Effect of potassium chloride on the blood pressure in two-kidney, one clip Goldblatt hypertensive rats.

With the technical assistance of Toby S. BrownSUMMARY Epidemiologies! and experimental data suggest blood pressure-lowering effects of dietary potassium. A randomized, double-blind clinical trial was used to assess blood pressure response to orally administered potassium, 120 mEq/day, and to placebo in 101 adults with mild hypertension. Blood pressure was measured with a random-zero sphygmomanometer every 2 weeks of this 8-week trial. Systolic blood pressure in the potassium-treated group decreased by 6.4 ± 13.7 (SD) mm Hg ( p < 0.025) compared with 0.11 ± 13.0 mm Hg in the placebo-treated group (p = 0.96). Diastolic blood pressure in the potassium-treated group decreased by 4.1 ± 8.3 mm Hg (p<0.05) compared with a 1.6 ± 6.5 mm Hg decrease in placebo-treated subjects (p= 0.09). Baseline blood pressure of potassium-treated subjects was unexpectedly higher than that of controls. After correcting for baseline variation, blood pressure still decreased 3.4/1.8 mm Hg more in potassium recipients than in placebo recipients (p = 0.14 and 0.24, respectively). Blood pressure decreased by 19/13 mm Hg in five blacks taking potassium vesus a 1/0 mm Hg increase in seven blacks taking placebo. Compliance with the potassium regimen was 91.5% by pill count; only one subject discontinued treatment because of side effects. In conclusion, 120 mEq/day of microencapsulated potassium chloride was well tolerated in adults with mild hypertension. An antihypertensive effect of potassium cannot be ruled out despite the fact that there was no statistically significant difference between potassium-treated and placebo-treated subjects after adjustment for differences in baseline blood pressure. Systolic blood pressure was affected more than diastolic blood pressure. Blacks may be particularly sensitive to blood pressure-lowering effects of potassium chloride. A larger clinical trial stratified by baseline blood pressure and race is required. (Hypertension 9: 444- In experimental models of renovascular, genetic, and salt-sensitive hypertension, high potassium intake has been shown to attenuate the development of hyper-

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Double-blind, placebo-controlled trial of potassium chloride in the treatment of mild hypertension.

LP¹,

Yarger²,

Feussner³

et al. 1987

“…In most studies, potassium supplementation has been found to ameliorate hypertension by causing an increase in urinary sodium excretion. 28 ' 30 In contrast, since total body sodium and plasma volume are increased in potassium depletion, 10 the protective effect of potassium depletion is independent of changes in sodium and volume and is related to potassium depletion per se.…”

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“…30 ' 31 Although a protective effect of both potassium depletion and potassium supplementation seems paradoxical, the mechanism of protection of these divergent maneuvers appears to differ. In most studies, potassium supplementation has been found to ameliorate hypertension by causing an increase in urinary sodium excretion.…”

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Potassium depletion ameliorates hypertension in spontaneously hypertensive rats.

Linas¹,

Marzec-Calvert²

1986

SUMMARY The hemodynamic effect of moderate K+ depletion in hypertension is unknown. Since severe K+ depletion reduces systemic vascular resistance in normotensive rats, we determined the effect of K+ depletion on the natural history of hypertension in spontaneously hypertensive rats (SHR). Wistar-Kyoto rats (WKY) and SHR were fed a K + -replete, a moderately K + -depleted, or a severely K + -depleted diet. After 6 weeks, systemic vascular resistance was reduced by 25% in WKY on the severely K + -depleted diet while mean arterial pressure and systemic vascular resistance were comparable in WKY on the other two diets. In SHR on the severely K + -depleted diet for 6 weeks, muscle K+ was reduced by 23% and growth rate by 65%. In SHR on the moderately K + -depleted diet, growth rate was reduced by 23% after 3 weeks. By 6 weeks, however, muscle K + was reduced by 5 to 6% and growth rate was comparable to that in SHR receiving the K + -replete diet. The administration of either K + -depleted diet prevented the development of hypertension (systolic blood pressure: severely depleted, 116 ± 4; moderately depleted, 122 ± 3; K + -replete, 155 ± 5 nun Hg; p < 0.001 compared with both K + -depleted groups) and reversed established hypertension (systolic blood pressure: severely depleted, 116 ± 4; moderately depleted, 128 ± 3; K+-replete, 171 ± 5 mm Hg; p<0.001 compared with both K + -depleted groups). The protective effect of K + depletion was mediated by a 40% reduction in systemic vascular resistance. These results suggest that K + depletion has a potent antihypertensive effect in SHR. The vasodilative effect of moderate K+ depletion also appears to be specific for hypertension since it did not occur in normotensive WKY. (Hypertension 8: 990-996, 1986) KEY WORDS • hypokalemia * electrolytes • hemodynamics • angiotensin F OR many years sodium was the only electrolyte considered relevant to the control of blood pressure in patients with essential hypertension. While recent studies have demonstrated that other electrolytes such as calcium 1 and chloride 2 ' 3 may also be of importance in the pathogenesis of hypertension, there have been few experimental studies on the hemodynamic effects of potassium in hypertension. This paucity of information on potassium is surprising since potassium is the major intracellular cation and since many of the 30 million hypertensive patients in the United States are treated with diuretic agents and manifest mild hypokalemia and a decrease in total body potassium. Although there have been few studies on the effect of potassium in hypertensive animals, there have been hemodynamic studies on the effects of potassium in normotensive animals. Acute hypokalemia, as occurs when vessels or limbs from normokalemic animals are perfused with hypokalemic solutions, results in vasoconstriction.5 " 7 In contrast, chronic, severe total body potassium depletion induced by diet or dialysis, or both, results in a decrease in systemic vascular resistance (SVR) and mean arterial pressure (MAP).8 " 10 Unfortunat...

“…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.…”

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

Battarbee¹,

Dailey²,

Meneely³

1983

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-