Hypotension drugs producing

Although vasodilators are effective in lowering blood pressure, these drugs are associated with a number of adverse effects. Reflex tachycardia often occurs because baroreflex responses attempt to compensate for the fall in vascular resistance that these drugs produce. This side effect is analogous to the increased heart rate occurring when alpha blockers are used to decrease peripheral vascular resistance. Other common reactions include dizziness, postural hypotension, weakness, nausea, fluid retention, and headache. Minoxidil also increases hair growth on the face, ears, forehead,... 

Both drugs produce sedation, and so would synergize, causing profound CNS effects. In addition, the hypotensive effects of antipsychotics would be markedly potentiated by the decrease in sympathetic activity produced by opiate agonists, causing severe cardiovascular complications. Both drugs affect skeletal muscle and medullary centers, as well, and may synergize to cause severe respiratory depression. 

Sodium nitroprusside is not an active hypotensive drug until metabolized to its active metabolite, NO, the mechanism of action of which has been previously described (Fig. 29.1). Studies with sodium nitroprusside suggest that it releases NO by its interaction with glutathione or with sulfhydryl groups in the erythrocytes and tissues to form a S-nitrosothiol intermediate, which spontaneously produces NO, which in turn freely diffuses into the VSM, thereby increasing intracellular cGMP concentration (6,9). NO also activates K channels, which leads to hyperpolarization and relaxation. 

Pre-soaked hydrophilic SCLs, as compared with an eye drop, extend the time that the dissolved drug will continue to be effective. For instance, SCLs pre-soaked in a 2% pilocarpine solution and placed on the cornea can maintain a significant reduction in lOP for almost 24 h." However, 90% of the drug is desorbed within a half hour, and the increase in the pulse necessary to achieve a full day s hypotensive therapy produces significant pilocarpine side-effects, such as increased miosis and myopia. 

Of the following drugs, which would not produce a syndrome of flushing, headache, nausea, vomiting, sweating, hypotension, and confusion after ethanol consumption ... 

Concurrent antiarrhythmic agents Concurrent antiarrhythmic agents may produce enhanced prolongation of conduction or depression of contractility and hypotension, especially in patients with cardiac decompensation. Reserve concurrent use of procainamide with other Class lA antiarrhythmic agents (eg, quinidine, disopyramide) for patients with serious arrhythmias unresponsive to a single drug and use only if close observation is possible. 

Cardiovascular disorders Use with extreme caution in patients with cardiovascular disorders because of the possibility of conduction defects, arrhythmias, CHF, sinus tachycardia. Ml, strokes, and tachycardia. These patients require cardiac surveillance at all dose levels of the drug. In high doses, TCAs may produce arrhythmias, sinus tachycardia, conduction defects, and prolonged conduction time. Tachycardia and postural hypotension may occur more frequently with protriptyline. Hyperthyroid patients Hyperthyroid patients or those receiving thyroid medication require close supervision because of the possibility of cardiovascular toxicity, including arrhythmias. 

The major toxic reactions to disopyramide administration include hypotension, congestive heart failure, and conduction disturbances. These effects are the result of disopyramide s ability to depress myocardial contractility and myocardial conduction. Although disopyramide initially may produce ventricular tachyarrhythmias or ventricular fibrillation in some patients, the incidence of disopyramide-induced syncope in long-term therapy is not known. Most other toxic reactions (e.g., dry mouth, blurred vision, constipation) can be attributed to the anticholinergic properties of the drug. 

Lidocaine may produce clinically significant hypotension, but this is exceedingly uncommon if the drug is given in moderate dosage. Depression of an already damaged myocardium may result from large doses. 

The reduction in plasma volume produced by p-blockers contrasts with the increased volume seen with other types of antihypertensives. Tolerance to the antihypertensive actions of p-blockers therefore is less of a problem than with the vasodilating drugs. An additional difference from the vasodilators is that plasma renin activity is reduced, rather than increased, by propranolol (Inderal). Orthostatic hypotension does not occur with p-blockers. 

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