Decreased cardiac baroreflex sensitivity is not due to cardiac hypertrophy in NG-nitro-L-arginine methyl ester-induced hypertension.

OBJECTIVE

To investigate the link between cardiac hypertrophy, elevated blood pressure level and baroreflex impairment, we assessed cardiac baroreflex function in a hypertensive model almost devoid of cardiac hypertrophy, obtained by nitric oxide synthesis inhibition.

METHODS

Thirteen adult male Wistar rats were treated orally with NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg per 24 h) for 4 weeks. Fifteen control rats received tap water. At the end of the treatment aortic blood pressure was recorded continuously and the baroreceptor-heart rate curve was assessed by bolus injections of phenylephrine and sodium nitroprusside (10 different doses of each).

RESULTS

Mean blood pressure was higher in L-NAME rats than in control rats, whereas body weight was similar. Total heart weight and left ventricular weight did not differ between the groups. Cardiac baroreflex was reset in hypertensive rats, as indicated by a rightwards shift of the mean blood pressure-heart rate curve. Its gain was decreased significantly in L-NAME rats, whereas the heart rate range was not different between the two groups.

CONCLUSION

L-NAME hypertensive rats exhibit an original impairment of cardiac baroreflex, characterized by a range-independent decreased gain which is not due to cardiac hypertrophy.