正常和自发性高血压大鼠血管中神经肽y诱导的肌醇磷脂水解。

E Vila, J L Reid, I M Macrae
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引用次数: 6

摘要

1. 神经肽Y (NPY)增加成年Wistar Kyoto (WKY)和自发性高血压(SHR)大鼠股动脉和静脉肌醇磷酸(IP)的形成。2. 去甲肾上腺素(NA, 10(-6) M)诱导两品系大鼠的IP积累。3.亚阈浓度的NPY(股静脉3 × 10(-9) M,股动脉10(-8)M)未能改变NA (10(-6) M)诱导的两种血管的IP形成。4. 这些结果表明,在成年SHR和WKY大鼠中,直接收缩效应而非na诱导的收缩增强可能与磷脂酰肌醇的转换直接相关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuropeptide Y-induced inositol phospholipid hydrolysis in blood vessels from normotensive and spontaneously hypertensive rats.

1. Neuropeptide Y (NPY) increased inositol phosphate (IP) formation in the femoral artery and vein of adult Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. 2. Noradrenaline (NA, 10(-6) M) induced IP accumulation in both strains of rats. 3. Subthreshold concentrations of NPY (3 x 10(-9) M for femoral vein and 10(-8) M for femoral artery) failed to modify NA (10(-6) M)-induced IP formation in both vessels. 4. These results suggest that the direct contractile effects but not the potentiation of NA-induced contractions may be directly linked to phosphatidylinositol turnover in adult SHR and WKY rats.

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