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.

A comparative electrocardiographic evaluation of changes in cardiac function in rats with hereditary arterial hypertension (NISAG strain) and normotensive (Wistar) rats in response to a single epinephrine injection revealed much more pronounced changes in NISAG rats, including an unfavorable time course of electrocardiographic waves (left ventricle overload) and impaired conduction (blockade) and excitability (extrasystoles). The results indicate that the myocardium of NISAG rats is much more responsive to the acute stimulation of adrenergic receptors by epinephrine than is the myocardium of normotensive rats. Key Words: hereditary arterial hypertension; heart; epinephrine; electrocardiographyThe strong reaction of the cardiovascular system to hormones, including epinephrine, that are secreted during stress is held to be one of the important mechanisms responsible for the development of arterial hypertension and associated complications such as myocardial infarction and stroke [1,6]. For this reason, adrenergic receptor blockers are used as agents to lower arterial pressure and protect the heart [8].A hypertensive rat strain, NISAG, was recently developed at the Institute of Cytology and Genetics of the Siberian Division of the Russian Academy of Sciences. The hypertensive status of these rats and the condition of their cardiovascular system can be judged by evaluating their responsiveness to epinephrine. Such an evaluation is of particular interest because arterial hypertension in this strain is established as a stress-dependent phenomenon [3, 4]. In the present electrocardiographic study we compared changes in cardiac function brought about by a single epinephrine injection in MATERIALS AND METHODSSix-month-old male Wistar and NISAG rats were used, 60 animals of each population. For the recording of the electrocardiogram (ECG), they were anesthetized with ether (etherrausch) and placed supine in a screened box. Needle electrodes were inserted under the skin of all four limbs and also in the chest region in three positions: one electrode along the midstemal line at the level of the apex beat and the other two 1 cm to the left and 1 cm to the fight of this line, which corresponds to the standard positions of the chest leads V~, V:, and V 3. The ECG was thus recorded in 3 standard leads, 3 augmented limb leads, and 3 unipolar chest leads. The recording was done on a Mingograph 34 cardiograph at a paper speed of 100 mm/sec and a channel sensitivity of 20 mm/mV. After the background ECG was recorded, each rat received a subcutaneous injection of epinephrine in a dose of 0.2 mg/100 g body weight. A second ECG was recorded ten minutes postinjection. The data were evaluated