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垂体-肾上腺活动的变化调节清醒自由活动雄性大鼠中由神经肽Y和肾上腺素诱导的中枢血管减压反应。

Changes in pituitary-adrenal activity regulate the central vasodepressor responses induced by neuropeptide Y and adrenaline in the awake unrestrained male rat.

作者信息

Aguirre J A, Fuxe K, Andbjer B, Eneroth P, Agnati L F

机构信息

Department of Histology, Karolinska Institute, Stockholm, Sweden.

出版信息

Acta Physiol Scand. 1991 Jan;141(1):35-44. doi: 10.1111/j.1748-1716.1991.tb09041.x.

Abstract

The central cardiovascular responses induced by neuropeptide Y (0.25 nmol) and adrenaline (2.00 nmol) given i.c.v. in close to maximal doses in the awake, unrestrained male rat were studied following changes in the pituitary-adrenal activity. Adrenalectomy (1 week) alone significantly reduced the vasodepressor response to i.c.v. adrenaline but not to i.c.v. neuropeptide Y. Corticosterone replacement treatment (5 mg kg-1 x 2, i.p., 1 week) significantly reduced both the maximal (peak) and overall (area) vasodepressor responses to i.c.v. adrenaline and neuropeptide Y (only overall responses) in the adrenalectomized rat. Corticosterone treatment alone in the sham-operated rat highly significantly reduced the vasodepressor responses to both i.c.v. adrenaline and neuropeptide Y. The bradycardic action of centrally administered neuropeptide Y was no longer significant after alterations in pituitary-adrenal activity. The present results suggest that corticosterone treatment can abolish the centrally evoked vasodepressor responses to close to maximal doses of adrenaline and neuropeptide Y, which may contribute to their hypertensive properties in man. Finally, after adrenalectomy the central vasodepressor responses to neuropeptide Y dominate, since the adrenergic vasodepressor responses are selectively reduced. This dominance is reduced by corticosterone replacement treatment. The results indicate an antagonistic role of adrenocortical steroids in control of centrally induced acute vasodepressor responses to neuropeptide Y and adrenaline.

摘要

研究了在清醒、不受约束的雄性大鼠中,经脑室内注射接近最大剂量的神经肽Y(0.25纳摩尔)和肾上腺素(2.00纳摩尔)所诱发的中枢心血管反应,观察垂体-肾上腺活动变化后的情况。单独进行肾上腺切除术(1周)显著降低了对脑室内注射肾上腺素的血管减压反应,但对脑室内注射神经肽Y的反应无影响。用皮质酮替代治疗(5毫克/千克×2,腹腔注射,1周)显著降低了肾上腺切除大鼠对脑室内注射肾上腺素和神经肽Y的最大(峰值)和总体(面积)血管减压反应(仅总体反应)。在假手术大鼠中,单独使用皮质酮治疗可极显著降低对脑室内注射肾上腺素和神经肽Y的血管减压反应。垂体-肾上腺活动改变后,中枢给予神经肽Y的心动过缓作用不再显著。目前的结果表明,皮质酮治疗可消除中枢诱发的对接近最大剂量肾上腺素和神经肽Y的血管减压反应,这可能有助于它们在人体中的升压特性。最后,肾上腺切除术后,对神经肽Y的中枢血管减压反应占主导,因为肾上腺素能血管减压反应被选择性降低。这种主导作用因皮质酮替代治疗而减弱。结果表明肾上腺皮质类固醇在控制中枢诱导的对神经肽Y和肾上腺素的急性血管减压反应中起拮抗作用。

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