Nishio I, Shima H, Tsuda K, Hano T, Masuyama Y
Department of Cardiology, Internal Medicine, Wakayama Medical College, Japan.
J Hypertens Suppl. 1988 Dec;6(4):S216-8. doi: 10.1097/00004872-198812040-00064.
In order to evaluate endogenous Na+,K+-ATPase inhibitor on sympathetic nerve endings, endogenous Na+,K+-ATPase inhibitor and plasma noradrenaline were determined in patients with essential hypertension under different sodium conditions. Compared with the plasma from non-salt-sensitive patients, that from salt-sensitive patients showed significantly higher Na+,K+-ATPase inhibitor and plasma noradrenaline levels. Salt-induced changes in endogenous Na+,K+-ATPase inhibitor and those in blood pressure or plasma noradrenaline showed positive correlations. These results suggest that the salt-induced increase in endogenous Na+,K+-ATPase inhibitor might induce blood pressure elevation in essential hypertension, at least partly via increased noradrenaline levels.
为了评估内源性钠钾ATP酶抑制剂对交感神经末梢的作用，我们测定了不同钠条件下原发性高血压患者体内的内源性钠钾ATP酶抑制剂及血浆去甲肾上腺素水平。与盐不敏感患者的血浆相比，盐敏感患者的血浆中钠钾ATP酶抑制剂及血浆去甲肾上腺素水平显著更高。盐诱导的内源性钠钾ATP酶抑制剂变化与血压或血浆去甲肾上腺素变化呈正相关。这些结果表明，盐诱导的内源性钠钾ATP酶抑制剂增加可能至少部分通过去甲肾上腺素水平升高，导致原发性高血压患者血压升高。
