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(Hypertension. 1997;29:1104-1108.)
© 1997 American Heart Association, Inc.

Articles

Distinct Mechanisms of Modulation of Angiotensin II Type I Receptor Gene Expression in Heart and Aorta

Donna H. Wang; Aqing Yao; Huawei Zhao; ; Donald J. DiPette

From the Department of Internal Medicine, Hypertension and Vascular Research Laboratories, University of Texas Medical Branch, Galveston.

Correspondence to Donna H. Wang, MD, Department of Internal Medicine, Hypertension and Vascular Research Laboratories, 8.104 Medical Research Building, University of Texas Medical Branch, Galveston, TX 77555-1065. E-mail dwang%intmeds1{at}mhost.utmb.edu

Abstract The purpose of the present study was to test the hypothesis that hypertension induced by reduced renal mass (RRM) upregulates gene expression of the type 1 angiotensin II (Ang II) receptor (AT₁) in the thoracic aorta and heart through an Ang II–dependent mechanism. Three groups of rats were given 1% NaCl water and subjected to RRM, RRM plus captopril (RRM+Cap, 30 mg/kg per day), or sham surgery. Tail-cuff systolic blood pressure was significantly elevated in RRM and RRM+Cap rats compared with sham-operated rats. The ratios of the medial wall area of the thoracic aorta and heart weight to body weight were significantly elevated in RRM and RRM+Cap rats compared with sham-operated rats. Northern blot analysis indicated that the ratio of AT₁ to GAPDH mRNA in the aorta was significantly higher in RRM (1.85±0.52) compared with sham-operated (0.21±0.04) and RRM+Cap (0.55±0.20) rats. In contrast, the ratio of AT₁ to GAPDH mRNA in the heart was significantly increased in both RRM (1.09±0.23) and RRM+Cap (1.00±0.09) compared with sham-operated (0.34±0.06) rats. Thus, RRM hypertension upregulates AT₁ mRNA expression in both the hypertrophied aorta and heart. Captopril treatment without altering blood pressure in RRM rats prevents the increase in AT₁ mRNA in the aorta but not the heart. These results suggest that different tissue-specific mechanisms of AT₁ gene regulation exist; ie, in aorta, an Ang II– or kinin-dependent mechanism is operant, whereas in heart, RRM-induced upregulation of AT₁ mRNA may be pressure dependent.

Key Words: aorta • hypertension, reduced renal mass • receptors, angiotensin II • heart • captopril

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