Dietary sodium and potassium-induced transient changes in blood pressure and catecholamine excretion in the Sprague-Dawley rat.

Abstract

SUMMARY When Sprague-Dawley derived rats were changed from a chow type diet to a moderately high sodium diet, rapid transient changes in blood pressure (BP) and catecholamine excretion were observed. After 1 dietary week, BP increased from 122 ± 1 mm Hg to approximately 145 mm Hg (p < 0.001), and there was a concomitant 20% reduction in urinary norepinephrine (UNEV) and cpinephrine (UEV) excretion (p < 0.05). Heart rates were reduced (p < 0.05). These data suggest that sodiuminduced increases in BP were initially associated with suppressed sympathetic nervous system activity. During dietary Weeks 2 and 3, some animals had a persistent moderate elevation in BP (BP =S 150 mm Hg), while others developed more severe increases. UNEV in moderately hypertensive animals returned to control levels during this period; but UEV and heart rates remained suppressed. UNEV in severely hypertensive animals exceeded (13% ± 3%, p < 0.05) that of controls. This increase coincided with their most severe hypertension (171 ± 1 mm Hg, p < 0.001). UE values and heart rate data indicate that systemic adrenergic tone was likely suppressed at this time and that the increased UNEV was renal in origin. By dietary Week 4, the BP of severely hypertensive animals had begun to fall, and indices of sympathetic nervous system tone were indistinguishable among all groups. Inclusion of a dietary potassium supplement ameliorated the development of hypertension only in those animals that became severely hypertensive, and appeared to prevent the early suppression of indices of sympathetic activity. Received May 20, 1982; revision accepted November 29, 1982. sium supplements would lower the elevated blood pressure of the sodium-fed, genetically heterogenous, Sprague-Dawley derived rat. A similar protective effect of potassium was observed in Kyoto spontaneously hypertensive rats (SHR) fed excess sodium, 16 Dahl 17 salt-sensitive rats (Dahl S), and in the two-kidney, one clip Goldblatt model. 18 The mechanisms of both the hypertensive effect of excess dietary sodium and the protective effect of potassium remain unknown.In the quest for initiating factors or "prime movers" in hypertension, 19 exhaustive studies of the relationship between sympathetic neural activity and essential hypertension have been conducted. The topic remains embroiled in controversy. Symbolic of this dispute is a recent review by Goldstein 20 who surveyed 32 studies in the area and found 88% of the investigators reporting higher plasma norepinephrine values (PNE) in hypertensives than in normotensives. Only 41% of these differences, however, reached a level considered statistically significant. These higher values were found mostly in young patients, suggesting greater sympa-