ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01606.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTThe radioligand binding technique has been proven useful in the study of altered responsiveness after exposure to adrenergic agents. A reduction in receptor number has generally been reported after interventions serving to increase the stimulatory input to the receptors prior to assay. Conversely a decrease in receptor stimulation has been demonstrated to induce an elevation in receptor density. These phenomena have been described for α‐ as well as for β‐adrenoceptors in various tissues under a variety of experimental conditions such as prolonged agonist exposure, chronic receptor blockade, denervation and interference with catecholamine turnover. A number of clinically relevant cardiovascular experimental models have been characterized by altered adrenoceptor densities, possibly reflecting a compensatory resetting of sympathetic tone in response to an aberrant haemodynamic pattern. The mechanisms underlying receptor density changes as those discussed have been suggested to involve an internalization process which may involve phospholipase and transglutaminase activation in the cell mem

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01607.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTMost β‐adrenergic effects are mediated by activation of the enzyme adenylate cyclase. Hormone binds to the receptor leading to an accelarated binding of GTP to the coupling protein, the N‐protein, which is activated. This causes an activation of the adenylate cyclase and an increased formation of cAMP, the intracellular second messenger. The same principles hold good for other hormones coupled to adenylate cyclase. The sensitivity of the adenylate cyclase may be altered in different clinical and experimental conditions. An increased sensitivity is seen in hyperthyroidism in man and in the rat, and during starvation in rats. A decreased sensitivity is seen in hypothyroidism, in patients with pheochromocytoma, pseudohypoparathyroidism type I or multiple symmetric lipomatosis. Several reasons for the altered sensitivity have been suggested. The number of hormone receptors, the coupling between receptor and N‐protein, the amount or function of the N‐protein or the PDE activity may all vary in different co

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01608.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTInsulin release is influenced by the autonomic nervous system. In the periphery the regulation occurs via both α‐adrenergic and β‐adrenergic receptors. The parasympathetic nervous system is important in the central regulation of insulin secretion. Nevertheless, adrenergic mechanisms are also concerned. This review discusses the mechanisms for the adrenergic regulation of insulin release and some clinical conditions where these mechanisms are conc

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01609.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTThis paper reviews the various possible relationships between thyroid hormones and the adrenergic nervous system. These concern the sympathetic influence on thyroid hormone secretion, thyroid hormone ‐ induced changes of sympathetic activity or adrenoceptor changes ‐ the effects of catecholamines on thyroid hormone metabolism and, finally, the clinical benefits of β‐adrenoceptor blocking drugs on symptoms and signs of hyperthyr

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01610.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTThis survey discloses the main mechanisms regulating renin release from the kidneys. Stimulation or inhibition of renin at least during a normal sodium intake seems to depend mostly on the sympathetic nervous system and be mediated through β1‐adrenoceptors. The suppression of renin release is maintained during long‐term treatment with both selective (β1) and non‐selective (β1+β2)‐adrenoceptor blocking drugs. The role of α‐adrenoceptors on renin release is less clear, both stimulating and suppressive effects having been described after treatment with α1‐adrenoceptor blocking therapy (i.e. prazosin). In certain conditions, i.e. when renal vascular resistance is increased or renal perfusion pressure augmented, renal prostaglandins (PG) especially PGE2, may play an important part in renin release. Angiotensin II (A II) and aldosterone generally follow the shifts in renin release. Thus, a decrease in both A II and plasma aldosterone is seen during long‐term treatment with β‐adrenoceptor‐blockade and may contribute to the blood‐pressure lowe

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01611.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTAdrenergic receptors are ubiquitous and mediate several important effects involving lipid metabolism. Thus, β‐adrenergic stimulation increases lipolysis and inhibits the activity of the lipoprotein lipase. In contrast, α‐adrenergic stimulation inhibits fat cell lipid mobilisation. Unexpectedly, β‐adrenergic blockade increases plasma triglyceride levels and tends to lower the high density lipoprotein (HDL‐cholesterol). These effects seem to be prevented or attenuated by concomitant α‐blockade. Possible mechanisms for the adrenergic effect on lipid metabolism

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01612.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTβ‐adrenoceptor antagonists influence almost all haemodynamic and metabolic actions in the body. High levels of sympathetic stimulation accompany aerobic exercise and it is known that β‐blockade results in a decreased working capacity. Furthermore it has also been questioned whether β‐blockade inhibits the normal response to physical training. Although adrenergic mechanisms are involved in muscle and liver glycogen breakdown, β‐blockade does not seem to reduce glycogen utilisation during exercise. Both selective and non‐selective β‐blockade inhibit lipolysis and result in less free fatty acids being available for muscle utilisation. Surgical and chemical sympathectomy in animals has been shown to inhibit the responses to physical training but results are now available showing that β‐adrenergic blockade does not prevent the effect of physical conditioning in patients treated with propranolol. It is concluded that β‐blockade during prolonged exercise a) does not reduce oxygen uptake by the working muscles b) decreases fat metabolism, which secondarily increases the use of carbohydrates, resulting in earlier hypoglycaemia and/or depletion of muscle glycogen with reduction in working capacity c) does not inhibit central and peripheral adaptation to

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01613.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTThis paper assesses mechanisms that may contribute to the higher incidence of increased muscle fatigue during exercise and reduced exercise performance as observed with selective compared with non‐selective β‐adrenoceptor antagonists. Published data and the results obtained in 8 healthy subjects (mean age 23 years) studied before and after acute β‐adrenoceptor blockade with pindolol (nonselective, 10 mg) and metoprolol (β1‐receptor selective, 100 mg) suggest that the differences in the cardiovascular and respiratory effects between the 2 types of antagonists are marginal and cannot explain the discrepancies concerning exercise perception and performance. Conversely, basic differences between the 2 types of antagonists were shown in different groups of hypertensive men (mean age 32 years) studied before and after 4 weeks of treatment with pindolol (15 mg), and with metoprolol (200 mg) and acebutolol (cardioselective, 500 mg), by single crossover technique. Whereas lipolysis was similarly inhibited by both selective and non‐selective antagonists, hypoglycaemia occurred only under nonselective blockade. It apparently reflects the inhibition of glycogen breakdown; concomitant rises in plasma adrenaline and ACTH probably reflect counter‐regulat

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01614.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY

摘要:

ABSTRACTThe metabolic effects of β‐adrenoceptor blocking agents during hypoglycaemia in patients prone to hypoglycaemia are of interest as diabetics are often treated with these drugs because of hypertension or angina pectoris. Compared with non‐diabetics these patients also have impaired glucose compensation after hypoglycaemia, partly secondary to deficient release of glucagon. This makes the diabetics more dependent on adrenergic mechanisms to recover from low blood glucose concentrations. Non‐selective β‐adrenoceptor blockade (propranolol) significantly impairs the glucose recovery rate after hypoglycaemia in insulin dependent diabetics, whereas selective β‐adrenoceptor blockade (metoprolol) does not have this side effect. The mechanism of the effect of propranolol is probably an attenuation of the gluconeogenesis secondary to deficient release of the important gluconeogenic substrates lactate

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1983.tb01615.x

出版商:Blackwell Publishing Ltd    

年代:1983

数据来源: WILEY