Mechanism of vasodilation induced by alpha‐human atrial natriuretic polypeptide in rabbit and guinea‐pig renal arteries.
Mechanism of vasodilation induced by alpha‐human atrial natriuretic polypeptide in rabbit and guinea‐pig renal arteries.
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α-人心房钠尿多肽诱导兔和豚鼠肾动脉血管舒张的机制。
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发表时间：
1986
期刊：
影响因子：
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通讯作者：
H. Kuriyama
中科院分区：
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作者：
K. Fujii;T. Ishimatsu;H. Kuriyama
研究了α-人心房利钠多肽（α - HANP）对豚鼠和兔肾动脉以及豚鼠肠系膜动脉平滑肌细胞的电学和力学特性的影响。α - HANP（高达10 nM）既不改变豚鼠和兔肾动脉平滑肌细胞的膜电位，也不改变其电阻。在豚鼠肠系膜动脉和肾动脉中，α - HANP（高达10 nM）对兴奋性接头电位的幅度和易化作用（肠系膜动脉）或抑制作用（肾动脉）以及动作电位均无影响。在豚鼠肾动脉中，α - HANP（高达10 nM）对去甲肾上腺素（NA）（高达10 μM）诱导的去极化无影响，但显著抑制NA诱导的收缩。α - HANP（10 nM）轻微抑制K⁺诱导的收缩。在兔肾动脉中，α - HANP（10 nM）抑制NA诱导的收缩，对K⁺诱导的收缩也有一定程度的抑制。在兔肾动脉中，在含有2 mM - EGTA的无钙溶液中研究了α - HANP对两次应用NA引起的细胞内储存钙释放及其再储存的影响。当在第一次应用0.5 μM - NA之前和期间应用5 nM - α - HANP时，收缩明显受到抑制，但第二次应用10 μM - NA时的收缩增强。如果第一次应用的NA剂量为10 μM，则影响非常小。在相同的实验条件下，硝酸甘油（10 μM）对NA诱导的收缩显示出与α - HANP几乎相同的作用。当在无钙溶液中咖啡因诱发第一次（3 mM）和第二次（10 mM）收缩时，α - HANP（5 nM）和硝酸甘油（10 μM）对两次收缩的抑制程度相同。在兔肾动脉中，应用α - HANP或硝酸甘油以剂量依赖的方式增加鸟苷3',5' - 磷酸（环磷鸟苷）的量。然而，硝酸甘油需要高得多的浓度（2×10³倍）。在兔肾动脉中，0.5 μM - NA激活的磷脂酰肌醇4,5 - 二磷酸（PI - P₂）的水解被α - HANP以剂量依赖的方式抑制，但10 μM - NA的激活不被α - HANP（高达100 nM）抑制。（摘要截断于400字）
Effects of alpha‐human atrial natriuretic polypeptide (alpha‐HANP) on electrical and mechanical properties of smooth muscle cells of the guinea‐pig and rabbit renal arteries and of the guinea‐pig mesenteric artery were investigated. alpha‐HANP (up to 10 nM) modified neither the membrane potential nor resistance of smooth muscle cells of the guinea‐pig and rabbit renal arteries. In the guinea‐pig mesenteric and renal arteries, alpha‐HANP (up to 10 nM) had no effect on the amplitude and facilitation (mesenteric artery) or depression (renal artery) of excitatory junction potentials nor on action potentials. In the guinea‐pig renal artery, alpha‐HANP (up to 10 nM) had no effect on the depolarization induced by noradrenaline (NA) (up to 10 microM) but markedly inhibited NA‐induced contraction. alpha‐HANP (10 nM) slightly inhibited the K‐induced contraction. In the rabbit renal artery, alpha‐HANP (10 nM) inhibited the NA‐induced contraction and to a lesser extent the K‐induced contraction. In the rabbit renal artery, the effects of alpha‐HANP on the release of Ca from the cellular storage by two applications of NA, and its re‐storage, were investigated in Ca‐free solution containing 2 mM‐EGTA. When 5 nM‐alpha‐HANP was applied before and during the first application of 0.5 microM‐NA, the contraction was markedly inhibited but the contraction to a second application of 10 microM‐NA was potentiated. If the first dose of NA was 10 microM the effect was very small. Under the same experimental procedures, nitroglycerine (10 microM) showed almost the same effects as alpha‐HANP on the NA‐induced contractions. When both the first (3 mM) and second (10 mM) contractions were evoked by caffeine in Ca‐free solution, alpha‐HANP (5 nM) and nitroglycerine (10 microM) inhibited both contractions to the same extent. In the rabbit renal artery, applications of alpha‐HANP or nitroglycerine increased the amount of guanosine 3',5'‐phosphate (cyclic GMP) in a dose‐dependent manner. However, a much higher concentration of nitroglycerine was required (2 X 10(3) times). In the rabbit renal artery, hydrolysis of phosphatidyl inositol 4,5‐bisphosphate (PI‐P2) activated by 0.5 microM‐NA was inhibited by alpha‐HANP, in a dose‐dependent manner, but activation by 10 microM‐NA was not inhibited by alpha‐HANP (up to 100 nM).(ABSTRACT TRUNCATED AT 400 WORDS)