DIETARY POTASSIUM AS A DETERMINANT OF BLACK HYPERTENSION

在正常血压和高血压的住院研究中，黑白 受试者，我们将调查这样一个假设，即饮食 足够的钾，每天30meq，会诱发或加剧 盐敏感现象，由盐敏感性的大小决定 当饮食中的氯化钠从 40-250meq/天，为期9天。以确定是否 饮食中适量的钾导致了这种情况的发生或 加重盐敏，我们会纠正温和的钾盐 补钾9天所致的体力衰竭 用40毫摩尔的碳酸氢钾(KHCO3)来增加摄入量 正常，70meq/天，而氯化钠水平持续。对…的影响 补钾与停钾后血压变化的关系 要下定决心。我们已经确定， 低正常范围的膳食钾，30-70meq/天，显著 调节血压对食盐的反应，一种由氯化钠诱导的 服用补充剂后血压的升高明显逆转 KHCO3，并在停止补充后迅速复发 碳酸氢钾。KHCO3的补充可显著提高小鼠血清中的含量。 血浆钾，但只在早晨禁食时有轻微的增加 句号。补钾也会导致大量的钠尿。 和体重减轻，其肾脏血流动力学相关性将是 调查过了。我们将确定，盐敏感性是诱导的还是 更严重的是，由于饮食中钾的摄入量略有充足， 患者：1)动脉僵硬增加，由增加的 脉搏波速度；2)增加的收缩峰值血压 颈动脉脉搏波波形测定评估的主动脉弓 通过压平眼压测量；3)增强动脉升压反应 静脉注射去甲肾上腺素；4)增加前臂 动脉阻力降低，前臂血流量降低；5)降低 动脉内注射乙酰胆碱引起的血管松弛和增强 对动脉注射酚妥拉明的反应。 鉴于有证据表明，氯化钠的高血压效应需要其 氯化物成分以及钠，并具有肾脏升压作用 氯离子本身，我们将检验氯离子的假设 氯化钾的成分限制了其降低高血压的能力。在……里面 一项关于黑人男性和男性的安慰剂对照、双盲门诊研究 高血压升高的女性，我们将确定是否口服 服用KHCO3降压效果优于KCl2。

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.