min after insulin administration during each study, the fractional rate of glucose recovery as determined by analysis of covariance was significantly slower during the naloxone infusions (P = 0.008). Plasma glucagon, serum cortisol, and serum GH concentrations were not different during glucose recovery on either study day. These studies suggest that endogenous opioids contribute to glucose recovery from insulin-induced hypoglycemia and therefore may be important to glucose homeostasis in normal man.

Blood Glucose↗