Peripheral vasculature vasodilators

Prazosin, terazosin, and doxazosin are selective cq-receptor blockers that inhibit catecholamine uptake in smooth muscle cells of the peripheral vasculature, resulting in vasodilation. 

Vasodilators Peripheral vasculature Lower vascular resistance by directly vasodilating peripheral vessels... 

Diltiazem (Cardizem, Dilacor). Like the other calcium channel blockers, diltiazem is able to vasodilate the coronary arteries and the peripheral vasculature. Diltiazem also produces some depression of electrical conduction in the sinoatrial and atrioventricular nodes, an effect that may cause slight bradycardia. This bradycardia can be worsened by beta blockers or in patients with myocardial conduction problems, and diltiazem should probably be avoided in these individuals.32,45... 

Peripheral vasculature. PGI2, PGE, and PGE2 induce vasodilation in heart, kidney, skeletal muscle, and mesentery, lowering vascular resistance and blood pressure. 

The calcium channel blockers inhibit the entrance of calcium into cardiac and smooth muscle cells of the coronary and systemic arterial beds. All calcium channel blockers are therefore vasodilators that cause a decrease in smooth muscle tone and vascular resistance. (See p. 187 for a description of the mechanism of action of this group of drugs.) At clinical doses, these agents affect primarily the resistance of vascular smooth muscle and the myocardium. [Note Verapamil mainly affects the myocardium, whereas nifedipine exerts a greater effect on smooth muscle in the peripheral vasculature. Diitiazem is intermediate in its actions.]... 

In addition to their prominent function in heart, P-ARs are located on vascular smooth muscle cells, where they mediate vasodilating effects of catecholamines. The P2-AR has been proposed to play a dominant role in catecholamine-induced vasodilation in both pulmonary and peripheral vasculature. Surprisingly, isomet-... 

Antihypertensive Vasodilators - A common characteristic of hypertensive patients, regardless of the etiology of their disease, is abnormally high peripheral vascular resistance. Drugs that act directly on peripheral vasculature to decrease resistance are, therefore, logical agents for the treatment of hypertension. Unfortunately, sympathetic reflex actions leading to cardiac stimulation, hyperreninemia and fluid retention limit the hypotensive action of vasodilators and they are used mainly in combination with 6-blockers and diuretics for the treatment of more severe hypertension. A vasodilator that may not cause undesirable reflex... 

D (peripheral) Renal, mesenteric, coronary vasculature vasodilation—in kidney T GFR, RBF and Na+ excretion... 

Intravenous administration of dopamine promotes vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels, via activation of Di receptors. Activation of the Di receptors in the renal vasculature may also induce natriuresis. The renal effects of dopamine have been used clinically to improve perfusion to the kidney in situations of oliguria (abnormally low urinary output). The activation of presynaptic D2 receptors suppresses norepinephrine release, but it is unclear if this contributes to cardiovascular effects of dopamine. In addition, dopamine activates Bj receptors in the heart. At low doses, peripheral resistance may decrease. At higher rates of infusion, dopamine activates vascular a. receptors, leading to vasoconstriction, including in the renal vascular bed. Consequently, high rates of infusion of dopamine may mimic the actions of epinephrine. 

Vascular smooth muscle tone is regulated by adrenoceptors consequently, catecholamines are important in controlling peripheral vascular resistance and venous capacitance. Alpha receptors increase arterial resistance, whereas 2 receptors promote smooth muscle relaxation. There are major differences in receptor types in the various vascular beds (Table 9-4). The skin vessels have predominantly receptors and constrict in the presence of epinephrine and norepinephrine, as do the splanchnic vessels. Vessels in skeletal muscle may constrict or dilate depending on whether ffor 13 receptors are activated. Consequently, the overall effects of a sympathomimetic drug on blood vessels depend on the relative activities of that drug at and 8receptors and the anatomic sites of the vessels affected. In addition, Di receptors promote vasodilation of renal, splanchnic, coronary, cerebral, and perhaps other resistance vessels. Activation of the Di receptors in the renal vasculature may play a major role in the natriuresis induced by pharmacologic administration of dopamine. 

Both presynaptic and postsynaptic adrenoceptors are present in the vasculature. Postsynaptic a - and 2-receptors mediate vasoconstriction, whereas postsynaptic /32-receptors induce vasodilation. Presynaptic a2-receptors inhibit norepinephrine release in the vasculature as well. Presynaptic /3i-adrenoceptors promote neurotransmitter release. Stimulation of peripheral DAj -receptors produces renal, coronary, and mesenteric vasodilation and a natriuretic response. Stimnlation of DA2-receptors inhibits norepinephrine release from sympathetic nerve endings and prolactin release and may in-dnce nansea and vomiting. DAj- and DA2-receptor stimulation also... 

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