Characterization of dopamine receptors by 3H-ADTN binding in calf adrenal zona glomerulosa.
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Biomedical subjects
Publications and source records attributed to M Bevilacqua.
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Metoclopramide, a dopaminergic inhibitor, injected in 9 normal volunteers, was followed by a prompt decrease of serum potassium (10--20 min; p less than 0.01) and by an increase of plasma aldosterone (p less than 0.01). Renin slightly increased at 45 min (p less than 0.05); insulin and cortisol did not show any significant increase. The urinary excretion of potassium rose after metoclopramide (p less than 0.05). A bolus of aldosterone (250 micrograms i.v.) in 4 normal subjects was not followed by any modification of serum potassium, but increased urinary potassium excretion (p less than 0.05); the injection of metoclopramide in two patients with an aldosterone-secreting adenoma of the adrenal and in one patient with Addison's disease induced a decrease of serum potassium in absence of any modification of plasma aldosterone. The decrease of serum potassium after metoclopramide is not explained by changes of aldosterone or insulin, considered the most important hormonal controls of potassium. The rapidity of potassium decrease implies a change of distribution of potassium between extra- and intracellular compartments, which, in turn, may stimulate aldosterone secretion. It is conceivable that the dopaminergic system has a role in the control of serum potassium.
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Normal subjects and patients with adult-onset diabetes received 10 gm. of aspirin in four days. On the fourth day, the fasting serum glucose and the glucose response to oral glucose were decreased in both groups. These changes were associated with increased levels of serum insulin and pancreatic glucagon, although the glucagon responses to oral glucose were unchanged. In the diabetic patients, aspirin therapy was followed by a decreased glucose response to I.V. glucose and by the appearance of an early insulin peak, which could not be demonstrated before treatment. Aspirin did not affect the I.V. glucose tolerance in normal subjects, although it did enhance the early insulin peak. A decrease in the fasting levels of free fatty acids was noted in both groups, whereas the fasting level of triglycerides decreased only in the diabetic patients. Cholesterolemia did not change in either group. A few preliminary observations indicate that, in normal subjects, ibuprofen and ketoprofen, two other presumed prostaglandin inhibitors, did not affect fasting glycemia, glucose tolerance, or the insulin response to glucose. No changes were noted after the administration of placebo.
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Respiratory function investigations (spirometry, capillary haemogasanalysis and Xenon 133), before and after dialysis, have been carried out in 10 uraemic patients. Methods of investigation and the results showing a post-dialysis improvement of the lung ventilation and perfusion function, are described.
Plasma Aldosterone (PA) response to metoclopramide (10 mg i.v.) was studied in 11 normal, 2 hypophysectomized subjects and in one patient with bilateral adrenal hyperplasia. All the subjects were kept on a normal sodium and potassium intake. Four normal subjects were pretreated with 1 mg of dexamethasone in order to inhibit endogenous ACTH. In all subjects metoclopramide elicited a prompt rise of PA comparable to that obtained with angiotensions or ACTH. No significant change of blood pressure, serum electrolytes, plasma renin activity, Plasma Cortisol (PC) was detected. The lack of PC response to metoclopramide and the PA increase in dexamethasone pretreated subjects rule out an ACTH mediated effect. The increase of PA in hypophysectomized subjects, in whom metoclopramide did not stimulate any prolactin release, rules out a prolactin mediated effect. Metoclopramide increases plasma aldosterone concentration probably via a direct action on the adrenal glomerular zone or throught another unknown mechanism.
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124 patients with obstructive broncho-pulmonary syndromes have bzen studied with 133Xe moving scanning. The method and the results are described; 5 cases are reported in detail.
The literature data concerning respiratory function in cirrhosis of the liver are cited and reference is made to the results of a spirometric, gas analysis and 133-Xenon investigation of this parameter in 38 patients. Spirometry pointed to slight ventilatory incapacity of the restrictive type. Arterial gas analaysis showed respiratory alkalosis, usually accompanied by metabolic acidosis and slight hypoxyaemia. Examination with 133-Xe indicated that hypoxyaemia was not due to a shunt effect, since there was no excess of perfusion with respect to district ventilation. It was clear, on the other hand, that the pulmonary capillary reserve was almost exhausted. Such complete perfusion of the capillary bed may be due to increased cardiac output and, in part, to reduction of the respiratory surface caused by raising of the diaphragm and hypoventilation of the lung bases.
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