环核苷酸依赖性蛋白激酶异喹啉磺酰胺抑制剂H-8对cAMP和cgmp介导的血管舒张的影响。

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158883
J T Daugirdas, H L Zhou, V V Tamulaitis, C W Nutting, R R Fiscus
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引用次数: 4

摘要

我们推测,H-8, N-[2-(甲氨基)乙基]-5-异喹啉磺酰胺,一种环核苷酸依赖性蛋白激酶抑制剂,可能是评估环核苷酸依赖性血管松弛的有用探针。然而,在大鼠尾动脉和主动脉中,我们发现即使大剂量的H-8也不会减少环AMP-和环gmp介导的松弛。例如,在尾动脉中,8-溴- cgmp (10(-5) M)对苯肾上腺素收缩的松弛作用不受H-8:对照33 +/- 6.2%的影响;10微米H-8, 41 +/- 12%;30微米H-8, 30 +/- 16% (p NS)。8-溴- camp的松弛量(3 × 10(-4) M)实际上增加了H-8:对照,29 +/- 7.6%;10微米H-8, 34 +/- 7.4%;30微米H-8, 80 +/- 14%。在大鼠主动脉中,H-8也不能减弱8-溴- cgmp、阿特罗肽II或硝普钠引起的松弛。在尾动脉和主动脉中,H-8本身引起α -肾上腺素能收缩的剂量依赖性抑制:例如,在尾动脉中,10或30微米H-8,对苯肾上腺素的峰值收缩分别降低到对照的70 (SEM) +/- 12%或52 +/- 7%。结果表明,蛋白激酶抑制剂H-8不是研究环核苷酸依赖性松弛的有用探针。
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Effect of H-8, an isoquinolinesulfonamide inhibitor of cyclic nucleotide-dependent protein kinase, on cAMP- and cGMP-mediated vasorelaxation.

We theorized that H-8, N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide, an inhibitor of cyclic nucleotide-dependent protein kinases, might be a useful probe to assess cyclic nucleotide-dependent relaxation of blood vessels. However, working in the rat caudal artery and aorta, we found that neither cyclic AMP- nor cyclic GMP-mediated relaxations were diminished by even large doses of H-8. For example, in the caudal artery, relaxation of a phenylephrine contraction by 8-bromo-cGMP (10(-5) M) was unaffected by H-8: control, 33 +/- 6.2%; 10 microM H-8, 41 +/- 12%; 30 microM H-8, 30 +/- 16% (p NS). The amount of relaxation by 8-bromo-cAMP (3 x 10(-4) M) was actually increased by H-8: control, 29 +/- 7.6%; 10 microM H-8, 34 +/- 7.4%; 30 microM H-8, 80 +/- 14%. In the rat aorta, H-8 also failed to diminish relaxation induced by 8-bromo-cGMP, or by atriopeptin II or sodium nitroprusside. In both caudal artery and aorta, H-8 of itself caused a dose-dependent suppression of alpha-adrenergic contraction: for example, in the caudal artery, with 10 or 30 microM H-8, peak contraction to phenylephrine was reduced to 70 (SEM) +/- 12% or 52 +/- 7% of control, respectively. The results suggest that the protein kinase inhibitor H-8 is not a useful probe to study cyclic nucleotide-dependent relaxation.

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