1981
DOI: 10.1016/s0140-6736(81)91157-0
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Haemodynamic, Hormonal, and Elecrolyte Responses to Withdrawal of Long-Term Captopril Treatment for Heart Failure

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1982
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Cited by 28 publications
(7 citation statements)
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“…For example, it has been shown that brief restoration of the integrity of the renin-angiotensin system is not accompanied by a deterioration of hemodynamic effects in patients with heart failure. 31 Converting enzyme inhibitors may increase circulating levels of bradykinin, by inhibition of the enzyme kinase II, which would result in venodilatation. 10 -32 -33 It is also possible that captopril prevents sodium and water retention that is characteristic of advanced heart failure.…”
Section: Discussionmentioning
confidence: 99%
“…For example, it has been shown that brief restoration of the integrity of the renin-angiotensin system is not accompanied by a deterioration of hemodynamic effects in patients with heart failure. 31 Converting enzyme inhibitors may increase circulating levels of bradykinin, by inhibition of the enzyme kinase II, which would result in venodilatation. 10 -32 -33 It is also possible that captopril prevents sodium and water retention that is characteristic of advanced heart failure.…”
Section: Discussionmentioning
confidence: 99%
“…No changes in plasma catecholamines have been detected during acute therapy with captopril (Morganti et al, 1980). No major withdrawal phenomena have been observed after abrupt cessation of captopril therapy (Maslowski et al, 1981). In a personal series of eight hypertensive patients receiving captopril, no untoward problems were associated with their anaesthetic management (Prys-Roberts, unpublished observations).…”
Section: Angiotensin-converting Enzyme Inhibitor*mentioning
confidence: 96%
“…In this renin-dependent phase of renovascular hypertension, both plasma renin and angiotensin II concentrations are high, and the use of specific angiotensin antagonists (Saralasin) or angiotension-converting enzyme inhibitors (captopril) restores pressures to normal (Ayers et al, 1974), or prevents the development of hypertension (Miller et al, 1975). Patients with hypertension of renovascular origin present special problems during anaesthesia (Prys-Roberts, 1982a).…”
Section: Adrenergic and Other Pathophysiological Mechanisms In Hypertmentioning
confidence: 99%
“…While this increased potassium is almost certainly the result of a fall in mean plasma aldosterone, the rise of potassium will limit the fall in aldosterone secretion resulting from reduced formation of angiotensin I1 (Atlas et al, 1979) and thus will alter the relationship between angiotensin I1 and aldosterone. Moreover, Maslowski et al (1981) have noted a rise in both plasma and urinary cortisol on withdrawing captopril treatment and have raised the question of an inhibitory effect of captopril on corticotrophin secretion. These various observations warn against overreliance on aldosterone measurements as a guide to angiotensin 11 suppression during captopril treatment.…”
Section: Discussionmentioning
confidence: 99%