Skrabal F, Kotanko P, Wach P, Kenner T, Lueger A, Raid H, Rieger E
Abteilung für Innere Medizin, Krankenhaus Barmherzige Brüder, Universität Graz.
Klin Wochenschr. 1991;69 Suppl 25:36-40.
The hypothesis, proposed by us since 1981, that genetically determined salt sensitivity exists in the normotensive population has been confirmed by other groups. We propose that in salt sensitive subjects an augmented upregulation of alpha-2 combined with simultaneous downregulation of beta-2 adrenoceptors by a high salt diet (resulting in an increase in the "operative" adrenoceptor ratio) is responsible for the rise of blood pressure. In salt resistant subjects the "operative alpha-2/beta-2 adrenoceptor ratio" does not increase on a high salt intake. The adrenoceptor changes in salt sensitive subjects probably lead to an increased central sympathetic outflow (through receptor changes in certain brain areas) and to simultaneous enhanced end-organ response in resistance vessels and in the kidney, causing enhanced vasoconstriction and enhanced sodium reabsorption. Long term follow up of salt sensitive normotensives will show, whether they develop "essential hypertension" in the future.
我们自1981年起提出的关于血压正常人群中存在基因决定的盐敏感性这一假说已得到其他研究团队的证实。我们提出，在盐敏感个体中，高盐饮食会导致α-2肾上腺素能受体上调增强，同时β-2肾上腺素能受体下调（导致“有效”肾上腺素能受体比例增加），这是血压升高的原因。在盐抵抗个体中，高盐摄入时“有效α-2/β-2肾上腺素能受体比例”不会增加。盐敏感个体中的肾上腺素能受体变化可能导致中枢交感神经输出增加（通过某些脑区的受体变化），并同时增强阻力血管和肾脏终末器官的反应，从而导致血管收缩增强和钠重吸收增强。对盐敏感的血压正常者进行长期随访将显示他们未来是否会发展为“原发性高血压”。
