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In previous studies (1-6) it has been determined that the aortic wall of rats with various forms of experimental hypertension contains an increased amount of sodium, potassium and water per unit of dry weight. The pertinence of these findings to hypertension has always been somewhat in question, since the aorta does not contribute much to the total peripheral resistance. In the normal circulation most of the peripheral resistance is provided by the arterioles, and hypertension is accompanied by a narrowing of these arterioles. Hence an analysis of the arterioles themselves would be expected to give more pertinent information concerning the pathogenesis of hypertension. This was attempted in the present experiment.The present study was also designed to offset another possible cause of misinterpretation. When an animal becomes hypertensive, the walls of the arterioles become thicker; some of this thickening is probably related to an increased content of acid mucopolysaccharides, which are known to bind sodium (7). In the present experiment a large number of rats was made hypertensive and thickening of the arterioles occurred in all of them. Half the hypertensive rats were then "cured" of their elevated blood pressure by removing the clip which narrowed their renal artery. We were then able to compare the arterioles of hypertensive and normotensive rats, both of which had comparable degrees of arteriolar thickening.Thus, the present experiment largely overcomes two weaknesses of previous studies. First, electrolytes are estimated in arterioles rather than arteries. Second, there is a similar degree of hypertrophy in both normotensive and hypertensive arterioles.* Supported by a grant from the American Heart Association and by Grant no. H2008, National Heart Institute, United States Public Health Service. METHODSA number of Wistar rats was made hypertensive by narrowing one renal artery with a clip and removing the opposite kidney. Seven months after the original operation, the rats with moderate to severe hypertension were culled out and divided into two groups which were evenly matched for arterial pressure. In one of the two groups, an operation was performed on each rat to remove the clip which narrowed the renal artery. On the rats of the other group, a similar sham operation was done but the clip was left intact. Exactly 7 days after either type of operation, the blood pressure was carefully determined on each rat with the microphonic method (8), and a number of mesenteric arterioles was removed for analysis with the aid of a stereomicroscope. The arterioles of completely normal rats of the same age were also analyzed concomitantly. The arterioles were handled in such a way that the lumen was free of blood before excision of the vessel. As little adventitia as possible was included in the tissue sample. The arterioles in the samples varied in outer diameter from about 25 to 140 A. By measuring serial cross sections of the arterioles, it was possible to compute the fraction of the total arteriolar sample which ...

Administration of chlorothiazide to rats for 9 weeks produces an increase of intracellular sodium and a decrease of intracellular potassium in skeletal muscle. However, in cardiac muscle, in the wall of mesenteric arterioles, in aortic wall, and in kidney there is no significant alteration in the amount of sodium, potassium, or chloride per unit of dry tissue weight. The water content of heart muscle, skeletal muscle, and kidney is not altered by chlorothiazide. The intracellular concentration of Na and K in heart muscle is likewise unaltered by chlorothiazide. However, chlorothiazide produces a highly significant 44% increase in the granularity of the juxtaglomerular cells. The data in general suggest that chlorothiazide decreases the volume of extracellular fluid, but does not reduce the content of intracellular Na. Extracellular K is reduced as well as the K inside skeletal muscle fibers. However, the amount of K inside cardiac muscle fibers is unchanged by chlorothiazide.

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