Labetalol binding to specific alpha- and beta-adrenergic sites in vitro and its antagonism of adrenergic responses in vivo

Greenslade, Forrest C.; Tobia, Alfonso J.; Madison, Sherrie M.; Krider, Kathryn M.; Newquist, Kathryn L.

doi:10.1016/0022-2828(79)90405-x

Cited by 9 publications

(2 citation statements)

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“…Furthermore, in hypertensive patients, 1) 50% of the rise of the systemic vascular resistance induced by phenylephrine is antagonized by labetalol [5]; and 2) the dose of phenylephrine required to increase diastolic blood pressure is more than doubled during labetalol therapy [6]. Furthermore, labetalol also binds to alphal-adrenergic receptors [8]. Furthermore, labetalol also binds to alphal-adrenergic receptors [8].…”

Section: Alpha1-adrenergic Blocking Qualities Of Labetalolmentioning

confidence: 99%

“…Substantial evidence obtained from animal experiments also shows that labetalol can antagonize alphal-adrenergic stimulation [7]. However, it should be noted that 1) labetalol has a much more powerful beta than alphal-adrenergic blocking effect [7], and 2) the binding of labetalol to alpha-adrenergic receptors is relatively weak when compared with phentolamine [8]. However, it should be noted that 1) labetalol has a much more powerful beta than alphal-adrenergic blocking effect [7], and 2) the binding of labetalol to alpha-adrenergic receptors is relatively weak when compared with phentolamine [8].…”

Section: Alpha1-adrenergic Blocking Qualities Of Labetalolmentioning

confidence: 99%

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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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