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Arch Intern Med (Chic). 1947;80(1):81-88. doi:10.1001/archinte.1947.00220130089008.
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IN RECENT years great strides have been made in the direction of determination of the pathogenesis of hypertensive vascular disease. However, there is conflicting opinion concerning the relation between basal heat production and hypertensive vascular disease.1 Clinically, an elevated basal metabolic rate has been noted in patients with hypertension. Mountain and his co-workers1h reported that there was a direct correlation between basal heat production and the height of the blood pressure; others2 failed to demonstrate this relation. The exact mechanism underlying these metabolic changes has not been definitely proved. Some investigators3 have indicated that an interrelationship among the brain, the thyroid and the adrenal sympathetic system exists. Hayasaka1f concluded that the basal metabolic rate remains unchanged in hypertensive patients with normal renal function but becomes elevated in those with renal insufficiency.

Because of these opposing viewpoints, it seemed of real value to reinvestigate the entire problem. In


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