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Biomedical subjects

M Bramnert

Publications and source records attributed to M Bramnert.

28 records · Page 2Linked to original sources
PubMed1988

The effect of naloxone on blood pressure, heart rate, plasma catecholamines, renin activity and aldosterone following exercise in healthy males.

There is evidence that endogenous opioids are involved in blood pressure regulation. In the present study the effect of naloxone on the cardiovascular, sympathoadrenomedullary and renin-aldosterone response to physical exercise was investigated in 8 healthy males. Each subject performed a submaximal work test twice, i.e. with and without naloxone. The test consisted of ergometer bicycling for 10 minutes on 50% of the maximal working capacity (MWC), immediately followed by 10 min on 80% of MWC. Ten minutes before exercise the subjects received in a single blind randomized order a bolus dose of naloxone (100 micrograms/kg) or a corresponding volume of the preservatives of the naloxone preparation (control) followed by a slow infusion of naloxone (50 micrograms/kg/h) or preservatives, respectively. Naloxone was without effect on the exercise-induced changes in systolic blood pressure, heart rate, plasma noradrenaline, renin activity and aldosterone, but the adrenaline response increased markedly. The present results indicate that opioid receptors are involved in the plasma adrenaline response to submaximal exercise, but not in the regulation of systolic blood pressure, heart rate, plasma noradrenaline, renin activity and plasma aldosterone.

Adult↗
PubMed1987

Naloxone enhances the increase in plasma growth hormone induced by alpha 2-adrenergic stimulation in healthy males.

There is evidence that the alpha 2-adrenergic agonist clonidine interacts with the opioid system. In the present investigations, the effect of naloxone on the increase in plasma GH induced by clonidine and the more specific alpha 2-agonist guanfacine was studied in man. In a single-blind study, five healthy males received in randomized order either the preservatives in the naloxone preparation (control) or naloxone at two different doses (10 or 100 micrograms/kg) followed by an infusion of either diluted preservatives or naloxone (5 or 50 micrograms X kg-1 X h-1, respectively). Fifteen min after the bolus dose, clonidine (3 micrograms/kg) or guanfacine (15 micrograms/kg) was infused over 10 min in a single-blind order. Both clonidine and guanfacine induced an increase in plasma GH (P less than 0.05). Pre-treatment with naloxone at the higher dosage resulted in an enhanced (P less than 0.05) GH response to clonidine and guanfacine, respectively, whereas the lower dosage of naloxone was without effect. The increase in plasma GH did not correlate with basal mean arterial blood pressure, nor with the changes in mean arterial blood pressure induced by clonidine or guanfacine. These results indicate that the increase in plasma GH induced by alpha 2-adrenergic stimulation in normotensive subjects involves opioid receptors with moderate sensitivity to naloxone.

Adrenergic alpha-Agonists↗
PubMed1987

The influence of naloxone on exercise-induced increase in plasma pituitary hormones and the subjectively experienced level of exhaustion in healthy males.

Opioid peptides seem to play a role as modulators of the pituitary function in man. In the present study, the effect of naloxone on exercise-induced pituitary hormone release and the subjectively experienced level of exhaustion were investigated in nine healthy males. A submaximal work test was performed on two occasions using a bicycle ergometer: 10 min on 50% of maximal working capacity (MWC), immediately followed by 10 min on 80% of MWC. Ten min before exercise, each subject received, in a single-blind randomized order, either a bolus dose of naloxone (100 micrograms/kg) followed by a slow infusion of naloxone (50 micrograms X kg-1 X h-1) or as a control a corresponding volume of the preservatives in the naloxone preparation as a bolus dose followed by an infusion of diluted preservatives. In the control studies, exercise induced a significant increase in GH, PRL, TSH and ACTH. The increase in ACTH was enhanced following naloxone. Naloxone was without effect on exercise-induced changes in GH, PRL and TSH. An increased level of exhaustion was experienced on 80% of MWC during naloxone. It is concluded that opioid receptors with a moderate sensitivity to naloxone are involved in the regulation of the ACTH response to exercise and also influence the subjectively experienced level of exhaustion.

Adrenocorticotropic Hormone↗
PubMed1985

Lack of effect of naloxone in a moderate dosage on the exercise-induced increase in blood pressure, heart rate, plasma catecholamines, plasma renin activity and plasma aldosterone in healthy males.

