alpha-adrenergic receptors


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α-ad·re·ner·gic re·cep·tors

adrenergic receptors in effector tissues capable of selective activation and blockade by drugs; conceptually derived from the ability of certain agents, such as phenoxybenzamine, to block only some adrenergic receptors and of other agents, such as methoxamine, to activate only the same adrenergic receptors. Such receptors are designated as α-receptors. Their activation results in physiologic responses such as increased peripheral vascular resistance, mydriasis, and contraction of pilomotor muscles.

α-ad·re·ner·gic re·cep·tors

(adrĕ-nĕrjik rĕ-septŏrz)
Those in effector tissues capable of selective activation and blockade by drugs; conceptually derived from the ability of certain agents, such as phenoxybenzamine, to block only some adrenergic receptors and of other agents, such as methoxamine, to activate only the same adrenergic receptors. Such receptors are designated as α-receptors. Their activation results in physiologic responses such as increased peripheral vascular resistance, mydriasis, and contraction of pilomotor muscles.
References in periodicals archive ?
It showed that blocking the beta-receptor alone promotes cardiac remodelling via growth of cardiac fibroblasts induced by alpha-adrenergic receptor signaling.
It is an alpha-2 receptor agonist which acts centrally on postsynaptic alpha-adrenergic receptors in the medulla oblongata.[1,2,4,12] This central effect results in decreased sympathetic outflow and enhanced vagal tone, lowering blood pressure and heart rate.[1-3,7,10,13-15] This may cause side effects of drowsiness, lethargy, dry mouth,[4,10] and parotidynia.[13] Clonidine may also act peripherally within the heart to inhibit norepinephrine release,[7,14,15] contributing to further reductions in heart rate.
This same lipolytic response is blunted by alpha-adrenergic receptors. It has been shown that beta-adrenergic responsiveness is lowered in the abdominal adipose tissue of the obese.

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