Objective: Active TGF-횩-induced ig-h3 molecule (棺ig-h3) is an extracellular matrix protein, highly induced by transforming growth factor 횩 (TGF-횩). TGF-횩 underlies the development of tissue fibrosis and arteriosclerosis, which are a major cause of cardiovascular disease. We, therefore, studied the clinical implication of 棺ig-h3 in patients with essential hypertension. Methods: One-hundred twelve normotensive subjects (53 year-old, 65% male, BP 118/82 mmHg) were compared with 220 hypertensive patients (51 year-old, 62% male, BP 161/104 mmHg). Fasting serum TGF-횩 1 and 棺ig-h3, and urinary 棺ig-h3 and creatinine excretion was measured by ELISA. Cardiac structure and function were evaluated by echocardiogram and arterial stiffness (augmentation index; AI and pulse pressure/stroke volume index; PP/SVI) by the pressure transfer function using radial pulse tonometry. Results: Hypertensives had significant increase of PP/SVI and central AI. Urinary 棺ig-h3 increased to 40짹2.8ng/mg Cr in hypertensives (vs 26.2짹2.3 in normotensives, p<0.01). By univariate analysis, urinary 棺ig-h3 correlated positively with female (r=0.21, p<0.05), SBP (r=0.14, p<0.05) and central AI (r=0.12, p=0.05). Serum 棺ig-h3 correlated positively with fibrinogen (r=0.14, p<0.05) and DBP (r=0.12, p=0.05). No correlation was found between serum TGF-棺 and urine or serum 棺ig-h3. By multivariate regression analysis, PP/SVI correlated with SBP (r=0.43, p<0.01), inversely with DBP. Six-month treatment with antihypertensive drugs decreased urinary 棺ig-h3 from 39.7짹7.0 to 17.7짹4.3 ng/ml.Cr (p<0.01). Serum 棺ig-h3 after treatment were decreased to 214짹20ng/ml from 389짹35 ng/ml (p<0.01). Conclusion: 棺ig-h3 in either serum or urine can offer an complimentary phenotypic finding to support the regression of vascular stiffness, in addition to BP lowering. Therefore, 횩ig-h3 can be used as an early marker of vascular damage of hypertension or an indicator of response to antihypertensive intervention in hypertension
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