AVP release induced by increased intrarenal NaCl through renal afferent nerves in conscious rats

Abstract

Previous study from our laboratory demonstrated that the renal sensory afferent fibers responded to NaCl concentration in the renal artery, i.e., the renal afferent nerve activity was increased by an intrarenal arterial infusion of hypertonic NaCl solution in a dose dependent manner. However, a physiological significance of the increased renal afferent nerve activity was still unclear. We hypothesized that the renal afferent nerves may contribute to body fluid homeostasis through controlling arginine vasopressin (AVP) release. To examine this, plasma AVP was measured, while intrarenal NaCl receptors were selectively stimulated by a small dose infusion of hypertonic NaCl in conscious rats. Under a gas anesthesia, a PE‐10 catheter for NaCl infusion was inserted into the right renal artery via the suprarenal artery and a PE‐50 catheter for blood sampling was inserted into the abdominal aorta via the left femoral artery; these catheters were exteriorized from the back of the neck and connected to a swivel. One day was elapsed to recover from anesthesia and the surgery. Hyperosmotic NaCl solution (616 mmol/L) was infused into the renal artery at a rate of 50 μL/min for 10 min. Plasma Na+ concentration was not affected by this infusion (from 142.8 ± 0.6 to 143.6 ± 0.4 mmol/L), while plasma K+ concentration was significantly decreased (4.3 ± 0.1 to 4.1 ± 0.1 mmol/L). The hypertonic NaCl infusion significantly increased plasma AVP concentration from 2.8 ± 0.2 to 3.4 ± 0.4 pg/mL. This response was completely abolished by renal denervation. These data indicate that the renal sensory afferent fibers might sense changes in the intrarenal arterial NaCl concentration and alter AVP release.