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(钠,钾)激活的三磷酸腺苷酶与DAHL盐敏感和抗性大鼠的高血压

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

作者信息

McPartland R P, Rapp J P

出版信息

Clin Exp Hypertens A. 1982;4(3):379-91. doi: 10.3109/10641968209060750.

Abstract

(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.

摘要

比较了 Dahl 盐敏感(S)大鼠和盐抵抗(R)大鼠的(钠,钾)-ATP 酶活性。当 S 大鼠和 R 大鼠维持在 1%氯化钠饮食时,它们 5 周龄时的血压相似,肾脏微粒体(钠,钾)-ATP 酶活性也相似。在 6 个月龄时,食用 1%氯化钠饮食,与 R 大鼠相比,S 大鼠的血压显著升高,且与 R 大鼠相比,S 大鼠的肾脏微粒体(钠,钾)-ATP 酶活性受到抑制。给年轻的 S 大鼠喂食 8%氯化钠饮食 5 周可诱发高血压,但未能改变肾脏或大脑的(钠,钾)-ATP 酶活性。无论血压的盐摄入量如何变化,与 R 大鼠相比,S 大鼠心脏的(钠,钾)-ATP 酶活性均升高。由于发现两种品系的肾脏(钠,钾)-ATP 酶分子的物理化学性质相似,因此肾脏(钠,钾)-ATP 酶分子结构位点的突变似乎与盐诱导高血压易感性的品系特异性差异无关。由于盐喂养和年轻 S 大鼠随后的血压变化并未改变肾脏(钠,钾)-ATP 酶活性,因此仅在老年 S 大鼠中观察到的肾脏(钠,钾)-ATP 酶活性受抑制可能是对长期肾脏损伤的反应,而不是对“利钠因子”的反应。S 大鼠心脏中升高的(钠,钾)-ATP 酶无法解释。

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