Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six normal subjects and six normotensive insulin-dependent diabetics underwent two insulin hypoglycaemia tests after administration for three days of either a placebo or of acebutolol--a cardioselective beta-blocker--at a dose of 400 mg per day. The order in which the tests were performed was decided by random selection. Acebutolol suppressed the tachycardia which occurred as a reaction to hypoglycaemia but did not interfere with other warning symptoms and signs. In both normal subjects and diabetics, acebutolol neither worsened the initial hypoglycaemia nor did it delay a return to normal values. The increase in lactate levels following hypoglycaemia was not reduced by acebutolol but free fatty acid rebound was suppressed. Hormonal responses (glucagon, cortisol, growth hormone) were unaffected by the beta-blocker. If they are confirmed by long term studies, these results would suggest that acebutolol is safer to use than non-cardioselective beta-blockers in the treatment of coronary insufficiency and of hypertension in diabetics exposed to the risk of hypoglycaemia.
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PMID:[The effects of acebutolol on endocrine and metabolic reactions induced by acute hypoglycaemia. Study in normal subjects and in insulin-dependent diabetics (author's transl)]. 39 44

Beta antagonists competitively block beta 1-adrenoceptors that mediate both the rate and force of myocardial contraction. Their precise mechanism of anti-anginal action is uncertain. A reduction in oxygen demand may relative pain and improve effort tolerance. Alternatively inhibition of the adrenergic drive to contraction may offset the increased ventricular wall tension due to incomplete relaxation. Partial agonist activity in a beta-antagonist does not influence efficacy nor protect against airflow obstruction. Membrane stabilising activity is clinically trivial. Cardioselectivity makes airflow obstruction less likely at low but not at high blood concentrations of drug. Alpha-receptor antagonism may also prevent broncho-constriction; it has not been assessed in coronary vasospasm. The dosage and choice of drugs are based on pharmaco-kinetic and dynamic data in animals and man. The major side-effects of beta-blockade are heart failure and airflow obstruction. Cardiotoxicity from overdosage may be treated with isoprenaline, dopamine or glucagon while beta 2-agonists will reverse bronchoconstriction. Since beta-antagonists raise-peripheral vascular impedance, reduction of preload with nitrates enhances their antianginal efficacy. Combining a beta-antagonist with nifedipine seems especially useful. Beta-blockade is worth trying in angina with normal coronary arteries. In acute coronary insufficiency beta-blockade reduces both the work-load on the heart and the somatic features of anxiety, so preparing patients for investigations, like coronary arteriography, aimed at definitive treatment.
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PMID:Clinical pharmacology of beta-adrenoceptor antagonism in angina pectoris: an overview. 611 11