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Efferent pathways in renal and cardiovascular responses induced by intravenous hypertonic saline (HS) infusion
Author(s) -
Pedrino Gustavo Rodrigues,
Schoorlemmer Guus HM,
Cravo Sergio L
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a513-b
Subject(s) - endocrinology , renal blood flow , medicine , natriuresis , renal circulation , antagonist , renal artery , saline , jugular vein , tonicity , hypertonic saline , vasopressin , denervation , chemistry , femoral artery , kidney , receptor
The present study sought to determine the involvement of oxytocin (OT) and the renal sympathetic nerves in renal and cardiovascular responses induced by HS. Male Wistar rats (280–320 g) were anesthetized with sodium pentobarbitone (40 mg/kg, iv.) and fitted with a blood flow probe around the renal artery and cannulas in the femoral artery and vein, jugular vein, and urinary bladder. HS (3 M NaCl, 0.18 ml/100 g bw) was infused over 60 s. In control rats (N=5), ten min after HS, renal blood flow (RBF) and vascular conductance (RVC) increased by 49±2 and 36±8%. In 6 rats treated with the OT receptor blocker Atosiban (40 μg*h −1 *Kg −1 iv.), the increases in RBF and RVC were significantly smaller (17±7 and 16±7% after 10 min). In rats treated with OT antagonist and subjected to renal denervation (N=5; OTRD‐rats) the increases in RBF and RVC were abolished (10±11% and 15±8%, after 10 min). The increase in urine flow induced by HS was blunted in rats treated with the OT antagonist (2.1±0.34 vs. 3.5±0.35 ml/h, after 10 min) and was further reduced in OTRD‐rats (1.3±0.29 after 10 min). The natriuresis induced by HS was transiently reduced by the OT antagonist (0.32±0.06 vs. 0.17±0.04 mmol/h, after 10 min), and abolished in OTRD‐rats (0.08±0.027 mmol/h after 10 min). These results suggest that OT and renal nerves are important for renal vasodilation and sodium excretion induced by acute plasma hypertonicity. Acknowledgements: CAPES, CNPq.