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血管紧张素I通过增加黏膜细胞中环磷酸腺苷来增强加压素对蟾蜍膀胱水流量的刺激作用。

Enhancing effects of angiotensin I on the vasopressin-stimulated water flow of toad bladder through increased cyclic AMP in mucosal cells.

作者信息

Marumo F

出版信息

Life Sci. 1986 Dec 15;39(24):2371-5. doi: 10.1016/0024-3205(86)90668-5.

Abstract

The effects of angiotensins I and II on 10 mU/ml vasopressin-stimulated water flow across toad bladder were examined. Angiotensin I at concentrations of 10(-6) and 10(-7) M enhanced the water flow, but angiotensin II failed to do so at these concentrations. Angiotensin I had no effect on 5 mM cyclic AMP-stimulated water flow. After being preincubated for 30 min with angiotensin II, angiotensin I failed to have any stimulatory effect on vasopressin-stimulated water flow. At 10(-6) M angiotensin I significantly enhanced vasopressin-stimulated cyclic AMP content in bladder mucosal cells. These results indicate that angiotensin I enhances vasopressin-stimulated water flow by increasing cyclic AMP production in bladder cells and that angiotensin II may possibly interfere with angiotensin I in a competitive manner.

摘要

研究了血管紧张素I和II对10 mU/ml血管加压素刺激的蟾蜍膀胱水流量的影响。浓度为10(-6)和10(-7) M的血管紧张素I增强了水流量,但血管紧张素II在这些浓度下未能如此。血管紧张素I对5 mM环磷酸腺苷刺激的水流量没有影响。在与血管紧张素II预孵育30分钟后,血管紧张素I对血管加压素刺激的水流量没有任何刺激作用。在10(-6) M时,血管紧张素I显著增强了膀胱黏膜细胞中血管加压素刺激的环磷酸腺苷含量。这些结果表明,血管紧张素I通过增加膀胱细胞中环磷酸腺苷的产生来增强血管加压素刺激的水流量,并且血管紧张素II可能以竞争性方式干扰血管紧张素I。

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