Abstract
INTRODUCTION Professor Maekawa presented a theory that the ultimate cause of hypertension is the disturbance in ATP-ATPase system, particularly the discharge in the blood stream of the renal ATPase which has property of being activated by sodium and inhibited by potassium. With regard to the genesis of the arterial and arteriolar necrosis which often associates the malignant hypertension in man and experimental animal, opinions have been discrepant, some regarding such necrosis as the result of the elevated pressure, some ascribing it to two factors, elevated blood pressure and excretory renal failure, but some, on the contrary, insisting that elevated arterial pressure is not the indispensable cause of such necrosis. In order to expand the above theory of Professor Maekawa, the author tried to disclose the relation between hypertension and histological changes, employing dogs and rats which were made hypertensive experimentally. This paper aims to report on the author's histopathological study with various genetic types of hypertension.EXPERIMENTAL NEUROGENIC HYPERTENSION Nine dogs were operated upon for bilateral section of the pressoreceptor nerves and their blood pressure was messured 2 to 3 times a week thereafter. The method of the blood pressure measurement was that of direct puncture in the femoral artery. Animals were sacrificed after various (3∼190 days) periods of observation by means of venesection, and organs were taken out and immersed in 10% formalin solution, for fixation. Specimens were made zelloidine or paraffine-sections and stained with hematoxylin-eosin, and Van Gieson's or Masson's method.RESULTS 1) Following the section of the pressoreceptor nerves, there was an immediate elevation of the blood pressure. At this time kidney showed swelling and exudation in glomeruli.2) As time elapses after the section of the nerves, fluctuation in blood pressure became less and less outstanding, while arteriolar change in the kidney became more pronounced. However, the degree of such change was independent of the degree of hypertension.3) Therefore, such vascular lesion as caused by this method evidently cannot be ascribed to the existing hypertension alone.4) Heart weight showed increase, but not proportionately to the degree of hypertension.
