Few humans studies are available that examine the effects of aging on renal and extrarenal adaptation to high potassium loads or dietary potassium deprivation. However, in two studies age-related decreases in both total body potassium and total exchangeable potassium, found in both men and women, were more evident in women (Davis et al., 1989; Rowe et al., 1992). Decreases in total body potassium may be due in part to the decrease in muscle mass that occurs with age (Rowe et al., 1992). In turn, the decrease in muscle mass with age may be, in part, a result of an inadequate intake of dietary potassium and its accompanying base (Frassetto et al., 1997).
In potassium adaptation studies in rats, the kaliuretic response to intravenous infusion of potassium chloride and the rise in plasma potassium have been shown not to be influenced by age (Friedman and Friedman, 1957; Rowe et al., 1992). However, when potassium intake was high, the efficiency of kaliuretic response to intravenous potassium chloride was impaired in the aging rat; a significantly greater plasma potassium concentration also occurred (Friedman and Friedman, 1957; Rowe et al., 1992). Following bilateral nephrectomy, the rise in plasma potassium concentration was also higher in the aged rats that were on a high potassium, but not normal potassium, intake. The renal and extrarenal impairment in potassium adaptation was associated with significant decreases in renal and colon Na+/K+-ATPase activity (Friedman and Friedman, 1957; Rowe et al., 1992). The applicablity of these findings to humans is still unclear.
Over the past several years there has been substantial attention paid to extrarenal potassium disposal. Beta-adrenergic mechanisms have been found to be responsible for potassium disposal during potassium infusion in healthy individuals across the adult age range (aged 23 to 85 years) (Rosa et al., 1980; Rowe et al., 1992). No observed effects of age on the extrarenal potassium disposal or the effect of β-adrenergic blockade was found. The effects of insulin concentration, β-adrenergic blockage, and age on potassium homeostasis during hyperinsulinemia was evaluated in 16 younger (22 to 37 years of age) and 10 older (63 to 77 years of age) men (Minaker and Rowe, 1982; Rowe et al., 1992). Increasing steady-state concentrations of insulin were associated with dose-dependent declines in plasma potassium concentration during the first hour of