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
MORLOCK CG. ARTERIOLES OF THE PANCREAS, LIVER, GASTROINTESTINAL TRACT AND SPLEEN IN HYPERTENSION. Arch Intern Med (Chic). 1939;63(1):100–118. doi:10.1001/archinte.1939.00180180110008
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