Chronic angiotensin-II treatment potentiates HR slowing in Sprague-Dawley rat during acute behavioral stress

This study examined the effect of 2-week infusion of angiotensin-II (Ang-II; 175 ng/kg/min) via minipump in rats (n = 7) upon the mean arterial blood pressure (mBP) and heart rate (HR) response to an acute stress as compared to rats infused with saline (n = 7). The acute stress was produced by a classical aversive conditioning paradigm: a 15 s tone (CS +) followed by a half second tail shock. Baseline mBP in Ang-II infused rats (167.7 ± 21.3 mm Hg; mean ± SD) significantly exceeded that of controls (127.6 ± 13.5 mm Hg). Conversely, baseline HR in the Ang-II infused rats (348 ± 33) was significantly lower than controls (384 ± 19 bpm). The magnitude of the mBP increase during CS + did not differ between groups, but the HR slowing during CS + in the Ang-II infused rats (− 13.2 ± 8.9 bpm) was significantly greater than that seen in controls (− 4.2 ± 5.5 bpm). This augmented bradycardia may be inferentially attributed to an accentuated increase in cardiac parasympathetic activity during CS + in the Ang-II infused rats. The mBP increased above baseline immediately post-shock delivery in controls, but fell in the Ang-II infused rats, perhaps because of a 'ceiling effect' in total vascular resistance. This classical conditioning model of 'acute stress' differs from most stress paradigms in rats in yielding a HR slowing concomitant with a pressor response, and this slowing is potentiated by Ang-II.