Association between transforming growth factor-β and hypertension

Abstract Discordant findings are reported on the left ventricular transforming growth factor-β1 (TGF-β1) mRNA levels in various rat models. Left ventricular TGF-β1 mRNA levels did not differ between spontaneously hypertensive rats (SHR) and normal rats, between deoxycorticosterone (DOCA)-salt and sham-operated hypertensive rats, but were increased in stroke-prone spontaneously hypertensive rats (SHRSP) and in post-myocardial infarction (MI) rats. Renal cortical TGF-β1 mRNA levels were, however, higher in DOCA-salt hypertensive rats. Angiotensin II subtype 1 receptor antagonism (AT1R) and angiotensin converting enzyme inhibition (ACEI) decreased left ventricular and vascular smooth muscle TGF-β1 mRNA levels in SHR and renal TGF-β1 mRNA in DOCA-salt hypertensive rats and in SHRSP. In post-MI rats ventricular TGF-β1 mRNA decreased by AT1R antagonism. In essential hypertensive patients, TGF-β1 protein as well as TGF-β1 mRNA levels are hyperexpressed. The TGF-β1 overproduction in hypertension can be attributed to various factors such as elevated angiotensin II, increased systemic blood pressure (BP) per se, increased fluid shear stress and a differential expression of TGF-β1 linked to DNA polymorphism in the promoter. The Arg25 polymorphism in the TGF-β1 gene is associated with higher BP. A higher plasma TGF-β1 concentration is found in hypertensive patients with microalbuminuria and left ventricle hypertrophy. In these patients, AT1R antagonism and ACEI reduced these plasma TGF-β1 levels significantly.