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Letters to the Editor will be published, if suitable, as space permits. They should not exceed 1,000 words (typed double-spaced) in length and may be subject to editing or abridgment. To the Editor: The nexus between salt (sodium chloride) intake and essential hypertension is not simple. (For a recent review, see Reference 1). Population studies have demonstrated a positive correlation between increased dietary salt intake and the incidence of essential hypertension, whereas intrapopulation studies have not always shown this relation. Established essential hypertension is expressed by a sustained increase in the peripheral vascular resistance (PVR) because of a reduction in the vascular lumen of the peripheral circulatory system. Thus, the high incidence of essential hypertension in populations consuming large quantities of sodium chloride is likely to reflect the chronic influence of a high salt intake on the cardiovascular system. This phenomenon is probably related to enhanced growth of the vascular media and peripheral vasoconstriction, both of which produce narrowing of the vascular lumen. However, a substantial increase of vascular smooth muscle (VSM) mass is unlikely to result from a brief exposure to a high salt intake. Yet, to characterize the nature of "salt-sensitivity," most investigations have monitored the blood pressure response in individuals subjected to an increased intake of salt for short periods ranging from days to months. A significant elevation of blood pressure in association with increased sodium intake was thus considered as indicative of salt-sensitivity. A recent insight into cellular mechanisms that mediate alterations of the PVR suggests that underlying causes for the increased incidence of essential hypertension in populations habitually consuming a high salt diet results from additional pathophys-iological processes to those responsible for blood pressure elevation during short periods of exposure to increased salt intake. A great number of vasoactive agents and growth factors stimulate pathways in VSM cells that may lead both to vasoconstriction and enhanced growth. These factors usually increase the cytosolic free calcium in concert with stimulation of the sodium-proton exchange. As expected, some vasoactive agents can function as growth factors for VSM cells, 2-5 and reciprocally, a number of growth factors can cause vasoconstrictionA 7 Such a concept is compatible with recent observations that structural vascular alterations in animal models of hypertension may not solely relate to the elevated blood pressure level but to the trophic influences of vasoactive hormones (for example, see Reference 8). These findings suggest the concept that a …

Salt sensitivity: trophic effect of growth and vasoactive factors.