Koepke J P
Washington University School of Medicine, Department of Pharmacology, St. Louis, Mo.
Miner Electrolyte Metab. 1989;15(1-2):83-7.
Environmental stress increases renal sympathetic nerve activity and decreases urinary sodium excretion to a greater degree in conscious hypertensive rats (spontaneously hypertensive rat; deoxycorticosterone-sodium chloride, Dahl salt-sensitive) than normotensive control rats. The dependence of the antinatriuretic response to environmental stress on the renal sympathetic nerves is indicated by the finding that renal denervation prevents the response. Central nervous system beta 2- and alpha 2-adrenoceptors mediated the renal sympathetic nerve activity and antinatriuretic responses to environmental stress in conscious spontaneously hypertensive rats. Increased renal sympathetic nerve activity and renal sodium retention may contribute to chronic stress hypertension.
与正常血压的对照大鼠相比,环境应激在清醒的高血压大鼠(自发性高血压大鼠;脱氧皮质酮-氯化钠,达尔盐敏感型)中会更大程度地增加肾交感神经活动并减少尿钠排泄。肾去神经支配可防止这种反应,这一发现表明环境应激引起的利钠反应依赖于肾交感神经。中枢神经系统β2-和α2-肾上腺素能受体介导了清醒自发性高血压大鼠的肾交感神经活动以及对环境应激的利钠反应。肾交感神经活动增加和肾钠潴留可能导致慢性应激性高血压。