Prazosin Beta blockers

Drugs that may be affected by beta blockers include flecainide, gabapentin, haloperidol, hydralazine, phenothiazines, anticoagulants, benzodiazepines, clonidine, disopyramide, epinephrine, ergot alkaloids, lidocaine, nondepolarizing muscle relaxants, prazosin, sulfonylureas, and theophylline. 

ALPHA-BLOCKERS BETA-BLOCKERS t efficacy of alpha-blockers t risk of first-dose 1 BP when alfuzosin, prazosin or terazosin is started in patients already taking beta-blockers Additive hypotensive effect may be used therapeutically Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (lightheadedness, dizziness on standing, etc.). Watch for first-dose 1 BP... 

Certain beta-blockers such as propranolol, metoprolol, and pindolol, and alpha-blockers such as prazosin, may cause impotence or a decrease in libido, which is usually dose related and should be... 

Clinically important, potentially hazardous interactions with albuterol, alpha-blockers, amitriptyline, amoxapine, atenolol, beta-blockers, carteolol, chlorpromazine, clomipramine, cocaine, desipramine, doxepin, ephedra, ergotamine, furazolidone, halothane, imipramine, insulin detemir, MAO inhibitors, metoprolol, nadolol, nortriptyline, oxprenolol, penbutolol, phenelzine, phenoxybenzamine, phenylephrine, pindolol, prazosin, propranolol, protriptyline, sympathomimetics, terbutaline, thioridazine, timolol, tranylcypromine, tricyclic antidepressants, trimipramine, vasopressors... 

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. 

Propranolol—but not prazosin—may decrease cardiac output. Prazosin may increase renin output (a compensatory response), but beta-blockers inhibit its release by the kidney. By reducing blood pressure, both may increase central sympathetic outflow (a compensatory response). Propranolol does not cause orthostatic hypotension. The answer is (D). 

PO/IV. Well absorbed, 80% metabolized in first pass. 90% protein bound. Metabolites are active. Half-life is 5 hrs but may be up to 20 hrs in patients with cirrhosis. Patient on IV blockers or digitalis. A-V node block, sick sinus syndrome, cardiogenic shock, heart failure, hypotension. Beta blockers or digitalis Increases likelihood of bradycardia or A-V blockade. Quinicfine or prazosin Increases hypotension. Digoxin levels are increased. Cimetidine reduces verapamil clearance. Calcium supplements may inhibit actions of verapamil. Depolarization (leading to contraction) of vascular smooth muscle is dependent on calcium entry. Vasodilation is induced by calcium entry blockers because they inhibit calcium influx. 

Displaces warfarin from plasma protein binding sites. Reduces natriuretic and diuretic effects of furosemide and antihypertensive effects of thiazides, beta blockers, prazosin, and captopril. 

A study in 40 men with essential hypertension (taking beta blockers, cap-topril, diuretics, methyidopa, prazosin or verapamil) who were moderate to heavy drinkers, found that when they reduced their drinking over a 6-week period from an average of 450 mL of alcohol weekly (about 6 drinks daily) to 64 mL of alcohol weekly, their average blood pressure fell by 5/3 mrnHg. The reasons for this effect are uncertain. 

Direct information is limited. Acute hypotension (dizziness, fainting) sometimes occurs unpredictably with the first dose of some alpha blockers (particularly, alfuzosin, prazosin and terazosin but see Alpha blockers , (p.83)), and this can be exaggerated if the patient takes or is already taking a beta blocker or a calcium-channel blocker (see Alpha blockers + Beta blockers , below, and Alpha blockers + Calcium-channel blockers , p.85). It would therefore seem prudent to apply the same precautions to ACE inhibitors, namely reducing the dose of the ACE inhibitor to a maintenance level if possible, then starting the alpha blocker at the lowest dose, with the first dose given at bedtime. Note that the acute hypotensive reaction appears to be short-lived. There is limited evidence that terazosin and tamsulosin may not cause an additional hypotensive effect in the longer term in patients with BPH who have hypertension already well-controlled with ACE inhibitors. Nevertheless, caution should be exercised in this situation, and a dose reduction of the ACE inhibitor may be required. 

The risk of first-dose hypotension with prazosin is higher if the patient is already taking a beta blocker. This is also likely to be true of other alpha blockers, particularly alfuzosin, bunazosin and terazosin. In a small study tamsulosin did not have any clinically relevant effects on blood pressure that was already well controlled by atenolol. Alpha blockers and beta blockers may be combined for additional lowering of blood pressure in patients with hypertension. 

Direct information seems to be limited to this study but what occurred is consistent with the way indometacin reduces the effects of many other different antihypertensives (e.g. see ACE inhibitors + NSAIDs , p.28, and Beta blockers + Aspirin or NSAIDs , p.835). It apparently does not affect every patient. If indometacin is added to established treatment with prazosin, be alert for a reduced antihypertensive response. It is not known exactly what happens in patients taking both drugs long-term, but note that with other interactions between antihypertensives and NSAIDs the effects seem to be modest. The manufacturers say that prazosin has been given with indometacin (and also aspirin and phenylbutazone) without any adverse interaction in clinical experience to date. Other manufacturers also... 

Of the drugs listed, only isoproterenol causes a decrease in mean blood pressure, because it activates beta receptors and has no effect on alpha receptors. This permits identification of drug 3 as isoproterenol. Prazosin is an alpha blocker, so one can anticipate that this drug would antagonize any increases in blood pressure that result from activation of (Xj receptors in the vasculature. Epinephrine (high dose), norepinephrine, and tyramine all exert pressor effects via activation of (Xj receptors. However, only epinephrine is active on P2 receptors, and this action would be revealed by vasodilation and a reversal of its pressor effects following treatment with an alpha blocker— epinephrine reversal. Thus, drug 4 can be identified as epinephrine. 

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