Full Access
Red blood cell sodium and potassium fluxes in psoriatic patients
A. SEMPLICINI,
M. G. MOZZATO, E. RIGON, O. PAROLIN, B. SAMÀ, S. PADOVAN, P. DEGAN, A. PESERICO,
A. C. PESSINA,
Corresponding Author
A. SEMPLICINI
Clinica Medica I University of Padova, Italy
2 Clinica Medica I, Policlinico Universitario, via Giustiniani 2, 35126 Padova, ItalySearch for more papers by this authorA. PESERICO
*Clinica Dermatologica, University of Padova, Italy
Search for more papers by this authorA. SEMPLICINI,
M. G. MOZZATO, E. RIGON, O. PAROLIN, B. SAMÀ, S. PADOVAN, P. DEGAN, A. PESERICO,
A. C. PESSINA,
Corresponding Author
A. SEMPLICINI
Clinica Medica I University of Padova, Italy
2 Clinica Medica I, Policlinico Universitario, via Giustiniani 2, 35126 Padova, ItalySearch for more papers by this authorA. PESERICO
*Clinica Dermatologica, University of Padova, Italy
Search for more papers by this authorAbstract
Abstract. Psoriasis might be a widespread membrane disorder. Therefore, the red blood cell sodium, potassium and lithium outward fluxes (through Na-K-ATPase, Na-K-Cl co-transport, Li-Na countertransport and passive permeability), as well as the Na and K content, were studied in 31 psoriatic patients and 23 normal controls. A significant increase in intracellular potassium content, in the maximal velocity of the Na-K ATPase and of Na-K-Cl co-transport as well as in the outward passive permeability for Na were found in the psoriatic patients compared with controls. On the contrary, no differences were observed in sodium content, Li-Na countertransport and passive potassium permeability between the two groups. These results are compatible with a selective increase in inward, as well as outward, membrane permeability to sodium, which is compensated for by increased activity of the Na-K pump, and of the outward Na-K-Cl co-transport with a secondarily increased erythrocyte potassium content. They indicate that the red blood cell might be a useful model for the study of membrane transport in psoriatics.
References
- 1 Krueger GG. Psoriasis: current concepts of its etiology and pathogenesis. In: RL Dobson, BH Thiers, eds. The Yearbook of Dermatology. Year Book Medical Publishers Inc., Chicago , 1981: 13–70.
- 2 Hendel L, Larsen JK, Ammitzboll T, Asboe-Hansen G. A study of cell proliferation kinetics in the small intestinal epithelium of psoriasis patients. Clin Exp Dermatol 1984; 9: 329–35.
- 3 Mahrle G, Orfanos CE. The plasma unit membrane. Membrane mediated growth control and its failure in psoriasis. Br J Dermatol 1977; 96: 215–23.
- 4 Orfanos CE. Scanning electron microscopy in psoriasis. In: EM Farber, AJ Cox, eds. Psoriasis. Proceedings of the International Symposium, Stanford University. Stanford University Press, California , 1971: 169–77.
- 5 Barriere H, Litoux P, Geraut C. Etude des cellules cornées du psoriasis en microscopic électronique à balayage. Dermatologica 1974; 149: 257–65.
- 6 Brody I. The ultrastructure of the epidermis in psoriasis vulgaris as revealed by electron microscopy. J Ultrastructural Res 1962; 6: 304–23.
- 7 Orfanos CE, Schaumber-Lever G, Mahile G, Lever WF. Alterations of cell surfaces as a pathogenetic factor in psoriasis. Possible loss of contact inhibition of growth. Arch Dermatol 1973; 107: 38–46.
- 8 Caputo R, Innocenti M, Gasparini G, Peluchetti D. Plasma membrane in psoriatic cells. A freeze-fracture study. J Invest Dermatol 1978; 71: 245–9.
- 9 Kumar R, Weiss VS, West DP, Chiero LA. Erythrocyte membrane phosphorylation in untreated and in etretinate-treated psoriatic patients. Br J Dermatol 1983; 109: 277–86.
- 10 Wright RK, Mandy SH, Halprin KM, Hsia SL. Defects and deficiency of adenyl cyclase in psoriatic skin. Arch Dermatol 1973; 107: 47–53.
