Effects of halothane on renal hemodynamics and interstitial nitric oxide in rabbits
Autor: | Akira Miyatake, Yasuharu Aki, Takatomi Syokoji, Youichi Abe, Wang Yue, Toshiki Fukui, Shoji Kimura, Kazuhito Kusudo, Akira Nishiyama |
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Rok vydání: | 1999 |
Předmět: |
Male
Nitroprusside Microdialysis medicine.medical_specialty Blood Pressure Arginine Kidney Nitric Oxide Cyclase Renal Circulation Nitric oxide chemistry.chemical_compound Internal medicine medicine Animals Drug Interactions Cyclic GMP Pharmacology Dose-Response Relationship Drug Chemistry medicine.anatomical_structure Endocrinology Guanylate Cyclase Vasoconstriction Renal blood flow Anesthetics Inhalation Rabbits Sodium nitroprusside medicine.symptom Halothane medicine.drug |
Zdroj: | European Journal of Pharmacology. 367:299-306 |
ISSN: | 0014-2999 |
DOI: | 10.1016/s0014-2999(98)00978-9 |
Popis: | The effects of halothane on renal hemodynamics and the nitric oxide (NO)-guanylate cyclase signaling pathway were examined in anesthetized rabbits using a renal microdialysis method. Halothane (0.5 and 2 vol%) caused dose-dependent decreases in blood pressure, renal blood flow and the renal interstitial concentrations of guanosine 3',5'-cyclic monophosphate (cGMP) or nitrate (NO2)/nitrite (NO3). Sodium nitroprusside (20 microg kg(-1) min(-1), i.v.) under the inhalation of halothane (2 vol%) increased the renal interstitial concentration of cGMP. L-Arginine (priming dose, 300 mg kg(-1) 10 min(-1); sustaining dose, 50 mg kg(-1) min(-1), i.v.) did not reverse halothane-induced reductions of cGMP and NO2/NO3. These findings demonstrate that halothane caused a renal vasoconstriction and inhibited the NO-guanylate cyclase signaling pathway in the kidney. Moreover, it is possible that the renal hemodynamic responses to halothane might have been induced, in part, through this inhibition. Finally, it can be assumed that halothane did not interfere with the activation process of guanylate cyclase by NO. |
Databáze: | OpenAIRE |
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