DIVERSE EFFECTS OF RENAL DENERVATION ON VENTRICULAR HYPERTROPHY AND BLOOD-PRESSURE IN DOCA-SALT HYPERTENSIVE RATS

Cardiac hypertrophy that accompanies hypertension seems to be a phenom enon of multifactorial origin whose development does not seem to depen d on an increased pressure load alone, but also on local growth factor s and cardioadrenergic activity. The aim of the present study was to d etermine if sympathetic renal denervation and its effects on arterial pressure level can prevent cardiac hypertrophy and if it can also dela y the onset and attenuate the severity of deoxycorticosterone acetate (DOCA)-salt hypertension. DOCA-salt treatment was initiated in rats se ven days after uninephrectomy and contralateral renal denervation or s ham renal denervation. DOCA (15 mg/kg, sc) or vehicle (soybean oil, 0. 25 mi per animal) was administered twice a week for two weeks. Rats tr eated with DOCA or vehicle (control) were provided drinking water cont aining 1% NaCl and 0.03% KCl. At the end of the treatment period, mean arterial pressure (MAP) and heart rate measurements were made in cons cious animals. Under ether anesthesia, the heart was removed and the r ight and left ventricles (including the septum) were separated and wei ghed. DOCA-salt treatment produced a significant increase in left vent ricular weight/body weight (LVW/BW) ratio (2.44 +/- 0.09 mg/g) and rig ht ventricular weight/body weight (RVW/BW) ratio (0.53 +/- 0.01 mg/g) compared to control(1.92 +/- 0.04 and 0.48 +/- 0.01 mg/g, respectively ) rats. MAP was significantly higher(39%) in DOCA-salt rats. Renal den ervation prevented (P>0.05) the development of hypertension in DOCA-sa lt rats but did not prevent the increase in LVW/BW (2.27 +/- 0.03 mg/g ) and RVW/BW (0.52 +/- 0.01 mg/g). We have shown that the increase in arterial pressure level is not responsible for cardiac hypertrophy, wh ich may be more related to other events associated with DOCA-salt hype rtension, such as an increase in cardiac sympathetic activity.