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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Phillips P A, Rolls K A, Burrell L M, Casley D, Aldred K L, Hardy K J

Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1994 Mar;21(3):223-6. doi: 10.1111/j.1440-1681.1994.tb02501.x.

The aim of these studies was to determine the role of endothelin in cyclosporin A ([CsA], 10 mg/kg per day, s.c., for 30 days) hypertension in the rat. 2. There were no significant differences in plasma endothelin concentrations, in vitro mesenteric vascular membrane [125I]-endothelin-1 (ET-1) binding characteristics or myographic vascular responses to endothelin-1 between the CsA and control groups (systolic blood pressure 135 +/- 1 vs 127 +/- 1 mmHg, respectively, P < 0.001). 3. Twenty-four hours after selective endothelin type A receptor blockade in vivo with BQ123, blood pressure in CsA hypertensive rats was lowered to levels of normotensive controls. 4. These results suggest that changes in endothelin synthesis rather than changes in vascular sensitivity and/or ET-1 receptor characteristics may contribute to CsA-induced hypertension.

这些研究的目的是确定内皮素在环孢素A（[CsA]，每天10mg/kg，皮下注射，共30天）诱导的大鼠高血压中的作用。2. CsA组和对照组之间的血浆内皮素浓度、体外肠系膜血管膜[125I] - 内皮素 - 1（ET - 1）结合特性或血管对内皮素 - 1的肌电图反应均无显著差异（收缩压分别为135±1mmHg和127±1mmHg，P < 0.001）。3. 用BQ123在体内选择性阻断内皮素A型受体24小时后，CsA高血压大鼠的血压降至正常血压对照组的水平。4. 这些结果表明，内皮素合成的变化而非血管敏感性和/或ET - 1受体特性的变化可能导致CsA诱导的高血压。

Phillips P A, Rolls K A, Burrell L M, Casley D, Aldred K L, Hardy K J

Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.

Clin Exp Pharmacol Physiol. 1994 Mar;21(3):223-6. doi: 10.1111/j.1440-1681.1994.tb02501.x.

The aim of these studies was to determine the role of endothelin in cyclosporin A ([CsA], 10 mg/kg per day, s.c., for 30 days) hypertension in the rat. 2. There were no significant differences in plasma endothelin concentrations, in vitro mesenteric vascular membrane [125I]-endothelin-1 (ET-1) binding characteristics or myographic vascular responses to endothelin-1 between the CsA and control groups (systolic blood pressure 135 +/- 1 vs 127 +/- 1 mmHg, respectively, P < 0.001). 3. Twenty-four hours after selective endothelin type A receptor blockade in vivo with BQ123, blood pressure in CsA hypertensive rats was lowered to levels of normotensive controls. 4. These results suggest that changes in endothelin synthesis rather than changes in vascular sensitivity and/or ET-1 receptor characteristics may contribute to CsA-induced hypertension.

这些研究的目的是确定内皮素在环孢素A（[CsA]，每天10mg/kg，皮下注射，共30天）诱导的大鼠高血压中的作用。2. CsA组和对照组之间的血浆内皮素浓度、体外肠系膜血管膜[125I] - 内皮素 - 1（ET - 1）结合特性或血管对内皮素 - 1的肌电图反应均无显著差异（收缩压分别为135±1mmHg和127±1mmHg，P < 0.001）。3. 用BQ123在体内选择性阻断内皮素A型受体24小时后，CsA高血压大鼠的血压降至正常血压对照组的水平。4. 这些结果表明，内皮素合成的变化而非血管敏感性和/或ET - 1受体特性的变化可能导致CsA诱导的高血压。