The Response of Arterial Muscular Coat to Elevated Blood Pressure

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Abstract
Persistent arterial hypertension could be induced in rats by unilateral application of silver clips on renal arteries. When the clamping was effective, blood pressure rose steadily, attained approximately its highest level in each case in 5 weeks and remained essentially at the same level to the 20th week after the operation. Severe arteriolar injuries were observed in renal arteries in cases with mean systolic blood pressure over 170 mm Hg. Histometrical treatments of renal artery revealed a regular relation between anatomical radius R and corresponding medial thickness D in the form of D=aRb, a and b being constants. Estimated D was calculated in each case from the above formula at R=100 [mu] and was correlated to the mean systolic blood pressure P. The relation could be defined by D=uPW, u and w being constants. The value of w was 0.75[plus or minus]0.19, which indicated that the increase of medial thickness was about 68% corresponding to blood pressure elevation by 100% at R= 100 [mu] of rat''s renal artery. Because the value of w was a little smaller than 1, it was concluded that the adaptation of arterial muscular coat to blood pressure elevation was more or less imperfect in character, and finally a limit was inevitably reached where the equilibrium between blood pressure and arterial muscular coat was disturbed. The incidence of arteriolar injuries was quantitatively expressed by an index of arteriolar lesions I, which was determined by the count of arterial lesions in a square centimeter of renal cortex in histological slides. The relation between I and P or between I and D was defined by an exponential Ip=Iopea[alpha]P or ID=IODe[beta]D, respectively. The results demonstrated that arteriolar injuries, when they began to appear, increased so rapidly that they practically attained the level of infinity within relatively narrow range of blood pressure elevation. The highest possible blood pressure in rats was estimated to be about 230 mm Hg and the maximum medial hypertrophy was about 100% of the normal arterial muscular coat. The development of arterial injuries in experimental hypertension was discussed in comparison to that in human hypertension. It was assumed that some process must precede histologically confirmable arterial lesions and lower the resistance of arterial wall, before renal artery succumbed to high blood pressure.

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