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CARL G. MORLOCK, M.D.

Arch Intern Med. 1939;63(1):100-118.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Bright's¹ epoch-making observation in 1836 of the association of cardiac hypertrophy with renal disease assumed new significance in 1868, when Johnson² noted coexistent thickening of the arterial walls in this condition. That renal damage need not necessarily precede the other two factors was pointed out by Mahomed³ in 1874 and later was substantiated by Allbutt.⁴

Subsequent to these fundamental observations, continued study has emphasized more and more that of the whole vascular tree, the arteriolar bed suffers most profoundly from the changes that are known to be rather characteristically associated with hypertension. This is not surprising, because Landis⁵ noted that the greatest pressure gradient in the frog and in the mammalian mesentery is in the arteriole and Ellis and Weiss⁶ found that with an increase in vascular tension the load of work carried by the arteriole is magnified relatively many more times than is that of any other . . . [Full Text PDF of this Article]

Author Affiliations
ROCHESTER, MINN.

From the Division of Medicine of the Mayo Clinic.

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