- 11 Mahrle G, Orfanos CE. Decreased membrane-bound ATP-hydrolytic activity in psoriatic epidermis. Br J Dermatol 1974; 91: 529–40.
- 12 Mahrle G, Orfanos CE. Ultrastructural localisation and differentiation of membrane bound ATP utilizing enzymes including adenyl-cyclase in normal and psoriatic epidermis. Br J Dermatol 1975; 93: 495–507.
- 13 Maridonneau I, Braquet P, Garay RP. Na+ and K+ transport damage induced by oxygen free radicals in human red cell membranes. J Biol Chem 1983; 258: 3107–13.
- 14 Garay RP, Nazaret C. Na+ leak in erythrocytes from essential hypertensive patients. Clin Sci 1985; 69: 613–24.
- 15 Hilton PJ. Cellular sodium transport in essential hypertension. N Engl J Med 1986; 314: 222–9.
- 16 Garay PR. Inhibition of the Na+/K+ cotransport system by ciclic AMP and intracellular Ca2+ in human red cells. Biochim Biophys Acta 1982; 688: 786–92.
- 17 Voorhees JJ. Commentary: cyclic adenosine monophosphate regulation of normal and psoriatic epidermis. Arch Dermatol 1982; 118: 869–74.
- 18 Van De Kerkhof PCM, Van Erp PEJ. Calmodulin levels are grossly elevated in the psoriatic lesion. Br J Dermatol 1983; 108: 217–8.
- 19 MacNeil S, Tucker WFG, Dawson RA, Bleehen SS, Tomlinson S. The calmodulin content of the epidermis in psoriasis. Clin Sci 1985, 69: 681–6.
- 20 Mazia D. The cell cycle: what happens in the living cell between the time it is born in the division of another cell and the time it divides again? New methods of investigation reveal four phases in the cycle. Sci Am 1974; 230: 54–64.
- 21 Blaustein MP. Sodium ions, calcium ions, blood pressure regulation and hypertension: a reassessment and a hypothesis. Am J Physiol 1977; 232: C165–73.
- 22 Dagher G, Garay RP. A Na+, K+ cotransport assay for essential hypertension. Can J Biochem 1980; 58: 1069–74.
- 23 Canessa M, Adragna N, Solomon HS, Connolly TM, Tosteson DC. Increased sodium-lithium countertransport in red cells of patients with essential hypertension. N Engl J Med 1980; 302: 772–6.
- 24 Siegel S. Non Parametric Statistics for the Behavioral Science. McGraw Hill, New York , 1956: 47–52.
- 25 Siegel S. Non Parametric Statistics for the Behavioral Science McGraw Hill, New York , 1956: 116–27.
- 26 Canessa M, Brugnara C, Cusi D, Tosteson DC. Modes of operation and variable stoichiometry of the furosemide-sensitive Na and K fluxes in human red cell. J Gen Physiol 1986; 87: 113–42.
- 27 Wiley JS, Cooper RA. A furosemide-sensitive cotransport of sodium plus potassium in the human red cell. J Clin Invest 1974; 53: 745–55.
- 28 Diez J, Hannaert P, Garay RP. Kinetic study of Na-K pump in erythrocytes from essential hypertensive patients. Am J Physiol 1987; 252: H1–6.
- 29 Garay RP, Nazaret P, Hannaert P, Price M. Abnormal Na, K cotransport function in a group of patients with essential hypertension. Eur J Clin Invest 1983; 13: 311–20.
- 30 Wiley JS, Ellory JC, Shumamn MA, Shaller CC, Cooper RA. Characteristics of the membrane defect in the hereditary stomatocystosis syndrome. Blood 1975; 46: 337–54.
- 31 Pandey GN, Sarkadi B, Haas M, Gunn RB, Dvis JM, Tosteson DC. Lithium transport pathways in human red blood cells. J Gen Physiol 1978; 72: 233–47.
- 32 Hajini GH, Hussain ST, Shah SNA: Sodium, potassium and phosphorus content of normal and psoriatic skin. Br J Dermatol 1976; 95: 674–5.
