(Na+,K+)-activated adenosinetriphosphatase and hypertension in DAHL salt- sensitive and -resistant rats

(Na+,K+)-ATPase activity was compared in Dahl salt-sensitive (S) and salt-resistant (R) rats. When S and R rats were maintained on 1% NaCl diet their blood pressures at 5 weeks of age were similar and their renal microsomal (Na+,K+)-ATPase activities were also similar. At 6 months of age, on 1% NaCl diet, S rats have markedly elevated blood pressure compared to R and renal microsomal (Na+,K+)-ATPase activity was suppressed in S compared to R. Feeding 8% NaCl diet for 5 weeks induced hypertension in young S rats but failed to alter renal or brain (Na+,K+)-ATPase activity. Heart (Na+,K+)- ATPase activity was elevated in S compared to R rats regardless of salt intake of blood pressure. It appears unlikely that mutations in the structural locus for the renal (Na+,K+)-ATPase molecule are involved in the strain specific differences in susceptibility to salt-induced hypertension since the physical-chemical properties of the enzyme from the two strains were found to be similar. Since renal (Na+,K+)-ATPase activities were unchanged by salt feeding and resultant blood pressure changes in young S rats, the suppressed renal (Na+,K+)-ATPase activity seen only in old S rats is probably a response to prolonged renal damage and not a response to "natriuretic factors." Elevated heart (Na+,K+)-ATPase in S-rat hearts is unexplained.