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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

Hockings G I, Grice J E, Walters M M, Jackson R V

University Department of Medicine, Greenslopes Hospital, Brisbane, Queensland, Australia.

Clin Exp Pharmacol Physiol. 1991 May;18(5):303-7. doi: 10.1111/j.1440-1681.1991.tb01451.x.

The effect of pretreatment with nifedipine on naloxone-stimulated corticotrophin-releasing hormone (CRH)-induced adrenocorticotrophin (ACTH) release in humans was investigated. The mean peak plasma ACTH and cortisol levels and the mean peak change in cortisol levels from basal were significantly lower in the nifedipine/naloxone test than in the naloxone alone test. The integrated areas under the ACTH-time and cortisol-time curves were reduced by 33 and 49%, respectively, in the nifedipine/naloxone test compared with the naloxone alone test. These results correlate well with published in vitro studies. 2. Acute administration of oral nifedipine partially inhibited naloxone-stimulated ACTH and cortisol release, probably by blockade of plasma membrane voltage-dependent L-type calcium channels normally activated following binding of CRH to pituitary corticotroph receptors. 3. Naloxone-induced CRH release may replace insulin hypoglycaemia testing of pituitary ACTH reserve in humans.

研究了硝苯地平预处理对纳洛酮刺激的促肾上腺皮质激素释放激素（CRH）诱导的人类促肾上腺皮质激素（ACTH）释放的影响。在硝苯地平/纳洛酮试验中，血浆ACTH和皮质醇的平均峰值水平以及皮质醇水平相对于基础值的平均峰值变化显著低于单独使用纳洛酮的试验。与单独使用纳洛酮的试验相比，硝苯地平/纳洛酮试验中ACTH-时间曲线和皮质醇-时间曲线下的积分面积分别减少了33%和49%。这些结果与已发表的体外研究结果高度相关。2. 急性口服硝苯地平部分抑制了纳洛酮刺激的ACTH和皮质醇释放，可能是通过阻断CRH与垂体促肾上腺皮质激素受体结合后正常激活的质膜电压依赖性L型钙通道。3. 纳洛酮诱导的CRH释放可能替代人类垂体ACTH储备的胰岛素低血糖试验。

Hockings G I, Grice J E, Walters M M, Jackson R V

University Department of Medicine, Greenslopes Hospital, Brisbane, Queensland, Australia.

Clin Exp Pharmacol Physiol. 1991 May;18(5):303-7. doi: 10.1111/j.1440-1681.1991.tb01451.x.

The effect of pretreatment with nifedipine on naloxone-stimulated corticotrophin-releasing hormone (CRH)-induced adrenocorticotrophin (ACTH) release in humans was investigated. The mean peak plasma ACTH and cortisol levels and the mean peak change in cortisol levels from basal were significantly lower in the nifedipine/naloxone test than in the naloxone alone test. The integrated areas under the ACTH-time and cortisol-time curves were reduced by 33 and 49%, respectively, in the nifedipine/naloxone test compared with the naloxone alone test. These results correlate well with published in vitro studies. 2. Acute administration of oral nifedipine partially inhibited naloxone-stimulated ACTH and cortisol release, probably by blockade of plasma membrane voltage-dependent L-type calcium channels normally activated following binding of CRH to pituitary corticotroph receptors. 3. Naloxone-induced CRH release may replace insulin hypoglycaemia testing of pituitary ACTH reserve in humans.

研究了硝苯地平预处理对纳洛酮刺激的促肾上腺皮质激素释放激素（CRH）诱导的人类促肾上腺皮质激素（ACTH）释放的影响。在硝苯地平/纳洛酮试验中，血浆ACTH和皮质醇的平均峰值水平以及皮质醇水平相对于基础值的平均峰值变化显著低于单独使用纳洛酮的试验。与单独使用纳洛酮的试验相比，硝苯地平/纳洛酮试验中ACTH-时间曲线和皮质醇-时间曲线下的积分面积分别减少了33%和49%。这些结果与已发表的体外研究结果高度相关。2. 急性口服硝苯地平部分抑制了纳洛酮刺激的ACTH和皮质醇释放，可能是通过阻断CRH与垂体促肾上腺皮质激素受体结合后正常激活的质膜电压依赖性L型钙通道。3. 纳洛酮诱导的CRH释放可能替代人类垂体ACTH储备的胰岛素低血糖试验。