DeFronzo R A, Sherwin R S, Dillingham M, Hendler R, Tamborlane W V, Felig P
J Clin Invest. 1978 Feb;61(2):472-9. doi: 10.1172/JCI108958.
To examine the role of basal insulin and glucagon secretion in potassium and sodium homeostasis, somatostatin, a potent inhibitor of insulin and glucagon secretion, was infused for 5 h into healthy human subjects, maturity-onset diabetes, juvenile-onset diabetics, and normal dogs. Infusion of somatostatin resulted in an increase in serum potassium (0.5-0.6 meq/liter) in normal subjects and maturity-onset diabetics, but not in juvenile-onset diabetics despite equivalent reductions in plasma glucagon in all three groups. A similar rise in serum potassium was observed in normal conscious dogs given somatostatin and was reversed by insulin replacement. Urinary excretion of potassium was unaffected by somatostatin. In dogs given intravenous potassium chloride in doses (0.375 meq/kg per h) which do not alter basal insulin levels, the rise in serum potassium (0.6 meq/liter in controls) increased 100% when somatostatin was administered together with the KCl infusion. Addition of replacement doses of insulin to the somatostatin infusion resulted in increments in serum potassium which were comparable to infusion of KCl alone. Urinary potassium excretion rose after KCl administration and was unchanged by the addition of somatostatin. Serum sodium concentration was unaffected by somatostatin administration in both the human and dog studies. However, urinary sodium excretion displayed a biphasic response falling by 20-60% within the first 2 h of somatostatin administration and then rising to values 50-80% above basal levels at 3-4 h. Inulin and p-aminohippurate clearances were unaffected by somatostatin. It is concluded that (a) potassium homeostasis is influenced by basal insulin levels in the absence of which serum potassium concentration rises and potassium tolerance declines; (b) this effect of insulin is mediated via extrarenal mechanisms of potassium disposal; (c) somatostatin has a biphasic effect on urinary sodium secretion, the mechanism of which remains to be established.
为研究基础胰岛素和胰高血糖素分泌在钾和钠稳态中的作用，将生长抑素（一种强效的胰岛素和胰高血糖素分泌抑制剂）持续5小时输注到健康人体受试者、成年型糖尿病患者、青少年型糖尿病患者以及正常犬体内。在正常受试者和成年型糖尿病患者中，输注生长抑素导致血清钾升高（0.5 - 0.6毫当量/升），但在青少年型糖尿病患者中未出现这种情况，尽管三组患者的血浆胰高血糖素均有同等程度的降低。给正常清醒犬输注生长抑素后观察到血清钾有类似升高，且胰岛素替代可使其逆转。生长抑素不影响钾的尿排泄。给犬静脉输注氯化钾（剂量为每小时0.375毫当量/千克），该剂量不改变基础胰岛素水平，当生长抑素与氯化钾输注同时进行时，血清钾的升高幅度（对照组为0.6毫当量/升）增加了100%。在生长抑素输注中添加替代剂量的胰岛素会导致血清钾升高，其幅度与单独输注氯化钾相当。输注氯化钾后尿钾排泄增加，添加生长抑素后无变化。在人体和犬的研究中，生长抑素给药均不影响血清钠浓度。然而，尿钠排泄呈现双相反应，在生长抑素给药的前2小时内下降20 - 60%，然后在3 - 4小时升至高于基础水平50 - 80%的值。菊粉和对氨基马尿酸清除率不受生长抑素影响。得出以下结论：(a)钾稳态受基础胰岛素水平影响，缺乏基础胰岛素时血清钾浓度升高且钾耐受性下降；(b)胰岛素的这种作用是通过肾外钾处置机制介导的；(c)生长抑素对尿钠分泌有双相作用，其机制尚待确定。
