Hypotensive drug systemic effects

Shock is a complex acute cardiovascular syndrome that results in a critical reduction in perfusion of vital tissues and a wide range of systemic effects. Shock is usually associated with hypotension, an altered mental state, oliguria, and metabolic acidosis. If untreated, shock usually progresses to a refractory deteriorating state and death. The three major mechanisms responsible for shock are hypovolemia, cardiac insufficiency, and altered vascular resistance. Volume replacement and treatment of the underlying disease are the mainstays of the treatment of shock. Although sympathomimetic drugs have been used in the treatment of virtually all forms of shock, their efficacy is unclear. 

Ingestion. Primarily from chronic use of Mg-containing drugs by people with renal dysfunction. Anesthesia, hypotension, electroardiograph abnormalities, secondary central nervous system effects. 

The primary clinical effects observed in beta blocker toxicity are cardiovascular in nature. Direct cardiac effects include bradycardia (sinus, atrioventricular node, and ventricular), all degrees of atrioventricular block, bundle branch blocks, and asystole. Ventricular arrhythmias may occur secondary to bradycardia. Torsades de pointes has been associated with chronic toxicity from sotalol. Hypotension occurs and is due to decreased cardiac output and/or vasodilation. Central nervous system effects of these drugs including lethargy, coma, and seizures are secondary to the cardiovascular toxicities. Seizures and coma may be secondary to hypoglycemia. Bronchospasm can occur secondary to beta-2 blockade. Hypoglycemia and hyperkalemia can occur. 

Because inhibitory effects on angiotensin-converting enzyme (ACE) activity, a key enzyme in the renin-angiotensin system, are reported for many hypotensive drugs and functional foods (37,38), the effects of CLA isomers on ACE activity were measured (Fig. 9.6). However, 10r,12c-CLA did not have an inhibitory effect on ACE, because no significant differences were found among the three groups in ACE activity in plasma. 

With the possibihty of new drugs targeting NC and its receptor, one must consider the potential systemic effects with such administration. NC has the potential to effect systems such as the cardiovascular and renal systems. IV administration of NC resulted in species-based cardiovascular changes in test animals, showing transient hypotension and bradycardia in test rats, but an increase in both heart rate and blood pressure in sheep [1]. With regard to renal function, IV administration of NC resulted in increased water excretion and decreased urinary sodium excretion according to one study. This effect is probably due to the inhibition of oxytocin and vasopressin by NC. ICV injection of NC in test animals led to an increase in food consumption [1]. However, unlike other effects, this one was shown to be antagonized by naloxone. 

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