[The effects of sufentanil and remifentanil in the isolated perfused rat kidney]. / Sufentanil ve remifentanilin izole perfüze rat böbregi üzerine etkileri.

ABSTRACT

In this study, the effects of indomethacin (prostaglandin synthase inhibitor), propranolol (beta adrenergic receptors blocker), tetraethylammonium (TEA) (calcium-dependent potassium channel blocker) and glibenclamide (ATP-sensitive potassium channel blocker), NG nitro-L-arginine (NO synthetase inhibitor) and naloxane (nonselective opioid receptor antagonists) on the responses induced by sufentanil and remifentanil were investigated in the isolated perfused rat kidney. Renal arter was cannulated. Then the kidney was perfused continuously with warmed (37 degrees C) and aerated (95% O2 and 5% CO2). Krebs Henselieit solution by using a peristaltic pump delivering a constant flow (8-10 ml/min). Vascular responses were detected as changes in perfussion pressure, which was monitored continuously with a pressure transuder and recorded on polygraph. After phenilephrine (PE)-induced vasoconstriction had reached a platoe, sufentanil or remifentanil were given. Vasodilatation was recorded. Antagonists or inhibitors were added and responses were recorded. At the end of each experiment; papaverine was used to obtain the maximum dilatation. None of the used antagonists or inhibitors were not effected the submaximum PE construction. The used opioids were not alter in basal perfusion pressure. Antagonists or inhibitors had no effect on papaverine-induced dilatation. Bolus addition of sufentanil and remifentanil produced concentration dependent vasodilation. Indomethacine L-NAME, propranolol, naloxone and glibenclamide did not significantly alter responses of both of the opioids (p > 0.05). But, sufentanil and remifentanil induced dilatation were significantly affected by TEA (p < 0.05). The present results demonstrated that sufentanil and remifentanil decrease perfusion pressure in the isolated rat kidney and such mechanism may involve the calcium active K+ channels activation.