PT  - JOURNAL ARTICLE
AU  - Gary Francis
AU  - Steven R. Goldsmith
TI  - Vasopressin receptor antagonists: Mechanisms of action and potential effects in heart failure
DP  - 2006 Jun 01
TA  - Cleveland Clinic Journal of Medicine
PG  - S20--S23
VI  - 73
IP  - 6 suppl 2
4099  - http://www.ccjm.org/content/73/6_suppl_2/S20.short
4100  - http://www.ccjm.org/content/73/6_suppl_2/S20.full
SO  - Cleve Clin J Med2006 Jun 01; 73
AB  - Increased arginine vasopressin (AVP) secretion in heart failure may lead to vasoconstriction, left ventricular remodeling, and water retention—actions that promote afterload, preload, and hyponatremia and thereby cause disease progression. Interfering with AVP-mediated signaling pharmacologically may be beneficial in heart failure. Selective antagonism of the vasopressin 2 (V2) receptor may facilitate a safe diuresis and normalize low serum sodium levels, as demonstrated in preliminary clinical trials. Pure V2 antagonism, however, may stimulate AVP secretion and enhance V1a signaling, while pure V1a receptor antagonism may lead to unwanted V2 stimulation and secondary water retention and volume expansion. Combined V1a and V2 receptor antagonism could potentially prove advantageous as a therapy for heart failure by acting synergistically to facilitate diuresis and improve hemodynamics.