THE NATURE OF THE PERIPHERAL RESISTANCE IN ARTERIAL HYPERTENSION WITH SPECIAL REFERENCE TO THE VASOMOTOR SYSTEM

Open Access
Publisher Website
Google Scholar
Abstract
By studying the blood flow in the human arm by the plethysmographic method, it was found that the average flow in 32 patients with hypertension of all types (benign, malignant, and secondary or renal) was no greater than the average flow in 18 normal controls. From this it is obvious that the increase in peripheral resistance in hypertension is generalized throughout the systemic circulation and not limited to the splanchnic area. If the increase in peripheral resistance were limited to the splanchnic area, the blood flow to the rest of the body would necessarily be increased since the cardiac output in hypertension is normal. The extent to which the arterioles in hypertension are capable of dilatation was studied by 3 methods: (1) direct application of heat to the arm, (2) reactive hyperemia in response to obstruction of the arterial blood flow, (3) combined effect of heat and reactive hyperemia. The blood vessels in all types of hypertension were capable of dilatation to allow an increase in blood flow of 15 to 20 times, an increase as great as found in normal subjects. The increased peripheral resistance in hypertension is evidently not due to organic rigidity of the vessel walls but to vascular hypertonus. To determine whether this vascular hyper-tonus in hypertension is vasomotor in origin, the authors measured the increase in blood flow in the arm which results from paralysis of the vasomotor nerves by pro-caine injection of the dorsal sympathetic ganglia, comparing the results in control subjects and patients with hypertension. It was found that sympathetic block produces no greater increase in blood flow in patients with hypertension of all types than in normal subjects. This disproves the vasomotor origin of hypertension. Such hypertonus must therefore be attributed to intrinsic spasm in the blood vessels themselves. Hypertension is evidently due to hypertonus of the arterioles generalized throughout the systemic circulation and this hypertonus is apparently not mediated through the vasomotor system.