Enhanced vascular reactivity to norepinephrine in salt-sensitive patients with hypertension.

Abstract

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-

Role of cellular calcium in salt sensitivity of patients with essential hypertension.

“…However, excessive sodium chloride intake does not always raise blood pressure, as several reports have shown marked interindividual differences in response of blood pressure to changes in dietary salt intake (i.e., salt sensitivity) in patients with essential hypertension. 1 The actual mechanism underlying the differences in salt sensitivity has not been fully clarified, although expansion of fluid volume, 1 inappropriate response of the humoral factors, 2 and enhanced vascular response to pressor substances 3 have been proposed to explain the mechanism.…”

“…Many investigators have reported disturbances in the calcium transport system across the cell membrane and intracellular binding process 3 and elevation of [Ca 2+ ]j 6 ' 7 in circulating blood cells of patients with essential hypertension. In addition, clinical findings of enhanced hypotensive response to calcium channel blockers in this disease provide suggestive evidence for an abnormality in cellular calcium movements.…”