SUMMARYTwenty patients with hypertension were studied under diets containing low and high salt to identify factors which might be involved in elevating blood pressure under sodium-loading. They were classified as "salt-sensitive" (SS) and "nonsalt-sensitive" (NSS) according to the presence or absence of greater than 10% increases in mean blood pressure when a low salt diet was replaced by a high salt diet. During high-sodium intake, the SS patients showed reduced urinary excretion of sodium and elevated plasma levels of aldosterone as compared with plasma renin activity. The SS patients also showed an enhanced pressor response to norepinephrine under both low-sodium and high-sodium diets.From these results, it is suggested that the sodium retention, which is probably related to nonsuppressed levels of PAC under sodium-loading, is one of the factors in elevating blood pressure in the SS patients. Moreover, the enhanced pressor response to norepinephrine seems to contribute, in part, to elevation of blood pressure in the SS patients under salt-loading.Additional Indexing Words: Salt-sensitive hypertension Nonsalt-sensitive hypertension Pressor response Norepinephrine Renin-aldosterone HE major effects of dietary salt on incidence of hypertension1) and development of hypertension2) have been investigated in a number of epidemiological and experimental studies. It has been proposed that the expansion of the extracellular fluid volume by salt-loading is an important event in the elevation of blood pressure and the development of hypertension.3) How-

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SUMMARY We investigated the effects of plasma from dogs with perinephritk hypertension on theReceived June 9, 1987; accepted March 24, 1988. cell for the putative humoral inhibitor in hypertension; intracellular ion concentrations are easily measured, facilitating data interpretation; and use of unprocessed plasma avoids creation, modification, release, or destruction of inhibitory or stimulatory factors by acidification, boiling, or freezing. 2 -3 There is evidence for humoral pump inhibitors in dogs with chronic one-kidney, one wrapped (1K1W) perinephritic hypertension.4 -5 However, the best evidence to date involves boiled plasma supernates assayed in rat tail artery strips. 3 In the present study, we used our homologous cultured cell assay to reexamine this form of hypertension. Fresh, unprocessed plasma obtained within 60 minutes of bleeding was layered over cultured dog aortic smooth muscle cells, and effects on 86 Rb + uptake were measured. To detect temporal changes in levels of humoral inhibitor, blood was assayed repeatedly over the first 6 weeks of hypertension. To detect endothelial cell modulation of the inhibition, we also assayed with cocultures. Finally, because there is evidence that humoral inhibitors in hypertensive rats may induce Na + -K + pump molecules in vascu-

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