Role of atrial natriuretic peptide and oxytocin in gastric emptying delay induced by right atrial stretch in rats.

Fluid volume and osmolality balance are maintained by complex neuroendocrine and liquid-salt intake behavior, cardiovascular and renal mechanisms, and gastrointestinal adjustments. Mechanical stretching of the right atrium [atrial stretch (AS)] enhances central venous pressure and heart rate while decreasing gastric emptying (GE) of liquid in rats. We evaluated the effect of AS on GE and plasma levels of atrial natriuretic peptide (ANP), oxytocin (OT), and corticosterone (CORT) to determine whether ANP contributes to the OT-mediated GE delay of liquids due to AS in awake rats. Initially, we performed thoracotomy followed by right appendectomy (AX) or sham thoracotomy. One week later, rats were randomly subjected to pretreatment with NaCl 0.15 M (control), atosiban (AT, OT-antagonist), anantin (ANT, ANP-antagonist), or dexamethasone (DEX). Afterward, 50 µL of AS was administered for 5 min or not (sham). Then, the rats were fed a test meal, and GE of liquids or solids was performed. The other animals were pretreated with NaCl 0.15 M, atosiban, anantin, or dexamethasone, followed by OT treatment for GE assessment. Compared with the sham group, 50 µL of AS decreased the GE of the liquid and solid test meals. This phenomenon was prevented by AT, ANT, DEX, and surgical procedures with AX. AS also increased plasma levels of ANP, OT, and CORT. In turn, oxytocin treatment decreased GE and increased plasma ANP, OT, and CORT levels, while AT, ANT, and DEX prevented OT-induced GE delay. Hence, AS delayed GE of liquid in rats, a phenomenon that involves oxytocinergic pathways and ANP activities. We suggest a cardiogastric reflex with the participation of neuroendocrine mediators, which contributes to regulating liquid balance in the animal's body. Atrial natriuretic peptide and oxytocin are substances recognized for participating in diuresis and regulating the transit of liquids in the gastrointestinal tract in situations of cardiac volume overload, as was simulated with atrial stretching in the present experimental model.