Long-term effects of AVP-induced neurohumoral interaction via area postrema on body fluid and blood pressure

Abstract

Arginine vasopressin (AVP) has been known to interact with the central nervous system via the area postrema (AP), resulting in suppression of renal sympathetic outflow in short-term studies. We hypothesize that if this sympathoinhibitory effect lasts long, then the neurohumoral interaction would enhance urinary output because of the suppression of neurogenic reuptake of sodium (Na+) and water. Intact (Int) and AP-lesioned (APX) rabbits were chronically catheterized and housed in metabolic cages. AVP was intravenously infused (0.1 mU ⋅ kg−1 ⋅ min−1) for 5 consecutive days. Urine volume and urinary Na+excretion rates in Int rabbits were lower than those in APX rabbits during AVP infusion. This smaller urinary output in Int rabbits was reconfirmed either from the daily balance of water and Na+or from the body weight, plasma Na+ concentration, and plasma osmolality data. This result contradicted the hypothesis. Mean arterial pressure was not altered in either group of rabbits while heart rate was suppressed in the Int rabbits. These data suggest that AP-mediated long-term action of AVP augments water retention and sustains bradycardia.