The influence of beta‐adrenoceptor blocking drugs with and without intrinsic sympathomimetic activity on the hormonal responses to hypo‐ and hyperglycaemia.

Schlüter, Kurt; Aellig, W. H.; Petersen, Karl-Georg; Rieband, H C; Wehrli, A; Kerp, L.

doi:10.1111/j.1365-2125.1982.tb01948.x

Cited by 22 publications

(8 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast to two earlier studies with propranolol and CRH injection (24,25) or propranolol and hypoglycemia (e.g. 24,26,27), this study extended the earlier view by consideration of molar hormone ratios such as cortisol/adrenocorticotropin (ACTH), cortisol/17-hydroxyprogesterone (17OHP), cortisol/DHEA, and DHEAS/DHEA. Furthermore, responses were separately calculated and depicted for female and male subjects.…”

Section: Introductionmentioning

confidence: 78%

“…In another experiment, the unspecific a1,2-adrenergic antagonist, phentolamine, had no influence on CRHstimulated ACTH and cortisol levels (24). Several studies induced hypoglycemia in order to activate the HPA axis and administered b-adrenergic and a-adrenergic agonists and antagonists: four independent studies noted a propranolol-induced increase in plasma ACTH and/or serum cortisol during hypoglycemia (24,26,27,33). However, these groups did not Figure 3 Time course of androstenedione, 17-hydroxyprogesterone (17OHP) and the ratio of serum cortisol/serum 17OHP before and during a hCRH test with (W) or without (X) prior propranolol administration in women and men.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH

Kizildere

Glück

Zietz

et al. 2003

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: In chronic inflammatory diseases, serum levels of dehydroepiandrosterone (DHEA) sulfate (DHEAS) are low. Interestingly, several non-inflammatory diseases display similarly low levels of DHEAS which points to other inhibitory factors such as an activated sympathetic nervous system (SNS) (e.g. in patients with heart failure, fibromyalgia, or cancer cachexia). We aimed to identify the influence of the SNS tone on stimulated adrenal steroid secretion in 16 male and 12 female healthy subjects. Methods: One group were given oral propranolol 2 h before a corticotropin-releasing hormone (CRH) test, and levels of adrenocorticotropin (ACTH), cortisol, 17-hydroxyprogesterone (17OHP), androstenedione, DHEA, and DHEAS were measured. Results: Propranolol treatment decreased heart rate (by 20%), diastolic blood pressure (by 20%), and plasma ACTH, and increased serum cortisol, serum DHEAS, and the molar ratio of cortisol/17OHP, cortisol/DHEA, and DHEAS/DHEA similarly in female and male subjects. Conclusions: A b-adrenergic influence seems to decrease CRH-stimulated cortisol in relation to ACTH and 17OHP, and decreases DHEAS in relation to DHEA. Although other workers have found b-adrenergic stimulation of steroid secretion in cultured adrenocortical cells, the overall systemic influence of the SNS via b-adrenoceptors seems to inhibit adrenal steroids under unstimulated and stimulated conditions. Sympathetic hyperactivity may be a common denominator for low levels of DHEAS in inflammatory and non-inflammatory diseases.

show abstract

Section: Introductionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH

Kizildere

Glück

Zietz

et al. 2003

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…In a study using animal experiments, this action was confirmed for another non-selective beta-receptor blocker (bupranolol) (5). In studies carried out by Schlflter et al (38), the C-peptide serum levels after oral administration of glucose were lower under metoprolol and propranolol than under pindolol and placebo. Our results show that under stress the endogenous insulin secretion is reduced to a minimum at the start of exercise and that under exercise conditions carteolol appears to have no influence on the reduced secretion.…”

Section: Discussionmentioning

confidence: 86%

An Examination of the Hemodynamic and Metabolic Effects of Carteolol during Different Workloads on a Bicycle Ergometer

