PATHOPHYSIOLOGY AND NATURAL HISTORY HYPERTENSION Venous responses to salt loading in hypertensive subjects

It has been previously suggested that salt loading produces structural changes of the arteries in hypertensive patients who respond to salt loading with a greater rise of blood pressure. This study examined the possibility that salt loading alters venous distensibility in hypertensive patients. Twenty-one patients with essential hypertension were placed on a low-sodium diet (70 meq) for 7 days and then were placed on a high-sodium diet (345 meq) for 7 days. Patients were arbitrarily divided into two groups based on the response of their blood pressure to salt loading: (1) those whose mean blood pressure increased by more than 10% while on the high-salt diet as compared with those on the low-salt diet (salt-responsive patients, n = 8) and (2) those whose mean blood pressure did not increase by more than 10% (salt-nonresponsive patients, n = 13). The venous pressure-volume relationship was determined in the forearm with a water-filled plethysmograph when patients were on the lowand high-salt diet. Venous pressure-volume curves were not different between salt-responsive and salt-nonresponsive patients while on the low-salt diet. High-salt intake shifted the curve toward the pressure axis for salt-responsive patients (p < .05) but not for salt-nonresponsive patients. Phentolamine, 1 mg administered intravenously for 5 min, did not significantly alter venous pressure-volume curves for either group while on the lowor high-salt diet. These results suggest that salt loading decreased venous distensibility in salt-responsive patients, which resulted from nonadrenergic mechanisms: structural changes of the veins could perhaps be included as one of these mechanisms. Circulation 69, No. 1, 50-56, 1984. EPIDEMIOLOGIC STUDIES suggest that an excessive intake of salt contributes to the prevalence of essential hypertension in humans.' However, the mechanisms by which an excessive intake of salt promotes hypertension in humans are not clear. Recent studies have indicated that the response of blood pressure to salt loading varies among hypertensive patients.2'5 Studies by Kawasaki et al.2 and Fujita et al.3 indicated that patients who had a greater increase in blood pressure in response to salt loading (saltresponsive patients) excreted less sodium in urine, gained more weight, and had a greater increase in cardiac output during salt loading than did patients who did not have an increase in blood pressure or whose blood pressure increased less in response to salt From the Research Institute of Angiocardiology and Cardiovascular Clinic,i Faculty of Medicine, Kyushu University, Fukuoka, Japan. Supported by a research grant for cardiovascular diseases (56A-4) from the Ministry of Health and Welfare, Japan. Address for correspondence: Akira Takeshita, M.D., Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812 Japan. Received May 31, 1983; revision accepted September 29, 1983. 50 loading (salt-nonresponsive patients). It was thus considered that the greater increase in blood pressure during salt loading in salt-responsive patients might be attributed to the greater increase in cardiac output that resulted from greater sodium retention.' We have recently suggested that in addition to greater sodium retention, an alteration of control of vascular resistance during salt loading may contribute to the salt-induced elevation of blood pressure in salt-responsive hypertensive patients.5 Salt loading increased vascular resistance in the forearm in salt-responsive patients but not in salt-nonresponsive patients. Furthermore, salt loading decreased maximal vasodilator capacity of the resistance vessels in the forearm in saltresponsive patients but did not alter it in salt-nonresponsive patients. These results suggested that salt loading produced structural changes of resistance vessels in the forearm in salt-responsive patients. Structural changes might involve the increased thickness of the vessel wall or the increase in sodium and/or water in the vessels. It is known that there are abnormalities in veins as CIRCULATION by gest on A ril 4, 2017 http://ciajournals.org/ D ow nladed from PATHOPHYSIOLOGY AND NATURAL HISTORY-HYPERTENSION well as in arteries in humans and animals with spontaneous hypertension.2 There is a possibility that salt loading might produce changes in veins as well as in arteries in salt-responsive patients. If salt loading produces changes in veins and decreases venous distensibility, such changes might contribute to redistribution of venous blood from peripheral to cardiopulmonary circulation and thus might lead to the elevation of blood pressure by increasing cardiac output. However, there are only a few studies that have examined the effects of salt loading on veins.'3 Brown et al.13 reported that salt loading did not alter venous distensibility in hypertensive patients. However, most of their patients were salt-nonresponsive patients. It is possible that the venous responses to salt loading may differ between salt-responsive and salt-nonresponsive patients as did the arterial responses to salt loading.' The aim of this study was to examine whether salt loading altered venous distensibility in salt-responsive hypertensive patients. It has been implied that augmented neural mechanisms may contribute to salt-induced vasoconstriction in salt-responsive hypertensive patients.'. ` Accordingly, we also examined the role of a-adrenergic mechanisms in changes in venous distensibility in salt-responsive patients.