{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T13:15:25Z","timestamp":1772889325807,"version":"3.50.1"},"reference-count":43,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:p>The present study evaluated the possible changes in the autonomic control of heart rate in the hypertensive model induced by the inhibition of nitric oxide synthase. Rats were treated with N<jats:sup>G<\/jats:sup>-nitro-l-arginine methyl ester (l-NAME group) in the drinking water during 7 days, whereas control groups were treated with tap water (control group) or with the N<jats:sup>G<\/jats:sup>-nitro-d-arginine methyl ester (d-NAME group), an inactive isomer of thel-NAME molecule. The l-NAME group developed hypertension and tachycardia. The sequential blockade of the autonomic influences with propranolol and methylatropine indicated that the intrinsic heart rate did not differ among groups and revealed a sympathetic overactivity in the control of heart rate in thel-NAME group. The spectral density power of heart rate, calculated using fast-Fourier transformation, indicated a reduced variability in the low-frequency band (0.20\u20130.60 Hz) for thel-NAME group. The baroreflex sensitivity was also attenuated in these animals when compared with the normotensive control or d-NAME group. 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