24 January 2001
Background/Aims: Several lines of evidence support that the kidney is involved in the increase of arterial blood pressure, and some genetic studies suggest that the thiazide-sensitive Na<sup>+</sup>:Cl<sup>–</sup> cotransporter could be implicated in the development of hypertension. In the present study, we analyzed the Na<sup>+</sup>:Cl<sup>–</sup> cotransporter mRNA levels in the kidney during the development of hypertension 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 Goldblatt hypertension studied at 7, 14, 21, and 28 days. The third model included 6 Wistar rats treated with N<sup>G</sup>-nitro- L-arginine methyl ester during 10 days. Respective controls were studied for all models. At the end of each experimental period, the systolic blood pressure was measured in the tail by plethysmography. Individual renal cortex total RNA was extracted, and the mRNA levels of the thiazide-sensitive Na<sup>+</sup>:Cl<sup>–</sup> cotransporter were assessed following a semiquantitative RT-PCR strategy. Results: All experimental models developed systemic hypertension. However, the level of mRNA expression of the Na<sup>+</sup>:Cl<sup>–</sup> cotransporter did not change in any of the models studied as compared with their respective controls. Conclusion: Our results suggest that a change in mRNA levels of the thiazide-sensitive Na<sup>+</sup>:Cl<sup>–</sup> cotransporter is not associated with the development of hypertension in spontaneously hypertensive rats, in rats with renovascular hypertension, nor in rats with hypertension induced by nitric oxide synthesis inhibition.