1970
DOI: 10.1136/bmj.4.5731.328
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Autonomic Control of Insulin Secretion and the Treatment of Heart Failure

Abstract: The families studied in the present work yield VA -0-65 for post-phenobarbitone phenylbutazone half-life corrected for height. These results are clearly of much the same order. The same genes do not control the two characters, since the postphenobarbitone phenylbutazone half-life data have been adjusted to a standard height. Therapeutic ImplicationsSome drugs are known to show a correlation between plasma level and (1) therapeutic effect and (2) occurrence of toxic (or adverse) effects. Bruck et al. (1954) sh… Show more

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Cited by 40 publications
(7 citation statements)
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“…There has been, however, the objection that many of these alpha-adrenoceptor blocking agents possess potent secondary properties which may be crucial for their antiarrhythmic actions (Daugherty et al 1986). For instance, phentolamine stimulates insuline secretion (Majid et al 1970) and inhibits platelet aggregation (Pfister and Imhof 1977). An importance of these effects can be clearly ruled out for this study, since the model uses isolated buffer perfused hearts and therefore avoids humoral or systemic interferences.…”
Section: Discussionmentioning
confidence: 99%
“…There has been, however, the objection that many of these alpha-adrenoceptor blocking agents possess potent secondary properties which may be crucial for their antiarrhythmic actions (Daugherty et al 1986). For instance, phentolamine stimulates insuline secretion (Majid et al 1970) and inhibits platelet aggregation (Pfister and Imhof 1977). An importance of these effects can be clearly ruled out for this study, since the model uses isolated buffer perfused hearts and therefore avoids humoral or systemic interferences.…”
Section: Discussionmentioning
confidence: 99%
“…Stimulation of a-receptors by catecholamines or /^-blockade suppressed insulin release whereas the yS-receptor agonist, isoproterenol, or a-receptor blockade with phentolamine potentiated the secretion of this hormone (Porte, 1969;Majid et al, 1970). Impairment of insulin release in MI is obviously a nonspecific phenomenon because similar disorders have been reported in congestive heart failure (Majid et al, 1970) ). In a fraction of patients with MI, glucose intolerance is not accompanied by lowered insulin activity; this indicates the presence of insulin antagonism which is likely to be due to increased cortisol and growth hormone levels and to an elevated content of FFA (Boden, 1971).…”
Section: Insulin Deficiencymentioning
confidence: 99%
“…Evidence for this has accumulated from studies on animals both in vitro (Coore and Randle, 1964) and in vivo (Kris et al, 1966) and on man (Porte et al, 1966). Stimulation of a-receptors by catecholamines or /^-blockade suppressed insulin release whereas the yS-receptor agonist, isoproterenol, or a-receptor blockade with phentolamine potentiated the secretion of this hormone (Porte, 1969;Majid et al, 1970). Impairment of insulin release in MI is obviously a nonspecific phenomenon because similar disorders have been reported in congestive heart failure (Majid et al, 1970) ).…”
Section: Insulin Deficiencymentioning
confidence: 99%
“…Infusion of catecholamines into the pancreatic artery of the dog results in severe but reversible histological changes confined to the islet beta-cells (Loubatieres et al,I965). Adrenergic alphastimulation and beta-blockade both suppress insulin release in normal man while alphablockade and beta-stimulation both potentiate insulin release (Majid et al, 1970). These observations show that the sympathetic nervous system has an important role in the control of insulin secretion.…”
Section: Secretion Of Insulin In Heart Failurementioning
confidence: 71%