Force and Work of Digital Arteriolar Smooth Muscle Contraction in Hypertension

¹ From the Department of Medicine and the Andre Meyer Department of Physics, The Mount Sinai Hospital, and from the Research Service, First (Columbia) Division, Goldwater Memorial Hospital, and the Department of Medicine, Columbia University, College of Physicians and Surgeons, New York City

Pressure and flow in the digital circulation were studied under standardized conditions before and after inhibition of sympathetic nerve discharge in thirty-six hypertensive and twenty-three normotensive subjects. This inhibition was tested by procaine block of the ulnar nerve and found to be nearly completely effective. Absolute and percentage changes in pressure-flow and flow-pressure ratios were calculated. A method was established for calculating the shift with vasoconstriction in the pressure axis intercept of the line defining the relationship of flow to pressure with decreasing mean pressure head. This made it possible to estimate the force and work of arteriolar smooth muscle contraction and the percentage of the maximal potential work represented by the actual work of vasoconstriction. The data suggest that the intrinsic narrowing of the digital vascular bed in hypertension is not produced by increased smooth muscle tone but probably by sclerosis or edema of the arterioles or both. They also support the thesis that neurogenic vascular smooth muscle contraction is increased in hyper-tension in the digital circulation, both absolutely and also in relation to the intrinsic caliber of the vessels.