alpha-adrenergic


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Related to alpha-adrenergic: beta-adrenergic, alpha-adrenergic blockers

alpha-adrenergic

(ăl′fə-ăd′rə-nûr′jĭk)
adj.
Of, relating to, or being an alpha-receptor.
References in periodicals archive ?
TCAs act by blocking presynaptic reuptake of norepinephrine or serotonin; they theoretically increase the effects of direct- or indirect-acting agonists at these synapses.[4] TCAs may also block alpha-adrenergic receptors, which causes hypotension resulting from reduction of myocardial contractility and systemic vascular resistance.[4],[5] TCAs inhibit Na/K-ATPase and act like quinidine-like antiarrhythmics by stabilizing excitable membranes and delaying His bundle conduction.
Although labetalol has both alpha and beta blocking properties, the ratio of alpha:beta antagonism is approximately 1 : 7 and could lead to unopposed alpha-adrenergic receptor stimulation [20].
Options include the tricyclic antidepressant amitriptyline (31); alpha-adrenergic agonists or antagonists (donidine, terazosin); and anti-muscarinic medications (benztropine, atropine, trihexyphenidyl, glycopyrrolate) (Table 2 (31)).
In some cases, it has been useful in situations where labetalol or sodium nitroprusside have not been beneficial.7 The optimization of this patient begins with alpha-adrenergic blockers (doxazosin and phenoxybenzamine), but faced with little improvement in myocardial contractility and instability of arterial pressure, magnesium sulfate is introduced starting in the acute crisis and during the surgical process up until the complete removal of the flow from the pheochromocytoma, ensuring a maximum level of magnesemia of 4.5mmol/l.
Sympathomimetics (alpha-adrenergic agonists) include apraclonidine (Iopidine), which has no human eye data, and brimonidine (Alphagan P), which has one case report in pregnancy and breastfeeding showing no fetal or nursing infant harm.
Some medications commonly used to reduce blood pressure are diuretics, angiotension-converting enzyme inhibitors, beta-adrenergic blockers, calcium antagonists and alpha-adrenergic blockers.
These can include trying a different stimulant or using a nonstimulant such as atomoxetine or an alpha-adrenergic agonist.
While the neuroanatomical interactions that govern the sympathetic nervous system are yet to be fully elucidated, sympathetic tone is recognised as an important mediator of cardiovascular function predominantly through its direct effects on beta-adrenergic receptors in the heart to modulate cardiac output and on alpha-adrenergic receptors in blood vessels to modulate arteriolar resistance and venous capacitance.
Beta-blockers should be added after a few days and in the presence of an effective alpha-adrenergic blockade since they can worsen the BP profile by inhibiting vasodilatation mediated by beta-2 adrenergic receptors and thus increasing vasoconstriction [16].
According to experimental data, it can be noted that usage of blockers caused the inhibition of alpha-adrenergic receptors by hydrazine in chronic intoxications.
A Cochrane Systematic Review of alpha-adrenergic drugs for treatment of female stress UI included 22 randomized and quasi-experimental studies, 11 of which were cross-over trials (Alhasso, Glazner, Pickard, & N'Dow, 2010).