Sodium transport in primary hypertension.
Humans and rats with primary hypertension may exhibit different and stable abnormalities in membrane Na+ transport systems: (i) Pump (-) = decreased apparent affinity of the pump for internal Na+, (ii) Co (-) = decreased apparent affinity of the Na+, K+ cotransport system for internal Na+ (iii) Leak (+) = increased passive Na+ permeability and (iv) = Counter (+) abnormality (increased maximal rate of Na+-Li+ and perhaps Na+-H+ exchange). Excess Na+ intake tends to be compensated by the transient secretion of endogenous "digitalis-like" and other natriuretic factors. The presence of Co(-) or Leak(+) abnormalities may amplify transitory cell Na+ rises induced by endogenous digitalis-like factors at the vascular wall. The Counter(+) abnormality may increase renal Na+ reabsorption and induce permanent hypersecretion of endogenous digitalis-like factors.
D000818:Animals; D001692:Biological Transport; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D012964:Sodium / Q000378:metabolism*
D012964:Sodium