Krümke

Mader²,

Michael³

et al. 1991

Int J Sports Med

View full text Add to dashboard Cite

The influence of 10 mg carteolol/day on the serum concentrations of insulin, C-peptide, glucagon, free fatty acids, adrenaline, noradrenaline, blood glucose, blood lactate levels, on heart rate and systolic blood pressure was investigated during different workloads on a bicycle ergometer in a placebo-controlled randomised double-blind study involving twelve male volunteers. The subjects performed standardized increasing exercises until subjective exhaustion as well as three 40-minute endurance exercises of varying intensity, corresponding to a lactate concentration of 1.0 to 2.0 mmol/l, 2.5 to 3.5 mmol/l and more than 3.5 mmol/l in the region of the anaerobic threshold, each exercise being followed by one rest day. The most important findings are: --the ISA of carteolol is of significance for the influence on the heart rate at rest but plays a minor role with respect to the degree of reduction in the heart rate and blood pressure under exercise; --carteolol exerts a minor influence on the metabolic parameters investigated in this study. This can be partly ascribed to the pronounced ISA of carteolol. In the case of endurance exercises, which lead to blood lactate concentrations of more than 3 mmol/l, the blood glucose levels showed a tendency to decrease. However, this was not statistically significant.

show abstract

“…clearance rate of insulin after metoprolol treatment [28,29]. It may also be a consequence of changes in the distribution volume for insulin [30], due to haemodynamic changes [15,31].…”

Section: Discussionmentioning

confidence: 99%

The effect of metoprolol treatment on insulin sensitivity and diurnal plasma hormone levels in hypertensive subjects

Guðbjörnsdóttir¹,

Fowelin²,

Elam³

et al. 1997

Eur J Clin Investigation

View full text Add to dashboard Cite

Abstract.To evaluate the effect of metoprolol on insulin sensitivity and diurnal plasma hormone levels, seven mildly hypertensive subjects were investigated (four men and three women, age 52 Ϯ 8, body mass index 25 . 4 Ϯ 1 . 9, mean Ϯ SD). The study had a placebo-controlled, double-blind, crossover design with 6 weeks' metoprolol treatment (100 mg b.i.d) vs. placebo. At the end of each treatment period 24-h blood samples were collected continuously for diurnal analysis of hormone levels and a hyperinsulinaemic euglycaemic clamp combined with [3-3 H]-D-glucose infusion was performed. Insulin sensitivity was evaluated by means of three different methods: diurnal plasma insulin and glucose levels; glucose consumption; and insulin sensitivity index during euglycaemic clamp conditions. Fasting blood glucose and insulin concentrations as well as mean plasma diurnal levels of insulin, growth hormone, testosterone and cortisol were similar after placebo and metoprolol treatment, whereas noradrenaline and adrenaline levels were significantly increased after metoprolol. During the clamp, plasma insulin was significantly higher after metoprolol treatment than after placebo treatment (56 Ϯ 3 vs. 64 Ϯ 2 mU L -1 , P < 0 . 05). Consequently, the insulin sensitivity index [glucose infusion rate (GIR)/ plasma insulin] was lower after metoprolol treatment (16 . 1 Ϯ 2 . 6 vs. 10 . 2 Ϯ 1 . 2, P < 0 . 05), although GIR was not significantly changed. We suggest that the insulin sensitivity index may not accurately reflect the insulin effect as the plasma level of insulin was significantly increased during insulin infusion but not at 24 h, possibly because of alteration of distribution and/or degradation rate of exogenous insulin. Thus, the likelihood of metoprolol inducing insulin resistance in hypertensive subjects may be less than previously proposed.

show abstract

The influence of beta‐adrenoceptor blocking drugs with and without intrinsic sympathomimetic activity on the hormonal responses to hypo‐ and hyperglycaemia.

Cited by 22 publications

References 28 publications

During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH

During a corticotropin-releasing hormone test in healthy subjects, administration of a beta-adrenergic antagonist induced secretion of cortisol and dehydroepiandrosterone sulfate and inhibited secretion of ACTH

An Examination of the Hemodynamic and Metabolic Effects of Carteolol during Different Workloads on a Bicycle Ergometer

The effect of metoprolol treatment on insulin sensitivity and diurnal plasma hormone levels in hypertensive subjects

Contact Info

Product

Resources

About