Vasopressin receptor cardiovascular effects

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

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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