Boegehold M A
Department of Physiology, West Virginia University School of Medicine, Morgantown 26506.
Am J Physiol. 1993 Jun;264(6 Pt 2):H1810-6. doi: 10.1152/ajpheart.1993.264.6.H1810.
This study evaluated the influence of high dietary salt intake on nitric oxide (NO) activity in the arteriolar network of rats resistant to salt-induced hypertension. The spinotrapezius muscle microvasculature was studied in inbred Dahl salt-resistant (SR/Jr) rats fed low (0.45%)- or high (7%)-salt diets for 4-5 wk. Arterial pressures were not different between groups at any time during the study. NO synthesis inhibition with NG-nitro-L-arginine-methyl ester (L-NAME) constricted arcade arterioles in low-salt SR/Jr and dilated arcade arterioles in high-salt SR/Jr. Arcade arteriole dilation to acetylcholine (ACh), but not sodium nitroprusside (SNP), was impaired in high-salt SR/Jr. In contrast, transverse and distal arteriole responses to L-NAME, ACh, and SNP were identical in high- and low-salt SR/Jr. These findings indicate that high salt intake, in the absence of increased arterial pressure, suppresses the influence of basal and evoked NO on vascular tone in arcading arterioles, but not in smaller transverse and distal arterioles. Unaltered SNP responses in high-salt SR/Jr suggest that this effect does not involve a change in arteriolar smooth muscle responsiveness to NO.
本研究评估了高盐饮食摄入对盐诱导高血压抵抗大鼠小动脉网络中一氧化氮（NO）活性的影响。在喂食低（0.45%）盐或高（7%）盐饮食4 - 5周的近交系达尔抗盐（SR/Jr）大鼠中，研究了斜方肌微血管系统。在研究期间的任何时候，各组之间的动脉血压均无差异。用NG - 硝基 - L - 精氨酸甲酯（L - NAME）抑制NO合成可使低盐SR/Jr大鼠的弓状小动脉收缩，而使高盐SR/Jr大鼠的弓状小动脉扩张。高盐SR/Jr大鼠对乙酰胆碱（ACh）而非硝普钠（SNP）的弓状小动脉扩张受损。相反，高盐和低盐SR/Jr大鼠的横行和远端小动脉对L - NAME、ACh和SNP的反应相同。这些发现表明，在动脉血压未升高的情况下，高盐摄入会抑制基础和诱发的NO对弓状小动脉血管张力的影响，但对较小的横行和远端小动脉则无此影响。高盐SR/Jr大鼠中SNP反应未改变表明，这种效应并不涉及小动脉平滑肌对NO反应性的改变。
