Thiazide-sensitive cotransporter mRMA expression is not altered in three models of hypertension

Background/Aims: Several fines of evidence support that the kidney is invol ved in the increase of arterial blood pressure, and some genetic studies su ggest that the thiazide-sensitive Na+:Cl- cotransporter could be implicated in the development of hypertension. In the present study, we analyzed the Na+:Cl- cotransporter mRNA levels in the kidney during the development of h ypertension in three experimental models. Methods: The first model included 18 spontaneously hypertensive rats studied at 4, 10, and 16 weeks of age. The second model included 28 Wistar rats with two-kidney, one-clip Goldblat t hypertension studied at 7, 14, 21, and 28 days. The third model included 6 Wistar rats treated with N-G-nitro-L-arginine methyl ester during 10 days . Respective controls were studied for all models. At the end of each exper imental period, the systolic blood pressure was measured in the tail by ple thysmography. individual renal cortex tota I RNA was extracted, and the mRN A levels of the thiazide-sensitive Na+:Cl- cotransporter were assessed foll owing a semiquantitative RT-PCR strategy. Results: All experimental models developed systemic hypertension. However, the level of mRNA expression of t he Na+:Cl- cotransporter did not change in any of the models studied as com pared with their respective controls. Conclusion: Our results suggest that a change in mRNA levels of the thiazide-sensitive Na+:Cl- cotransporter is not associated with the development of hypertension in spontaneously hypert ensive rats, in rats with renovascular hypertension, nor in rats with hyper tension induced by nitric oxide synthesis inhibition. Copyright (C) 2001 S. Karger AG, Basel.