Mechanisms for altered endothelium-dependent vasorelaxation in isolated kidneys from experimental hypertensive rats.
Mechanisms for altered endothelium-dependent vasorelaxation in isolated kidneys from experimental hypertensive rats.
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实验性高血压大鼠离体肾脏改变内皮依赖性血管舒张的机制。
DOI：
10.1152/ajpheart.1993.264.5.h1535
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Masaaki Hirobe
中科院分区：
文献类型：
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作者：
Hiroshi Hayakawa;Yasutaka Hirata;Eriko Suzuki;Tokuichiro Sugimoto;Hiroaki Matsuoka;K. Kikuchi;T. Nagano;Masaaki Hirobe
为了研究高血压患者内皮依赖性血管松弛减弱的机制，我们检测了乙酰胆碱（ACh）对自发性高血压大鼠（SHR）、醋酸脱氧皮质酮（DOCA）盐性高血压大鼠（DOCA salt）和达尔盐敏感（Dahl S）大鼠肾脏血管阻力（RVR）和内皮源性松弛因子（EDRF）释放率的影响。与血压正常的对照组相比，高血压大鼠乙酰氨基酚对RVR的降低幅度较小。以硝酸亚硝酸盐为指标估计的一氧化氮进入灌注液的释放率在SHR和Wistar-Kyoto大鼠（WKY）之间没有差异。然而，DOCA盐大鼠和Dahl S大鼠的EDRF释放率明显低于正常对照组（10(-7)M ACh: DOCA盐45 +/- 6比对照组410 +/- 60 pmol.min-1）。g-1肾wt， P < 0.001)。在SHR中，高k +灌注或用格列本脲预处理，内皮衍生超极化因子（EDHF）抑制剂仅在WKY中显著降低ach诱导的血管松弛，导致SHR和WKY之间的RVR降低无差异。因此，在DOCA盐大鼠和Dahl S大鼠中，乙酰胆碱钠引起的SHR肾血管松弛的减弱可能归因于EDHF的减少，而不是EDRF的减少。
To study mechanisms for attenuated endothelium-dependent vasorelaxation in hypertension, we examined the effects of acetylcholine (ACh) on renal vascular resistance (RVR) and release rates of endothelium-derived relaxing factor (EDRF) in kidneys isolated from spontaneously hypertensive rats (SHR), deoxycorticosterone acetate (DOCA) salt-hypertensive (DOCA salt) rats, and Dahl salt-sensitive (Dahl S) rats. Decreases in RVR by ACh were smaller in hypertensive rats than in their normotensive controls. The release rate of nitric oxide into the perfusate, which was estimated using nitrite-nitrate as an index, did not differ between SHR and Wistar-Kyoto rats (WKY). However, the release rate of EDRF was markedly decreased in both DOCA salt rats and Dahl S rats compared with their normotensive controls (10(-7) M ACh: DOCA salt 45 +/- 6 vs. control 410 +/- 60 pmol.min-1.g-1 kidney wt, P < 0.001). In SHR, high-K+ perfusion or pretreatment with glibenclamide, inhibitors of endothelium-derived hyperpolarizing factor (EDHF), significantly reduced ACh-induced vasorelaxation only in WKY, resulting in no differences in the RVR reduction between SHR and WKY. Thus attenuated ACh-induced vasorelaxation in the SHR kidney may be attributed to a decrease in EDHF, but to a decrease in EDRF in DOCA salt rats and Dahl S rats.