Nurkiewicz T R, Boegehold M A
Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26505-9229, USA.
Am J Physiol. 1999 Nov;277(5):H1946-55. doi: 10.1152/ajpheart.1999.277.5.H1946.
The purpose of this study was to determine if local nitric oxide (NO) activity attenuates the arteriolar myogenic response in rat spinotrapezius muscle. We also investigated the possibility that hypertension, dietary salt, or their combination can alter any influence of local NO on the myogenic response. Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) fed low-salt (0.45%, LS) or high-salt (7%, HS) diets were enclosed in a ventilated airtight box with the spinotrapezius muscle exteriorized for intravital microscopy. Mean arterial pressure was unaffected by dietary salt in WKY but was significantly higher and augmented by dietary salt in SHR. In all experiments, elevation of microvascular pressure by box pressurization caused a 0-30% decrease in the diameter of large (arcade bridge) arterioles and a 21-27% decrease in the diameter of intermediate (arcade) arterioles. Inhibition of NO synthase with N(G)-monomethyl-L-arginine (L-NMMA) significantly enhanced myogenic responsiveness of arcade bridge arterioles in WKY-LS and SHR-LS but not in WKY-HS and SHR-HS. L-NMMA significantly enhanced the myogenic responsiveness of arcade arterioles in all four groups. Excess L-arginine reversed this effect of L-NMMA in all cases, and arteriolar responsiveness to the NO donor sodium nitroprusside was not different among the four groups. High-salt intake had no effect on the passive distension of arterioles in either strain during box pressurization. We conclude that 1) local NO normally attenuates arteriolar myogenic responsiveness in WKY and SHR, 2) dietary salt impairs local NO activity in arcade bridge arterioles of both strains, and 3) passive arteriolar distensibility is not altered by a high-salt diet in either strain.
本研究的目的是确定局部一氧化氮（NO）活性是否会减弱大鼠斜方肌的小动脉肌源性反应。我们还研究了高血压、饮食盐分或二者联合是否会改变局部NO对肌源性反应的任何影响。将喂食低盐（0.45%，LS）或高盐（7%，HS）饮食的Wistar-Kyoto大鼠（WKY）和自发性高血压大鼠（SHR）置于通风密闭箱中，将斜方肌外置用于活体显微镜检查。平均动脉压在WKY中不受饮食盐分影响，但在SHR中显著更高且因饮食盐分而升高。在所有实验中，通过箱内加压升高微血管压力导致大（弓状桥）小动脉直径降低0 - 30%，中（弓状）小动脉直径降低21 - 27%。用N(G)-单甲基-L-精氨酸（L-NMMA）抑制NO合酶可显著增强WKY-LS和SHR-LS中弓状桥小动脉的肌源性反应性，但在WKY-HS和SHR-HS中则不然。L-NMMA显著增强了所有四组中弓状小动脉的肌源性反应性。过量的L-精氨酸在所有情况下均逆转了L-NMMA的这种作用，并且四组中小动脉对NO供体硝普钠的反应性没有差异。高盐摄入对两种品系在箱内加压期间小动脉的被动扩张均无影响。我们得出结论：1）局部NO通常会减弱WKY和SHR中小动脉的肌源性反应性；2）饮食盐分损害了两种品系弓状桥小动脉中的局部NO活性；3）高盐饮食在两种品系中均未改变小动脉的被动扩张性。
