Haddy F J
Department of Physiology, Uniformed Services University, Bethesda, Maryland 20814-4799.
Clin Invest Med. 1987 Nov;10(6):547-54.
A local increase in extracellular potassium concentration [K+]o, up to about 8 mEq/liter, by topical application or intra-arterial infusion of iso-osmotic solutions of K+ salts, causes arteriolar dilation and decreased resistance to blood flow in systemic vascular beds. A local decrease in [K+]o over physiologic ranges induces arteriolar constriction and increased resistance to blood flow. K+ vasodilation is accompanied by hyperpolarization of the smooth muscle cell, whereas the vasoconstriction is accompanied by depolarization. All of these responses can be blocked by ouabain, a potent Na+,K+-ATPase inhibitor. Thus it is thought that K+ vasodilation results from stimulation of the electrogenic Na+-K+ pump, and that the constriction results from its inhibition. Acute generalized inhibition of the Na+,K+-ATPase and Na+-K+ pump (hypokalemia, strophanthidin, methylguanidine, vanadate) in the anesthetized dog can raise blood pressure. In experiments in animals, myocardial Na+,K+-ATPase and vascular Na+-K+ pump activities were decreased in low-renin hypertension, and vascular Na+-K+ pump activity was decreased following acute volume expansion, changes associated with bioassay evidence of a Na+-K+ pump inhibitor in the plasma. The inhibitor appears to arise in, or to be influenced by the area of the anteroventral third ventricle of the brain. It induces electrogenic depolarization of vascular smooth muscle cells and may inhibit norepinephrine uptake by adrenergic nerve terminals. Potassium and a circulating endogenous Na+,K+-ATPase inhibitor of unknown molecular structure may partly regulate the mechanical activity of cardiovascular muscle and participate in the genesis of certain forms of hypertension. Potassium may be of value in the prevention and therapy of hypertension, partly by virtue of its vasodilator activity.
通过局部应用或动脉内输注等渗钾盐溶液，使细胞外钾浓度[K⁺]ₒ局部升高至约8毫当量/升，可引起小动脉扩张，并降低全身血管床的血流阻力。在生理范围内，[K⁺]ₒ局部降低会导致小动脉收缩，并增加血流阻力。钾引起的血管舒张伴随着平滑肌细胞的超极化，而血管收缩则伴随着去极化。所有这些反应都可被哇巴因（一种强效的钠钾ATP酶抑制剂）阻断。因此，人们认为钾引起的血管舒张是由电生性钠钾泵的刺激所致，而血管收缩则是由其抑制作用引起的。在麻醉犬中，急性全身性抑制钠钾ATP酶和钠钾泵（低钾血症、毒毛花苷、甲基胍、钒酸盐）可使血压升高。在动物实验中，低肾素性高血压时心肌钠钾ATP酶和血管钠钾泵活性降低，急性容量扩张后血管钠钾泵活性降低，这些变化与血浆中钠钾泵抑制剂的生物测定证据相关。该抑制剂似乎产生于脑前腹侧第三脑室区域，或受其影响。它可诱导血管平滑肌细胞发生电生性去极化，并可能抑制肾上腺素能神经末梢对去甲肾上腺素的摄取。钾和一种分子结构未知的循环内源性钠钾ATP酶抑制剂可能部分调节心血管肌肉的机械活动，并参与某些形式高血压的发生。钾可能在高血压的预防和治疗中具有价值，部分是由于其血管舒张活性。
