Tachycardia prazosin

Correct answer = D. Propranolol is a nonspecific p blocker that interferes with Pi receptors on the heart, causing bradycardia, that is, a slowing of the heart rate, Phenoxybenzamine blocks a receptors and prevents vasoconstriction of peripheral blood vessels by endogenous catecholamines. This leads to a decrease in blood pressure and peripheral resistance, which causes a reflex tachycardia. Isoproterenol is a potent p agonist that promotes tachycardia. Phentolamine is an a blocker that causes hypotension, which may set off refiex tachycardia. Prazosin is not indicated for tachycardia. 

OC-Adrenoceptor Blockers. Nonselective a-adrenoceptor blockers (Table 6), such as phentolamine, which block both a - and a2 adrenoceptors, produce vasodilation by antagonizing the effects of endogenous norepinephrine. They also produce severe tachycardia and have been replaced by selective a -adrenoceptor blockers, such as prazosin, terazosin, and doxazosin, which do not usually cause severe tachycardia. 

Prazosin, a selective a -adrenoceptor antagonist, exerts its antihypertensive effect by blocking the vasoconstrictor action of adrenergic neurotransmitter, norepinephrine, at a -adrenoceptors in the vasculature (200,227,228). Prazosin lowers blood pressure without producing a marked reflex tachycardia. It causes arteriolar and venular vasodilation, but a significant side effect is fluid retention. Prazosin increases HDL cholesterol, decreases LDL cholesterol, and does not cause glucose intolerance. 

Prazosin is a selective aradrenergic receptor antagonist that, at therapeutic doses, has little activity at a2-adrenergic receptors and clinically insignificant direct vasodilating activity The drug does not cause the other effects attributed to phentolamine. Most important, it produces less tachycardia than does phentolamine and, therefore, is useful in the treatment of essential hypertension. 

Doxazosin, also a selective a i-blocker, resembles prazosin in most aspects, but it has a better pharmacokinetic profile, at least for long-term use as in essential hypertension. Owing to its slow onset of action, doxazosin causes far less orthostatic hypotension and reflex tachycardia than prazosin. As a result of its long duration of action, it can be administered once daily in the long-term treatment of essential hypertension. 

In the treatment of hypertension a selective O -adrenoceptor agent is preferable to the older, non-selective (ai - - a2)-blockers. Doxazosin is preferable to prazosin, because it has a slower onset and longer duration of action. It therefore causes less or no reflex tachycardia and orthostatic hypotension. 

Prazosin is a piperazinyl quinazoline effective in the management of hypertension (see Chapter 11). It is highly selective for i receptors and typically 1000-fold less potent at k2 receptors. This may partially explain the relative absence of tachycardia seen with prazosin compared with that of phentolamine and phenoxybenzamine. Prazosin relaxes both arterial and venous vascular smooth muscle, as well as smooth muscle in the prostate, due to blockade of K receptors. Prazosin is extensively metabolized in humans because of metabolic degradation by the liver, only about 50% of the drug is available after oral administration. The half-life is normally about 3 hours. 

Prazosin (see structure in Figure 12.2), the prototypic drug in this class, decreases peripheral vascular resistance in arterioles and veins by blocking alpha receptors on vascular smooth muscle. It does not decrease cardiac output. Because of this effect, patients taking prazosin are more prone ( 50 percent) to postural hypotension, particularly following the first dose. In some cases, the hypotension is so severe that the patient may lose consciousness. In an attempt to compensate, the baroreceptors may produce an accompanying tachycardia. 

Prazosin, oxazosin and terazosin (see p. 73) produce a competitive block of oci adrenoceptors. They decrease peripheral vascular resistance and lower arterial blood pressure by causing the relaxation of both arterial and venous smooth muscle. These drugs cause only minimal changes in cardiac output, renal blood flow, and glomerular filtration rate. Therefore, long-term tachycardia and increased renin release do not occur. Postural hypotension may occur in some individuals. Prazosin is used to treat mild to moderate hypertension and is prescribed in combination with propranolol or a diuretic for additive effects. Reflex tachycardia and first dose syncope are almost universal adverse effects. Concomitant use of a p-blocker may be necessary to blunt the short-term effect of reflex tachycardia. 

BETA-BLOCKERS ALPHA-BLOCKERS t efficacy of alpha-blockers t risk of first-dose 1 BP with alfuzosin, prazosin and terazosin Additive hypotensive effect may be used therapeutically. Beta-blockers prevent the ability to mount a tachycardia in response to 1 BP this T the risk of first-dose 1 BP when starting alpha-blockers in patients already on beta-blockers Monitor BP at least weekly until stable watch for first-dose 1 BP. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)... 

The first-dose effect (profound postural hypotension and reflex tachycardia) is a weU-recognized complication of the first dose of prazosin and related agents. This phenomenon is dose-related and can usually be avoided by using a low initial dosage taken at bedtime. During long-term treatment, orthostatic hypotension and dizziness is reported by about 10% of patients. 

Indoramin is a postsynaptic selective alphai-adrenoceptor antagonist that is chemically distinct from the quinazo-lines. Unlike some other alpha-blockers, indoramin lowers blood pressure without a resulting reflex tachycardia or postural hypotension (1). However, it has largely been supplanted by more modern drugs, such as doxazosin, prazosin, and terazosin. 

Prazosin prototype otj selective blocker (others include doxazosin, terazosin, amsulosin). Less reflex tachycardia (because NE feedback mechanism is intact), but postural hypotension occurs (first-dose syncope). Clinical uses include mild-to-moderate HTN and benign prostatic hyperplasia (BPH). 

Do drugs such as prazosin and terazosin result in reflex tachycardia ... 

Selective alpha-blockers Because prazosin and its analogs block vascular a, receptors much more effectively than the a,-modulatory receptors associated with cardiac sympathetic nerve endings, these drugs cause much less tachycardia than the nonselective alpha-blockers when reducing blood pressure. 

E. Adrenoceptor Blockers Alpha -selective agents (eg, prazosin) and beta-blockers (eg, propranolol) are effective antihypertensive drugs. Alpha-blockers reduce vascular resistance and venous return. The nonselective alpha-blockers (phentolamine, phenoxybenzamine) are of no value in chronic hypertension because of excessive compensatory responses, especially tachycardia. Alpha,-selective adrenoceptor blockers are relatively free of the severe adverse effects of the nonselective alpha-blockers and postganglionic nerve terminal sympathoplegic agents. 

I. Mechanism of toxicity. All these drugs dilate peripheral arterioles to lower blood pressure. A reflex sympathetic response results in tachycardia and occasionally cardiac arrhythmias. Prazosin and other newer alpha-1-specific agents are associated with little or no reflex tachycardia however, postural hypotension is common, especially in patients with hypovolemia. 

Like all vasodilators, prazosin too causes an increase in heart rate Seedat recorded tachycardias of 120—180 a minute in patients who developed syncopes with, at that... 

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