Effect of maturation on renal Na+/K+-atpase and its susceptibility to nitric oxide-deficient hypertension in rats.
1. The present study deals with the effect of maturation on the kinetic properties of renal Na(+)/K(+)-ATPase and its susceptibility to nitric oxide (NO)-deficient hypertension induced by the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME). 2. Immature (4-week-old) and adult (12-week-old) male Wistar rats were administered L-NAME (40 mg/kg per day) in their drinking water for 4 weeks. 3. The properties of the ATP- and Na(+)-binding sites of Na(+)/K(+)-ATPase were investigated by activation of the enzyme with increasing concentrations of the energy substrate ATP and/or cofactor Na(+). Unchanged values of K(m) suggest that energy utilization by the enzyme in the kidney of control rats remains unaffected during maturation. Conversely, the decrease in K(Na) values (the concentration of Na(+) necessary to achieve half-maximal reaction velocity) indicates improved affinity for Na(+) in the older group of control rats. 4. Application of L-NAME to all young animals had no significant effect on the functional properties of Na(+)/K(+)-ATPase. 5. In adult animals, the V(max) values remained unchanged after treatment with L-NAME, but the affinities of the ATP- and Na(+)-binding sites were decreased, as indicated by significant increase in K(m) and K(Na) values. 6. Maturation of control rats was accompanied by an increase in the Na(+) affinity of renal Na(+)/K(+)-ATPase without affecting ATP utilization. However, maturation increased the susceptibility of renal Na(+)/K(+)-ATPase to the harmful effects of L-NAME.
Javorková
Veronika
V
Institute for Heart Research, Department of Biochemistry, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Vlkovicova
Jana
J
Kunes
Jaroslav
J
Pechanova
Olga
O
Zicha
Josef
J
Vrbjar
Norbert
N
D000255:Adenosine Triphosphate / Q000378:metabolism; D000367:Age Factors; D000375:Aging / Q000378:metabolism*; D000818:Animals; D001665:Binding Sites; D001794:Blood Pressure; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced / Q000201:enzymology / Q000378:metabolism* / Q000503:physiopathology; D007668:Kidney / Q000201:enzymology*; D007700:Kinetics; D008297:Male; D008954:Models, Biological; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000172:deficiency / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012965:Sodium Chloride / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D009569:Nitric Oxide; D012965:Sodium Chloride; D000255:Adenosine Triphosphate; D019001:Nitric Oxide Synthase; D000254:Sodium-Potassium-Exchanging ATPase; D019331:NG-Nitroarginine Methyl Ester