Katovich M J, Soltis E E, Field F P
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1984;78(2):369-72. doi: 10.1016/0742-8413(84)90100-2.
The effect of chronic salt treatment on systolic blood pressure and vascular adrenergic responsiveness was studied in rats. Vascular reactivity of aortic smooth muscle to potassium chloride and sodium nitrite was similar in both groups, indicating that salt treatment did not alter the regular contraction and relaxation process of the smooth muscle. Isoproterenol-induced relaxation was similar for both treated and control groups demonstrating that salt treatment had no effect on vascular beta-adrenergic responsiveness. However, when aortic smooth muscle was incubated with angiotensin II or norepinephrine, a significant increase in responsiveness was observed in the aortic smooth muscle of the salt-treated group compared to the control group. Collectively, these results suggest that salt, per se, does not affect systolic blood pressure or peripheral beta-adrenergic responsiveness, but does result in a significantly enhanced alpha-adrenergic responsiveness. The implication of these results for experimental hypertension are discussed.
在大鼠中研究了慢性盐处理对收缩压和血管肾上腺素能反应性的影响。两组大鼠主动脉平滑肌对氯化钾和亚硝酸钠的血管反应性相似，表明盐处理未改变平滑肌的正常收缩和舒张过程。异丙肾上腺素诱导的舒张在处理组和对照组中相似，表明盐处理对血管β-肾上腺素能反应性无影响。然而，当主动脉平滑肌与血管紧张素II或去甲肾上腺素一起孵育时，与对照组相比，盐处理组的主动脉平滑肌反应性显著增加。总体而言，这些结果表明，盐本身不影响收缩压或外周β-肾上腺素能反应性，但确实导致α-肾上腺素能反应性显著增强。讨论了这些结果对实验性高血压的意义。
