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Epinephrine is also used as a bronchodilator for asthma if specific β 2 agonists are unavailable or ineffective. [39] Because of the high intrinsic efficacy (receptor binding ability) of epinephrine, high drug concentrations cause adverse side effects when treating asthma. The value of using nebulized epinephrine in acute asthma is unclear. [40]
Alpha 1 blockers cause vasodilation by relaxing smooth muscles that control blood vessel diameter, leading to lower blood pressure. [1] FDA-approved uses of these drugs include treating conditions like benign prostatic hyperplasia, hypertension, pheochromocytoma, extravasation management, and reversal of local anesthesia. [1]
Adrenaline, also known as epinephrine, is a hormone and medication [10] [11] which is involved in regulating visceral functions (e.g., respiration). [10] [12] It appears as a white microcrystalline granule. [13] Adrenaline is normally produced by the adrenal glands and by a small number of neurons in the medulla oblongata. [14]
The blockade of beta-2 receptors will result in vasoconstriction and smooth muscle constriction, [6] and the effects are similar to the agonism of alpha-1 receptors. The side effects include hypertension, tachycardia, arrhythmia and subcutaneous ischemia at the site of injection. [3]
Examples of sympathomimetic effects include increases in heart rate, force of cardiac contraction, and blood pressure. [1] The primary endogenous agonists of the sympathetic nervous system are the catecholamines (i.e., epinephrine [adrenaline], norepinephrine [noradrenaline], and dopamine ), which function as both neurotransmitters and hormones .
Epinephrine (adrenaline) reacts with both α- and β-adrenoreceptors, causing vasoconstriction and vasodilation, respectively. Although α receptors are less sensitive to epinephrine, when activated at pharmacologic doses, they override the vasodilation mediated by β-adrenoreceptors because there are more peripheral α 1 receptors than β ...
In smooth muscle cells of blood vessels the principal effect of activation of these receptors is vasoconstriction.Blood vessels with α 1-adrenergic receptors are present in the skin, the sphincters [4] of gastrointestinal system, kidney (renal artery) [5] and brain. [6]
Adrenergic antagonists reverse the natural cardiovascular effect, based on the type of adrenoreceptor being blocked. For example, if the natural activation of the α 1-adrenergic receptor leads to vasoconstriction, an α 1-adrenergic antagonist will result in vasodilation. [3]