K transport and red cell dehydration in sickle and normal erythrocytes

Article type: Research Article

Authors: Brugnara, C.^;

Affiliations: Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.

Note: [] Correspondence to Carlo Brugnara, Department of Pathology, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.

Abstract: Cell dehydration due to loss of KCl is an important determinant in the pathogeneSiS of sickle cell anemia. The polymerization of hemoglobin S and cell sickling are markedly affected by an increase in the intracellular concentration of hemoglobin. Dense, dehydrated cells have been implicated in the vascular and vasoocclusive manifestations of this disease. Two systems for K transport, the KCl cotransport and the Ca-activated K channel, can lead to dehydration of sickle cells. Cellular acidification leads to activation of the KCl cotransport whereas transient increases in free cytoplasmic Ca lead to opening of the Ca-activated K channel. Maturation of normal reticulocytes takes place through a loss of membrane area and of cell K, Cl and water. The KCl cotransport system is a major determinant of the K loss and cell dehydration of normal maturing reticulocytes. Therefore, common mechanisms leading to K loss and dehydration are operative in normal red cells and in sickle erythrocytes.

Keywords: Sickle cell, anemia, K transport, erythrocyte

DOI: 10.3233/CH-1992-12202

Journal: Clinical Hemorheology and Microcirculation, vol. 12, no. 2, pp. 177-184, 1992