The diabetogenic effect of prolactin observed in patients with pathological hyperprolactinaemia was verified in healthy subjects. Plasma prolactin elevation was induced by administration of a dopamine antagonist drug domperidone (Motilium 10 mg orally, 9 subjects) and 2 h later the oral glucose tolerance test was performed. The influence of dopamine receptor stimulation on glucose homeostasis was tested by dopamine infusion (0.3 mg in saline or 20 % glucose, 1 g/min for 60 min, 11 subjects). After the blockade of dopamine receptors, a significant and prolonged increase of prolactin concentration was found. However, the levels of glucose, insulin, and C- peptide either before or after the glucose load were not different from control ones. The decreased number of insulin receptors (1.97±0.41 vs 0.51 ±0.14 pmol per 2.109 red blood cells) was compensated by increased affinity (0.51 ±0.17 vs 1.00±0.22 K* 108 mol.-1 per 1]) of insulin receptors. The stimulation of dopamine receptors showed a negligible effect on glucose regulation. It may be suggested that an endogenous increase of prolactin concentration in the physiological range does not participate in the regulation of glucose homeostasis in healthy subjects.
Glucose was found to exert an In vitro regulatory effect on prolactin secretion. Its role in the modulation of stimulated secretion of prolactin in man is, however, not clear. To evaluate the effect of hyperglycaemia on prolactin release, three stimulatory tests with different mechanisms of stimulation were employed. Healthy male subjects served as volunteers during submaximal exercise, TRH test (0.2 mg i.v.) and administration of haloperidol (2 mg i.v.). Glucose (100 g in 400 ml) or an equal volume of water was given 30 min before the tests. Blood for glucose and prolactin analysis was taken via an indwelling catheter. The plasma prolactin concentration increased in response to each of the stimuli applied. However, the prolactin increase during hyperglycaemia did not differ from values obtained in tests performed in normoglycaemia after water administration. These results indicate that prolactin release in healthy man is not modulated by hyperglycaemia.
The purpose of this study was to compare, in the same subjects, hormonal responses to 30-min head-up tilt (HUT) and lower body suction (LBNP) of different intensity (24° and 70°, and 15 and 35 mm Hg, respectively). Basal pooled individual data from -10 min (n=32) were within normal reference limits: norepinephrine (NE) averaged 318±23 pg/ml; epinephrine, 34.0±5J> pg/ml; plasma renin activity (PRA), 0.72±0.08 ng ATII/ml/h; aldosterone, 164±20 pg/ml; atrial natriuretic peptide (ANP), 29.9±2.0 pg/ml; cGMP, 6.29±0.59 mmol/1; cortisol, 95.7±5.8 ng/ml; and ACTH, 50.3±2.6 pg/ml. The low-level stimuli failed to induce consistent changes in hormone levels. From the onset of the stimulus (minute 0) to its termination (minute 30), norepinephrine (NE) increased by 101 % with LBNP-35, and by 70 % with HUT70, respectively. The NE increase with LBNP-35 was higher (p<0.05) than with HUT70. Epinephrine rose with HUT70 (by 162 %) only. PRA increased by 157 % with LBNP-35, and by 119 % with HUT70, respectively; these responses were not significantly different. Aldosterone rose equally (by 85 and 89 %) with LBNP-35 and HUT70 but not with the low-level stimuli. No consistent changes were observed in ANP, c-GMP or ACTH concentrations. Cortisol values fell during the LBNP and HUT24 situations but rose transiently after HUT70. We conclude that the hormones investigated respond differently to head-up posture and lower body suction and in a specific manner. Greater effects of high-level stimuli (HUT70, LBNP-35) were noted as compared to low-level stimuli (HUT24, LBNP-15). The application of combined sets of models stimulating the cardiovascular system may aid in the analysis of responses of hormonal systems in man.
Cardiovascular and neuroendocrine responses to exercise in a physically fit and an untrained group of young healthy subjects were compared to study the significance of physical fitness for performance in a discipline for which the athletes were not trained. Ten wrestlers of national rank prepared for an international competition (age 18 years) and 9 untrained healthy males (age 21 years). Exercise consisted of 27-min swimming, freestyle, in water of 29 °C, with last 3 min increased to maximal effort. The blood pressure, heart rate and sublingual temperature were measured and blood samples were withdrawn before exercise, immediately after and after a 30 min period of rest. Catecholamines were analyzed by radioenzymatic method and plasma renin activity (PRA) using commercial kits. Systolic blood pressure and heart rate after swimming were increased comparably in the two groups, diastolic pressure was unchanged in the controls and decreased in the wrestlers. Plasma cortisol remained unchanged. Plasma glucose tended to increase in the controls and so decrease in wrestlers, with a significant difference between them after swimming (p<0.05). However, plasma adrenaline was concomitantly increased in both groups (p<0.01). Noradrenaline and PRA were increased after swimming in both the control and trained group. The increments of noradrenaline and PRA in wrestlers were significantly reduced compared to the control group (p<0.01, p<0.05, respectively). Higher physical fitness in athletes significantly reduced plasma noradrenaline and angiotensin responses to maximal exercise demanding special skill in work performance which had not been included in their training program. Training of wrestlers did not cause an exaggerated plasma adrenaline response to exercise.
In rats, neonatal administration of monosodium glutamate (MSG) causes serious damage in some hypothalamic and circumventricular areas. The resulting loss of appropriate neurons important for the regulation of blood pressure (BP) may modulate cardiovascular system receptivity in these animals. In the present study, the reactivity of the cardiovascular system to intravenous injection of ai-adrenergic receptor agonist phenylephrine (200 ^g/kg/ml) and angiotensin II (500 ng/kg in 0.6 ml for 2 min) was investigated in adult rats which had been neonatally treated with MSG or vehicle. BP parameters measured directly in conscious cannulated rats were continuously registered using a computerized system. Under basal conditions, MSG-treated rats had slightly lower systolic, diastolic and mean BP with significant differences in pulse pressure (systolic - diastolic BP). In MSG-treated animals, the maximal increase of mean arterial BP after phenylephrine and the duration of BP elevation after both agents were significantly reduced. Slopes of the linear portion of baroreceptor function curves in control and MSG-treated rats did not differ significantly, indicating that baroreflex efficacy was unchanged. The results obtained by perfusion of the hindlimb vascular bed in situ showed that the pressure responses to increasing doses of noradrenaline in MSG-treated rats were reduced. These findings demonstrate that neonatal treatment of rats with MSG lowers the responsiveness of the cardiovascular system, particularly in response to a-adrenergic stimulation. It is suggested that the attenuation of cardiovascular reactivity in MSG-treated rats is, at least partly, caused by diminished vascular responsiveness.