Antianginal and Haemodynamic Effects of α1-Adrenoceptor Blockade

Dj, Sheridan; Thomas, P; Culling, W.; Collins, Peter

doi:10.1097/00005344-198600082-00029

Cited by 6 publications

(2 citation statements)

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“…However, the fall in the coronary vascular resistance was only small (13%) and at a low level of significance (0.05%); furthermore, during exercise, when the evidence for alpha-adrenergic mediated increase in coronary tone is stronger [25], there was no change during labetalol therapy. Indirect evidence with the alphal-blocking agent indoramin, added to preexisting beta-blockade (therefore with some similarities to labetalol) shows that the coronary vascular resistance fell as the coronary sinus outflow rose [28]. Indirect evidence with the alphal-blocking agent indoramin, added to preexisting beta-blockade (therefore with some similarities to labetalol) shows that the coronary vascular resistance fell as the coronary sinus outflow rose [28].…”

Section: Evidence For a Coronary Vasodilator Activity Of Labetalolmentioning

confidence: 99%

Role of vasobilation in the antihypertensive and antianginal effects of labetalol: Implications for therapy of combined hypertension and angina

Opie

1988

Cardiovasc Drug Ther

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Beta-adrenergic blockade is established therapy in the management of both hypertension and angina pectoris. This review evaluates the use of combined alpha-adrenergic and beta-adrenergic blockade for these conditions, with reference to labetalol. There are three major differences between labetalol and propranolol or similar conventional beta-blockers. First, in the mechanism of the antihypertensive effect, peripheral vasodilation plays a prominent role during the use of labetalol. In particular, acute therapy with labetalol rapidly reduces the blood pressure because of this reduction in the systemic vascular resistance. During prolonged therapy with labetalol over many years, blood pressure remains reduced with a sustained fall in the systemic vascular resistance. Second, in patients with combined hypertension and angina pectoris, fixed doses of labetalol (200 mg twice daily) gave the same blood pressure values, effort tolerance, and nitrate usage as did atenolol 100 mg once daily in a double-blind, double-dummy, crossover study. Labetalol gave higher heart rates at rest and during exercise (both p less than 0.01). The higher heart rate with labetalol could be an advantage in some patients with effort angina and a disadvantage in others. Third, in hypertensive asthmatics, labetalol appears to have a relative bronchosparing effect, when compared with propranolol. The possession by labetalol of beta2-stimulating qualities (intrinsic sympathomimetic activity) may explain part of the dilating effect and the bronchosparing quality. Thus labetalol 1) lowers blood pressure by a mechanism involving vasodilation, 2) has an equiantianginal effect to atenolol yet a higher heart rate, and 3) may be bronchosparing. Differences among various beta-blockers may be important in matching the properties of the beta-blocker chosen to the requirements of the individual patient.

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Section: Evidence For a Coronary Vasodilator Activity Of Labetalolmentioning

confidence: 99%

Role of vasobilation in the antihypertensive and antianginal effects of labetalol: Implications for therapy of combined hypertension and angina

Opie

1988

Cardiovasc Drug Ther

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“…From Gewirtz et al (1984) with permission of the authors and the American Heart Association, Inc. the A2-receptors , which stimulate the formation of cyclic AMP in vascular smooth muscle, thereby causing coronary artery dilation. Nonetheless, alpha-adrenergic blockade is not an established antianginal procedure, although there are reports of benefits of the following agents: nonspecific alphablockers (phentolamine; Gould, 1973), alphal-blockers (indoramin; Sheridan et al, 1986), or combined alphal-beta blockers (labetalol; Quyyumi et al, 1985), which are all effective in effort angina. Adenosine does, however, have some beta stimulatory properties on the myocardium, presumably by virtue of the activity of the A2-receptors, which are probably not limited to the vessel wall.…”

Section: Effect Of Adenosine On Purinergie Receptorsmentioning

confidence: 99%

Pharmacology of acute effort angina

Opie

1989

Cardiovasc Drug Ther

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From the pharmacologic point of view, each of the major types of antianginal agents--calcium antagonists, beta-blockers, and nitrates--seem to act at least in part by an improvement of the myocardial blood supply. The recently elucidated mechanism of action of nitrates, acting on a common pathway with the endothelium-derived relaxation factor (EDRF), suggests an important role for guanylate cyclase and cyclic GMP in maintaining coronary artery patency in patients with coronary atheroma. The efficacy of calcium antagonists, even in effort-induced angina, is in accord with a current hypothesis that physical exercise in the presence of coronary stenosis can cause relative coronary vasoconstriction, or at the least, failure of full dilation. Therefore, calcium antagonists all act, at least in part, on the "supply" side of the supply-demand equation. Beta-adrenergic blockers appear to have as their major mode of action a reduction of heart rate, which not only reduces the oxygen demand but, through an anti-ischemic effect, also appears to improve the endocardial blood supply (in relation to the heart rate). Thus beta-blockade indirectly enhances the supply side of the equation. The intriguing situation arises whereby all three major types of antianginal compounds may also act by a common mechanism of anginal relief, namely, improvement in the coronary blood supply, in addition to the diverse mechanisms specific to each type of compound. That conclusion does not mean the the "demand" side of the equation can be ignored. Rather, the critical importance of a reduced myocardial blood supply in the production of anginal syndromes is highlighted.

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