The role of prostaglandins in the stimulated release of vasopressin during activation of afferent renal nerves

• Published in: Japanese Journal of Pharmacology 1994, Vol.64 (suppl.1), p.253-253
• Main Authors: Yamamoto, Akira, Kagawa, Susumu, Aki, Yasuharu, Kimura, Shoji, Tamaki, Toshiaki, Abe, Yoichi
• Format: Article
• Language: eng ; jpn
• ISSN: 0021-5198
• DOI: 10.1016/S0021-5198(19)50647-3

Objective; We have previously shown that activation of renal mechanoreceptors (MR) and chemoreceptors (CR) stimulates the release of vasopressin (AVP) by way of afferent renal nerves (ARN). The present studies investigated the role of prostaglandins (PGs) in AVP responses to MR and CR activation. Methods; In anesthetized rabbits, renal MR or CR were activated for 10min before and after inhibition of PGs synthesis with indomethacin (5 mg/kg). Renal MR were activated by increasing intrapelvic pressure to 50 mmHg (n=9). Renal CR were activated by intrarenal infusion of bradykinin (500 ng/min, n=7). Blood samples were collected 0 min, 5 min, 10 min and 30 min. These samples were analyzed for plasma AVP concentration (PAVP) and plasma osmolality (Posm). Results; With increased pelvic pressure, PAVP increased from 10.2±3.3 to 32.0±13.7 at 5 min (p＜0.01) and to 31.2±113.7 pg/ml at 10min (p＜0.01). Mean arterial pressure (MAP) increased from 78±4 to 83±4mmHg (p＜0.01). There was no change in heart rate (HR) and Posm. Renal infusion of bradykinin increased PAVP from 1.3±0.2 to 20.7±8.1 at 5min (p＜0.01) and to 23.7±8.1 pg/ml at 10min (p＜0.01). HR increased from 233±10 to 25±11 beats/min (p＜0.05). MAP and Posm did not change. Indomethacin pretreatment abolished the PAVP and MAP responses to increased pelvic pressure. Indomethacin also attenuated the increases in PAVP and HR produced by renal bradykinin. Conclusion; Stimulated release of AVP during ARN activation is dependent upon PGs.