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血清肌酸激酶释放与α和β肾上腺素能受体

Serum creatine kinase release and alpha- and beta-adrenergic receptors.

作者信息

Jingu Y, Aoki Y, Itoh H, Saruta T

出版信息

Arch Int Pharmacodyn Ther. 1986 Aug;282(2):262-75.

PMID:3021077
Abstract

Changes in the serum creatine kinase (CK) activity and the mechanism of its release after administration of two kinds of beta-blockers to rats were studied in order to determine the mechanism of the increase in serum CK accompanying administration of beta-blockers. When pindolol or propranolol was administered at a dose of more than 10 mg/kg of body weight, the serum CK activity was increased in proportion to the dose. Also when an alpha-stimulator or an alpha, beta-stimulator such as noradrenaline and adrenaline was administered, the serum CK activity was increased. When the beta-stimulator isoproterenol or the alpha 1-blocker prazosin was administered, there was no increase in the serum CK activity. In terms of consecutive administration of a combination of beta-blockers and adrenaline, the serum CK activity was not increased by the second and succeeding administrations. As for the use of adrenaline alone, on the other hand, the serum CK activity after the second administration was equal to that after the first administration. The increase in CK activity after administration of adrenaline as the second treatment following administration of a beta-blocker as the first treatment was approximately the same as that after single administration of adrenaline. From the fact that the serum CK activity in rats was increased by administration of an alpha-stimulator and of a beta-blocker, it is possible that CK release in the blood is due to the action of alpha-receptors rather than beta-receptors. In the case of consecutive administration of a beta-blocker, the serum CK activity was not increased after the second administration. However, the serum CK activity was increased by the administration of an alpha-stimulator. This finding suggests the possibility that CK release is due to the disturbance of the balance between alpha-receptor and beta-receptor. Most of the CK isoenzymes released in the blood after administration of a beta-blocker were of the MM type.

摘要

为了确定β受体阻滞剂给药后血清肌酸激酶(CK)活性增加的机制,研究了给大鼠注射两种β受体阻滞剂后血清CK活性的变化及其释放机制。当吲哚洛尔或普萘洛尔以超过10mg/kg体重的剂量给药时,血清CK活性随剂量增加而升高。同样,当给予α刺激剂或α、β刺激剂如去甲肾上腺素和肾上腺素时,血清CK活性也会升高。当给予β刺激剂异丙肾上腺素或α1阻滞剂哌唑嗪时,血清CK活性没有增加。就连续联合给予β受体阻滞剂和肾上腺素而言,第二次及后续给药时血清CK活性没有增加。另一方面,单独使用肾上腺素时,第二次给药后的血清CK活性与第一次给药后相同。在第一次给予β受体阻滞剂后第二次给予肾上腺素,其CK活性增加幅度与单次给予肾上腺素后的增加幅度大致相同。从大鼠血清CK活性因给予α刺激剂和β受体阻滞剂而升高这一事实来看,血液中CK的释放可能是由于α受体而非β受体的作用。在连续给予β受体阻滞剂的情况下,第二次给药后血清CK活性没有增加。然而,给予α刺激剂后血清CK活性增加。这一发现提示CK释放可能是由于α受体和β受体之间平衡失调所致。给予β受体阻滞剂后血液中释放的大多数CK同工酶为MM型。

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