DIETARY POTASSIUM AS A DETERMINANT OF BLACK HYPERTENSION

在血压正常和高血压的住院研究中，黑人和白色 受试者，我们将调查的假设，饮食轻微 足够的钾，30毫克当量/天，将诱导或加剧 盐敏感性现象，由盐敏感性的大小决定。 当饮食中氯化钠含量从 40-250 meq/天，持续9天。 以确定是否 少量充足的膳食钾引起的发生或 盐敏感性加剧，我们将纠正轻度钾 补充膳食钾9天引起的耗竭 40 mmol碳酸氢钾（KHCO 3），以增加摄入量， 正常，70 meq/天，同时持续NaCl水平。 的影响 血压的补充钾和它的中断将 下定决心。 我们已经确定， 膳食钾超过低正常范围，30-70 meq/天，显着 调节对饮食NaCl的血压反应，NaCl诱导的 增加血压显着扭转与补充 KHCO 3，并在停止补充后迅速复发 KHCO3 KHCO_3的补充诱导了大幅度增加， 血浆钾，但只有一个轻微的增加，在早晨空腹 期 补钾也引起大量尿钠排泄 和体重减轻，肾血流动力学相关性将是 研究了 我们将确定，盐敏感性是否诱导或 加剧，通过勉强足够的膳食摄入钾， 参与：1）动脉僵硬度增加，通过增加 脉搏波速度; 2）增加收缩期峰值血压在 主动脉弓，如通过确定的颈动脉脉搏波形评估的 压平眼压计; 3）增强动脉升压反应， 静脉注射去甲肾上腺素; 4）前臂增加 动脉阻力降低，前臂血流量低; 5）降低 血管舒张反应动脉内乙酰胆碱和6）增强 对动脉内酚妥拉明的反应 鉴于证据表明，氯化钠的高血压效应需要其 氯化物成分以及钠，并给予肾血管加压作用 氯化物本身，我们将测试的假设，氯化物 KCl的组分限制了其减轻高血压的能力。 在 一项针对黑人男性的安慰剂对照、双盲门诊研究， 高血压增加的女性，我们将确定是否口服 在降低血压方面，给予KHCO 3比KCl更有效。

In inpatient studies of normotensive and hypertensive black and white subjects, we will investigate the hypothesis that a diet marginally adequate with respect to potassium, 30 meq/day, will induce or exacerbate the phenomenon of salt-sensitivity, as determined by the magnitude of increase in blood pressure when dietary sodium chloride is increased from 40-250 meq/day for a period of 9 days. To determine whether the marginally adequate dietary potassium caused the occurrence or exacerbation of the salt-sensitivity, we will correct the mild potassium depletion induced by supplementing dietary potassium for a 9 day period with 40 mmol, of potassium bicarbonate (KHCO3) to increase intake to normal, 70 meq/day, while the NaCl level is continued. The effect on blood pressure of the supplement of potassium and its discontinuance will be determined. We have already determined that the small change in dietary potassium over the low-normal range, 30-70 meq/day, significantly modulates the blood pressure response to dietary NaCl, a NaCl-induced increase in blood pressure significantly reversing with the supplement of KHCO3 and rapidly reoccurring after discontinuance of the supplement of KHCO3. The supplement of KHCO3 induced a substantial increase in the plasma potassium, but only a minimal increase in the morning fasting period. The potassium supplement also induced a substantial natriuresis and loss of weight, the renal hemodynamic correlates of which will be investigated. We will determine, whether salt sensitivity induced or exacerbated, by marginally adequate dietary intake of potassium is attended by: 1) increased arterial stiffness, as assessed by an increased pulse wave velocity; 2) augmented systolic peak blood pressure in the aortic arch, as assessed by the carotid artery pulse wave form determined by applanation tonometry; 3) enhanced arterial pressor response to intravenous administration of norepinephrine; 4) increased forearm arterial resistance and reduced forearm blood low; 5) reduced vasorelaxation in response to intraarterial acetylcholine and 6) enhanced response to intraarterial phentolamine. Given the evidence that the hypertensive effect of NaCl requires its chloride component as well as Na, and given the renal vasopressor effect of chloride per se, we will test the hypothesis that the chloride component of KCl constrains its capacity to attenuate hypertension. In a placebo controlled, double blind outpatient study of black men and women with increased hypertension, we will determine whether orally administered KHCO3 is more effective than KCl in lowering blood pressure.