Hansell P, Isaksson B, Sjöquist M
Department of Physiology, University of Uppsala, Biomedical Center, Uppsala, Sweden.
Acta Physiol Scand. 2000 Jan;168(1):257-66. doi: 10.1046/j.1365-201x.2000.00670.x.
Abnormalities in dopamine (DA) and noradrenaline (NA) activities and sodium handling may be involved in the pathogenesis of hypertension. The present study was designed to investigate whether any differences exist between normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) in urinary excretion of DA, NA and sodium after 15 weeks on a low, medium or high sodium diet and during a subsequent elevation of the cerebroventricular fluid sodium concentration (CNS-induced natriuresis). Seven features were noted: (1) Basal sodium and DA excretion after the diet regimen was correlated to the dietary sodium content in both strains, except that sodium and DA excretion in SHR showed no further increase after the high sodium diet over and above that after medium sodium diet. (2) For any given sodium diet, SHR excreted more DA and NA as compared with WKY. (3) Blood pressure in SHR, as opposed to that in WKY, was higher after medium and high sodium diet than after low sodium diet. (4) During CNS-induced natriuresis NA excretion decreased or remained unchanged in WKY, but increased in SHR. (5) The DA/NA excretion ratio during CNS-induced natriuresis increased in WKY while decreased in SHR, which would not favour a natriuretic/vasodilatory response in the latter. (6) The ability of SHR to respond with CNS-induced natriuresis was attenuated after high sodium diet. (7) The magnitude of CNS-induced natriuresis was in both strains correlated to the sodium diet; the higher the dietary sodium content, the greater the natriuretic response. In conclusion, the study shows some clear differences in the catecholamine and sodium handling between WKY and SHR which may be involved in the pathogenesis of hypertension in SHR. Furthermore, increased sodium in the diet sensitizes the brain and kidney to increase the ability to respond with natriuresis for a given sodium stimulus.
多巴胺(DA)和去甲肾上腺素(NA)活性以及钠代谢异常可能参与高血压的发病机制。本研究旨在调查正常血压的Wistar-Kyoto大鼠(WKY)和自发性高血压大鼠(SHR)在低、中或高钠饮食15周后以及随后脑脊液钠浓度升高(中枢神经系统诱导的利钠作用)期间,尿中DA、NA和钠的排泄是否存在差异。观察到七个特征:(1)饮食方案后的基础钠和DA排泄与两种品系的饮食钠含量相关,但SHR在高钠饮食后的钠和DA排泄量在中等钠饮食后并未进一步增加。(2)对于任何给定的钠饮食,SHR比WKY排泄更多的DA和NA。(3)与WKY相反,SHR在中等和高钠饮食后的血压高于低钠饮食后。(4)在中枢神经系统诱导的利钠作用期间,WKY的NA排泄减少或保持不变,但SHR增加。(5)中枢神经系统诱导的利钠作用期间,WKY的DA/NA排泄率增加,而SHR降低,这不利于后者的利钠/血管舒张反应。(6)高钠饮食后,SHR对中枢神经系统诱导的利钠作用的反应能力减弱。(7)两种品系中枢神经系统诱导的利钠作用的幅度与钠饮食相关;饮食钠含量越高,利钠反应越大。总之,该研究表明WKY和SHR在儿茶酚胺和钠代谢方面存在一些明显差异,这可能参与SHR高血压的发病机制。此外,饮食中钠的增加使大脑和肾脏敏感,以增加对给定钠刺激的利钠反应能力。