SALIVARY KALLIKREIN EXCRETION IN HYPERTENSION

被引:11
作者
HEIDLAND, A
ROCKEL, A
SCHMID, G
机构
[1] Abteilung für Nephrologie, Med. Univ.-Klinik Würzburg, Würzburg, D-8700
来源
KLINISCHE WOCHENSCHRIFT | 1979年 / 57卷 / 19期
关键词
Experimental hypertension in rats; Human essential and renoparenchymal hypertension; Kallikrein; Parotid saliva; Sodium transport; Sympathetic activity;
D O I
10.1007/BF01479990
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
According to immunohistochemical investigations kallikrein in the majors salivary glands is located predominantly at the apical border of the striated duct cells and as a luminal rim in the main excretory ducts. Comparatively the highest concentrations are observed in the submandibular gland of rats and cats in the cytoplasmic granules of the granular tubules. In normal humans and rats the kallikrein activity of parotid saliva is inversely related to flow rate and sodium concentration. An increased salivary kallikrein concentration is found in human essential hypertension and renoparenchymal hypertension associated with impaired kidney function. Furthermore in rats with various forms of hypertension (genetic hypertension, DOCTMA salt and renovascular hypertension) the salivary kallikrein secretion - as determined by the BAEE-esterase activity - is enhanced. In contrast to the kallikrein secretion the flow dependent sodium concentration of parotid saliva is reduced in human essential and renoparenchymal hypertension as well as in rats with various forms of experimental and genetic hypertension, which indicates an enhanced sodium reabsorption in the glandular duct system. Furthermore in most forms of hypertension, there is a tendency of higher potassium levels in the saliva. The pathogenesis of the enhanced glandular kallikrein secretion in hypertension is discussed with regard to a counterregulatory mechanism in hypertension as well as to a sympathicoadrenergic activation. The enhanced sodium reabsorption in the duct system in the various forms of hypertension could be the cause as well as a consequence of the enhanced kallikrein secretion. © 1979 Springer-Verlag.
引用
收藏
页码:1047 / 1052
页数:6
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