Erythrocyte ion transport and membrane lipid composition in young and adult rats with NO-deficient hypertension.
The aim of our study was to search for abnormalities of sodium and potassium transport in erythrocytes of male Wistar rats subjected to chronic L-NAME treatment (40 mg/kg/day) for 4 weeks either from weaning (4-week-old) or in adulthood (12-week-old). Sodium content, Na(+),K(+)-pump and Na(+),K(+)-cotransport activity, cation leaks as well as membrane cholesterol and phospholipid contents were determined in fresh erythrocytes. Chronic inhibition of NO synthase elicited similar blood pressure rise in both age groups which did not differ in the degree of NO synthase inhibition. No significant ion transport abnormalities were disclosed in erythrocytes of young NO-deficient rats, whereas erythrocyte Na(+) content, outward Na(+),K(+)-cotransport and inward Na(+) leak were significantly reduced in adult hypertensive animals compared to age-matched controls. It should be noted that the erythrocytes of adult control rats were characterized by higher activity of Na(+),K(+)-pump and Na(+),K(+)-cotransport, increased Na(+) and Rb(+) leaks and elevated membrane cholesterol content compared to those of young normotensive controls. Increased Na(+) leak and elevated membrane cholesterol content but reduced membrane phospholipid content were revealed in erythrocytes of adult hypertensive rats when compared to young hypertensive rats. It can be concluded that young and adult Wistar rats did not differ in the extent of NO synthase inhibition and blood pressure rise elicited by chronic L-NAME treatment. Our results exclude the important participation of classical sodium transport abnormalities in the pathogenesis of this NO-deficient form of experimental hypertension.
Vokurková
Martina
M
Center for Experimental Cardiovascular Research, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Dobesová
Zdena
Z
Pechánová
Olga
O
Kunes
Jaroslav
J
Zicha
Josef
J
D000818:Animals; D001693:Biological Transport, Active; D004195:Disease Models, Animal; D004910:Erythrocyte Membrane / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D017136:Ion Transport; D008297:Male; D008563:Membrane Lipids / Q000032:analysis / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000633:toxicity; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D008563:Membrane Lipids; D009569:Nitric Oxide; D012964:Sodium; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D019331:NG-Nitroarginine Methyl Ester