NATURE OF PERIPHERAL RESISTANCE IN ARTERIAL HYPERTENSION

Abstract

The increased peripheral resistance present in arterial hypertension cannot be reduced to the normal level in the skin of the hand and the foot, the muscles of the forearm, or in the brain by powerful vasodilating stimuli. The blood flow in the hand and foot at 43[degree]C. and in the muscles of the forearm after exercise shows no significant difference between the normal and hypertensive subjects. In postural expts. after the adm. of Na nitrite, subjects with arterial hypertension develop syncope with a much higher arterial pressure than do normal subjects. Cerebral anoxia in hypertensive subjects apparently does not reduce the peripheral resistance in the brain vessel to normal levels. In 1 subject with arterial hypertension, a marked fall in arterial pressure after malaria produced no change in the blood flow in the foot at 43[degree] C, indicating the absence of structural changes in the vessels. In a 2d subject, the blood flow in the foot at 43[degree] C. was decreased when the arterial pressure fell, indicating that irreversible vascular damage had occurred. Sensory stimuli, such as a pinch, a noise, and a deep breath, produce a similar degree of vasoconstriction in normal and in hypertensive subjects. When the arterial pressure is lowered following malaria, these vasoconstrictor responses remain unchanged. These results indicate that in arterial hypertension the peripheral resistance is uniformly raised throughout the area of the greater circulation, and it is not increased in the splanchnic area to any greater extent than in other tissues. The finding of a uniform degree of elevation of the peripheral resistance throughout the body is strong evidence against the neurogenic origin of the usual types of clinical hypertension since the nervous vasomotor control is not the same in each of the tissues investigated.