cGMP level that reduces cardiac myocyte O2 consumption is altered in renal hypertension.

cGMP level that reduces cardiac myocyte O2 consumption is altered in renal hypertension.
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肾性高血压中降低心肌细胞 O2 消耗的 cGMP 水平发生改变。

DOI:
10.1152/ajpheart.1997.273.4.h1949
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发表时间:
1997
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Weiss,HR
Weiss,HR
中科院分区:
--
文献类型:
--
作者:
Straznicka,M;Gong,G;Tse,J;Scholz,PM;Weiss,HR

文献摘要

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我们验证了高血压(一肾一夹;1K,1C)心肌肥厚兔心肌细胞需要更高的鸟苷3‘,5’-环一磷酸(CGMP)以同样比对照心肌细胞更低的O2消耗的假说,并且这种影响是由鸟苷环化酶活性的差异引起的。用硝普钠、一氧化碳或鸟苷素(10⋅8~10−5M)刺激鸟苷环化酶后,获得正常和1K、1C新西兰大白兔心肌细胞耗氧量(NL O2)和cGMP(fmol/105细胞)水平。同时测定了可溶性鸟苷环化酶的活性。基础cGMP在1K、1C组较对照组升高(176±28比85±13)。硝普钠、一氧化碳和鸟苷素刺激后,1K、1C和对照心肌细胞cGMP均升高。1K、1C组心肌细胞鸟苷环化酶活性与对照组相比无统计学差异。1K、1C心肌细胞的基础氧耗量与对照组相当(307±1比299±22)。当刺激鸟苷环化酶时,O2的消耗也同样减少。控制回归方程为:CO的O2消耗量=−1.46cGMP+444.65(r=0.96),硝普钠的O2消耗量=−0.58cGMP+328.48(r=0.82),鸟苷素的O2消耗量=−1.25cGMP+389.15(r=0.88)。1K,1C回归方程分别为:氧耗=−1.36⋅[cGMP]+537.81(r=0.97),氧耗=−0.23⋅[cGMP]+307.30(r=0.88),鸟苷=−1.27⋅[cGMP]+502.91(r=0.89)。这些数据表明,1K、1C肥大的心肌细胞在各个氧耗量水平上cGMP含量均高于对照组。这种影响不是由于基础或最大鸟苷环化酶活性的差异造成的。
We tested the hypothesis that cardiac myocytes from hypertensive (one kidney, one clip; 1K,1C) cardiac-hypertrophied rabbits require higher guanosine 3′,5′-cyclic monophosphate (cGMP) to similarly lower O2consumption than control myocytes and that this effect is caused by differences in guanylate cyclase activity. Using isolated myocytes from control and 1K,1C New Zealand White rabbits, we obtained O2consumption (nl O2⋅ min−1⋅ 105cells) and cGMP (fmol/105cells) levels after stimulation of guanylate cyclase with nitroprusside, CO, or guanylin (10−8–10−5M). Soluble guanylate cyclase activity was also determined. Basal cGMP was elevated in 1K,1C vs. control (176 ± 28 vs. 85 ± 13) myocytes. cGMP increased in 1K,1C and control myocytes after stimulation with nitroprusside, CO, and guanylin. Guanylate cyclase activity in 1K,1C vs. control myocytes was not statistically different. Basal O2consumption in 1K,1C vs. control myocytes was comparable (307 ± 1 vs. 299 ± 22). O2consumption was similarly decreased when guanylate cyclase was stimulated. Control regression equations correlating cGMP and O2consumption were O2consumption = −1.46 ⋅ [cGMP] + 444.65 (r= 0.96) for CO, O2consumption = −0.58 ⋅ [cGMP] + 328.48 (r= 0.82) for nitroprusside, and O2consumption = −1.25 ⋅ [cGMP] + 389.15 (r= 0.88) for guanylin. The 1K,1C regression equations were O2consumption = −1.36 ⋅ [cGMP] + 537.81 (r= 0.97) for CO, O2consumption = −0.23 ⋅ [cGMP] + 307.30 (r= 0.88) for nitroprusside, and O2consumption = −1.27 ⋅ [cGMP] + 502.91 (r= 0.89) for guanylin. These data indicate that 1K,1C hypertrophic myocytes had higher cGMP than controls at every level of O2consumption. This effect was not caused by differences in basal or maximal guanylate cyclase activity.