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首页> 外文期刊>American Journal of Physiology >High dietary salt alters arteriolar myogenic responsiveness in normotensive and hypertensive rats.
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High dietary salt alters arteriolar myogenic responsiveness in normotensive and hypertensive rats.

机译：高饮食盐会改变血压正常和高血压大鼠的小动脉肌源性反应性。

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We evaluated arteriolar myogenic responsiveness in normotensive, salt-loaded and hypertensive rats and investigated the potential influence of luminal blood flow or shear stress on myogenic responses under each of these conditions. Wistar-Kyoto (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. Dietary salt did not affect mean arterial pressure (MAP) in WKY, whereas MAP in SHR was significantly higher and augmented by dietary salt. In all groups, box pressurization caused similar increases in MAP that were completely transmitted to the arterioles. After these pressure increases, large arteriole diameters decreased by 0-30% and intermediate arteriole diameters decreased by 21-27%. Arteriolar myogenic responsiveness was not different between WKY-LS and SHR-LS. Large arterioles in WKY-HS displayed an attenuated pressure-diameter relationship compared with that in WKY-LS. Large arterioles in SHR-HS displayed an augmented pressure-diameter relationship compared with that in SHR-LS. There were no correlations between resting flow or wall shear rate and the magnitude of initial myogenic constriction in any group or vessel type. The capacity for sustained myogenic constriction was unrelated to secondary decreases in flow (14-41%) or increases in wall shear rate (21-88%) in each group. We conclude that 1) dietary salt impairs the myogenic responsiveness of large arterioles in normotensive rats and augments the myogenic responsiveness of large arterioles in hypertensive rats, 2) hypertension does not alter arteriolar myogenic responsiveness in this vascular bed, and 3) flow- or shear-dependent mechanisms do not attenuate myogenic responses in the intact arteriolar network of normal, salt-loaded, or hypertensive rats.
机译：我们评估了正常血压，盐负荷和高血压大鼠的小动脉肌源性反应，并研究了在每种情况下腔内血流量或切应力对肌源性反应的潜在影响。将Wistar-Kyoto（WKY）和进食低盐（0.45％，LS）或高盐（7％，HS）饮食的自发性高血压大鼠（SHR）封闭在通风的密闭盒中，将斜方肌肌肉外部化以进行活体显微镜检查。饮食盐不影响WKY中的平均动脉压（MAP），而SHR中的MAP显着更高，并且受饮食盐的影响而增加。在所有组中，框式加压都导致MAP的相似升高，并完全传递给小动脉。在这些压力增加之后，大动脉直径减小了0-30％，中间动脉直径减小了21-27％。 WKY-LS和SHR-LS之间的小动脉肌原性反应性没有差异。与WKY-LS相比，WKY-HS中的大动脉显示出减弱的压力-直径关系。与SHR-LS中相比，SHR-HS中的大动脉显示出增加的压力-直径关系。在任何组或任何类型的血管中，静息流量或壁剪切速率与初始肌收缩的幅度之间均无相关性。每组中持续的肌收缩能力与血流的继发性减少（14-41％）或壁切变率增加（21-88％）无关。我们得出的结论是：1）食盐会损害正常血压大鼠大动脉的肌反应性，并增加高血压大鼠大动脉的肌反应性; 2）高血压不会改变此血管床的小动脉肌反应性，以及3）流量或剪切力依赖的机制不会减弱正常，盐负荷或高血压大鼠完整小动脉网络中的肌源性反应。

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