Alpha, agonists vascular effects

Mechanism of Action An alpha-adrenergic agonist that stimulates alphaj-adrenergic receptors. Inhibits sympatheticcardioaccelerat or and vasoconstrictor center to heart, kidneys, peripheral vasculature. Therapeutic Effect Decreases systolic, diastolic blood pressure (BP). Chronic use decreases peripheral vascular resistance. Pharmacohinetics Well absorbed from gastrointestinal (GI) tract. Widely distributed. Protein binding 90%. Metabolized in liver. Excreted in urine and feces. Not removed by hemodialysis. Half-life 6 hr. 

Mechanism of Action An alpha-adrenergic receptor agonist that causes vasoconstriction, reflex bradycardia, inhibits GI smooth muscle and vascular smooth muscle supplying skeletal muscle and increases heart rate and force of heart muscle contraction. Therapeutic Effect Increases both systolic and diastolic pressure. 

Mechanism of Action A vasopressor that forms the active metabolite desglymido-drine, an alphaj-agonist, activating alpha receptors of the arteriolar and venous vasculature. Therapeutic Effect Increases vascular tone and BP. 

Alpha receptors are widely expressed in vascular beds, and their activation leads to arterial and venoconstriction. Their direct effect on cardiac function is of relatively less importance. A relatively pure agonist such as phenylephrine increases peripheral arterial resistance and decreases venous capacitance. The enhanced arterial resistance usually leads to a dose-dependent rise in blood pressure (Figure 9-... 

Agonist 1 increases HR, presumably through direct activation of cardiac Pj receptors because the effect is blocked by propranolol but is not influenced by the alpha blocker (prazosin), the ganglion blocker (trimethaphan), or blockade of M receptors (atropine). Only two of the listed drugs directly activate cardiac receptors epinephrine and norepinephrine. For NE, any direct cardiac stimulation is counteracted by reflex bradycardia resulting from the increase in mean BP via its activation of (Xj receptors in blood vessels (it has no effects on p2 vascular receptors). Therefore, agonist 1 is identified as epinephrine (presumably at low dose). 

I. Pharmacology. Norepinephrine is an endogenous catecholamine that stimulates mainly alpha-adrenergic receptors. It is used primarily as a vasopressor to increase systemic vascular resistance and venous return to the heart. Norepinephrine is also a weak beta-1-adrenergic receptor agonist, and it may increase heart rate and cardiac contractility in patients with shock. Norepinephrine is not effective orally and is erratically absoihed after subcutaneous injection. After intravenous administration, the onset of action is nearly immediate, and the duration of effect is 1-2 minutes after the infusion is discontinued. 

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