Plasma and lymph electrolyte and endocrine parameters in rats with genetically-determined arterial hypertension

Abstract

Hemolymphatic interactions of electrolytes and plasma contents of aldosterone and insulin are studied in rats with genetically-determined stress-induced arterial hypertension (NISAG) and in normotensive rats (Wistar). Correlation analysis shows that alterations in electrolyte metabolism in NISAG are strongly determined by endocrine influences. These alterations are regarded, on the one hand, as a mechanism responsible for generically-determined arterial hypertension, and, on the other hand, as a variant of "adaptation disease" accompanied by transformation of primarily adaptive reactions into a pathogenic factor of arterial hypertension. Key Words: hypertension; electrolytes; hormones; blood; lymphArterial hypertension (AH) is a polymorphic pathology involving numerous endo-and exogenous factors. The exchange of electrolytes (Na and K) largely determines both vascular tone and fluid homeostasis in the organism [3]. Although lymph vessels play substantial role in the regulation of fluid homeostasis [8], the contribution of the lymph flow impairments to the genesis of AH has not been evaluated. Moreover, the compensatory potential of lymphatic system under pathological conditions (including cardiovascular disorders) is poorly investigated [1,2], and the information regarding hemolymphatic interactions is scarce. There is little evidence on modifications of hormonal systems and generally it does not provide any information on qualitative interhormonal interactions in AH. Although aldosterone and insulin belong to different hormonal systems, they have common targets, and Na-K exchange may be one of Institute of Physiology, Siberian Division of the Russian Academy of Medical Sciences, Novosibirsk; Novosibirsk Medical Institute; Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences, Novosibirsk them. In this study we investigated hemolymphatic interactions between electrolytes (Na and K), aldosterone and insulin, and their correlations in nonnoand hypertensive rats. MATERIALS AND METHODSMale normotensive rats (Wistar) and rats with genetically-determined stress-induced All (NISAG) were used. The rats weighed 180-200 g. NISAG rats were bred at the Laboratory of Evolutionary Genetics, Institute of Cytology and Genetics (Siberian Division of the Russian Academy of Sciences). Arterial pressure in stress was 205+2 mm Hg, basal level being 172+2 mm Hg. Lymph was collected from the thoracic duct under intraperitoneal Nembutal anesthesia. Blood was collected after decapitation. The contents of Na and K were determined by flame photometry in a Hitachi-180-80 spectrophotolneter. Plasma concentrations of aldosterone and insulin were determined by radioimmune assay. The results were analyzed using standard statistical methods, Student's t test, and correlation analysis.

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“…Diuretics act by diminishing sodium chloride reabsorption at different sites in the nephrons, thereby increasing urinary sodium chloride and water losses and consequently leading to decreased plasma levels of these electrolytes. Antonov et al [ 24 ] reported that plasma electrolyte contents increased significantly in hypertensive rats. Impaired function of Na, K-ATPase and the Na-H antiport, which is typical of arterial hypertension, may promote an increase in plasma electrolytes.…”

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“…Many diuretics act by diminishing sodium chloride reabsorption at different sites in the nephrons, thereby increasing urinary sodium chloride and water losses, and consequently leading to decreased plasma levels of these electrolytes. Antonov et al [ 23 ] reported that plasma electrolyte contents increase significantly in hypertensive rats. Impaired function of Na, K-ATPase, Na-H antiport, which is typical of arterial hypertension, may promote an increase in plasma electrolytes.…”

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“…Diuretics act by diminishing sodium chloride reabsorption at different sites in the nephrons, thereby increasing urinary sodium chloride and water losses, consequently leading to decreased plasma levels of these electrolytes. Antonov et al [ 25 ] reported that plasma electrolyte contents increased significantly in hypertensive rats. Impaired function of Na, K-ATPase and the Na-H antiport, which is typical of arterial hypertension, may promote an increase in plasma electrolytes.…”