There is evidence that opioid peptides influence blood pressure and heart rate in animals and man. In the present investigation the effect of naloxone on the exercise-induced increase in blood pressure, heart rate, plasma catecholamines, plasma renin activity (PRA) and plasma aldosterone was investigated in nine healthy men. A submaximal work test was performed on two occasions. The test consisted of ergometer bicycling for 10 min on 50% of maximal working capacity immediately followed by 10 min on 80% of maximal working capacity. Ten minutes before exercise the subjects received in a randomized manner a bolus dose of naloxone (10 micrograms/kg) or a corresponding volume of saline followed by a slow infusion (15 ml/h) of naloxone (5 micrograms h-1 kg-1) or saline, respectively. After exercise systolic blood pressure, heart rate, plasma catecholamines, PRA and plasma aldosterone increased during both saline and naloxone infusion. The changes were similar in both studies. Accordingly, opiate receptors sensitive to naloxone in a moderate dosage seem not to be involved in the cardiovascular response and the increase in plasma catecholamines, PRA and plasma aldosterone induced by exercise.

Adult↗
PubMed1984

Partial blockade by naloxone of clonidine-induced increase in plasma growth hormone in hypertensive patients.

Studies in animals and man indicate a functional interaction between the adrenergic and the opiate systems. In the present study the effect of the opiate receptor blocker naloxone on the increase in plasma GH induced by clonidine was investigated in eight patients with essential hypertension. In a randomized order the patients received a bolus dose of naloxone (10 micrograms/kg) or physiological saline followed by a slow infusion of naloxone (5 micrograms/kg X h) or saline, respectively. Fifteen minutes after the bolus dose of saline or naloxone, clonidine (3 micrograms/kg) was infused for 10 min. Clonidine induced a significant increase in plasma GH. Naloxone pretreatment resulted in a significantly reduced GH increase after the clonidine infusion. These results indicate that the clonidine-induced increase in plasma GH in hypertensive man is partly mediated via activation of opiate receptors which can be blocked by naloxone.

Clonidine↗
PubMed1983

Failure of naloxone to reduce the clonidine induced reduction of blood pressure and plasma noradrenaline in patients with essential hypertension.

Studies in animals and man indicate a functional interaction between the adrenergic and the opiate systems. In the present study the effect of the opiate receptor blocker naloxone on the reduction of blood pressure and plasma noradrenaline induced by the alpha 2-agonist clonidine was investigated in nine patients with essential hypertension. In a randomised manner the patients received a bolus dose of naloxone (10 micrograms/kg) or physiological saline followed by a slow infusion of naloxone (5 micrograms/kg/h) or saline, respectively. Fifteen minutes after the respective bolus dose, clonidine (3 micrograms/kg) was infused over 10 minutes. Naloxone had no effect on the clonidine induced hypotension and reduction of plasma noradrenaline. Accordingly, there is no evidence that the clonidine induced reduction of blood pressure and plasma noradrenaline involves opiate receptors that can be blocked by naloxone. Plasma adrenaline increased significantly during the early phase of naloxone infusion.

Adult↗
PubMed1981

The effect of captopril on catecholamines, renin activity, angiotensin II and aldosterone in plasma during physical exercise in hypertensive patients.

The studies were designed to explore the effect of the converting enzyme inhibitor captopril on the activity of the sympathetic nervous system during basal conditions and following graded physical exercise in patients with essential hypertension. Seven males and two females, aged 36-59 years, were hospitalized under metabolic ward conditions and treated for 7 days with captopril given orally in increasing dosages, the final dose being 600 mg daily. The patients were subjected to an individual, graded submaximal work test (bicycling) for 20 min before medication and then again in an identical manner during medication with 600 mg captopril. Blood samples were drawn before exercise and then after 10 and 20 min of work for the determination of plasma angiotensin II (PA II), plasma aldosterone (PAC), plasma renin activity (PRA), plasma noradrenaline (PNA) and plasma adrenaline (PA). Before medication blood pressure (mmHg) was 195/133 immediately before exercise, 230/129 after 10 min of moderate exercise and 263/105 following 20 mon of nearly maximal work. During treatment with captopril the respective blood pressure values were 154/110, 200/100 and 245/98. Captopril had no significant effect on the changes in heart rate following physical exercise. PA II and PAC were substantially reduced and PRA considerably increased by captopril. PA II, PAC and PRA increased in response to exercise both before and following captopril. The exercise stimulated increase in PNA and PA was almost identical before and during captopril. Thus, captopril had no major effect on the activity of the sympathetic nervous system in patients with essential hypertension, neither during basic conditions nor during heavy physical exercise in spite of a profound decrease in PA II.

Adult↗