State of the myocardium in rats of a new hypertensive strain

Abstract

lease in an atherosclerotic plaque as well as formation of autoimmune complexes in situ require further investigations. 2. G. Hansson and S. Stemme, Atherosclerosis X, F. Woodford et al. (eds.), Elsevier Sci. Study of the heart in a new strain of rats with hereditary stress-induced hypertension (NISAG) reveals a complex of structural and functional changes which are analogous to the manifestations of essential hypertension. These changes are shown to be adaptivecompensatory in nature and indicative of limited functional reserves of the hypertrophic myocardium.

Functional activity of the sympathoadrenal system in hypertensive NISAG rats

“…Other neurohormonal mechanisms cannot be excluded (e.g., increase in thyroid activity [6], adrenocortical hyperfunction, and potentiation of vasoconstriction by glucocorticoid hormones). The increase in basal blood pressure can result from morphological changes in the target organs of NISAG rats [2,4,5]. The frequency of episodes of blood pressure elevation increases due to hyperreactivity of the sympathoadrenal system in NISAG rats, which contributes to progression of these changes.…”

Delayed Effect of Hypotensive Drugs on Blood Pressure and Structure of the Myocardium in Hypertensive ISIAH Rats during Chronic Stress

“…They are typical of the hypertensive state and age of ISIAH rats [4]. Morphological signs of acute structural alteration in animals of various groups were not found after CS.…”

“…All signs of hypertrophy are observed in the heart of adult male ISIAH rats, including greater relative weight, moderate cardiosclerosis, cardiomyocyte hypertrophy, thick walls, and reduced lumen of coronary arteries (compared to normotensive Wistar rats of similar age) [4]. Morphological signs of left ventricular hypertrophy appear from the 3rd to the 5th week of postnatal development [3], when genetically determined hypersensitivity to stress manifests in persistent increase in BP [2].…”