Defects in membrane transport of ions as possible pathogenic factors in hypertension.

Although abnormalities in cellular ion transport have been shown in a variety of cells of essential hypertensives, the mechanistic link between these abnormalities and elevated blood pressure is poorly understood. Reduced sodium-potassium ATPase activity, with and without elevated levels of a circulating inhibitor of this transport system, has been reported by a number of studies. The recent characterization of the endogenous ouabain or its isomer will facilitate the testing of the hypothesis that salt-sensitive essential hypertension relates to higher levels of this factor. The erythrocyte sodium-lithium countertransport may serve as a marker for a subpopulation of essential hypertensives. However, this transport system has no physiologic counterpart and thus does not provide insight into mechanisms associated with altered cellular ionic homeostasis in essential hypertension. Increased activity of the sodium-hydrogen antiport in essential hypertension relates to an alkaline shift in the cytosolic pH set-point for activation of this transport system. This process may reflect increased cytosolic free calcium concentration with or without augmented protein kinase C activity.