Autonomic components of the cardiovascular responses to an acoustic startle stimulus in rats

1 A loud acoustic stimulus was administered to rats prior to and after treatment with autonomic blockers in order to unravel the autonomic mechanisms of the blood pressure (BP) and heart rate (HR) responses to startle. 2 Six rats, implanted with a BP telemetric system, were used in a randomized crossover saline-controlled (saline vs. autonomic blocker) study with a washout period of 7 days between each active session. A first acoustic stimulus (110 dB, 0.7 s) was administered. An autonomic blocker i.e. atropine methylnitrate (15 mg, kg(-1)), atenolol (15 mg. kg(-1)) or prazosin HCl (1 mg. kg(-1)), or physiological saline was administered i.p. 40 min prior to a second identical acoustic stimulus, 3 The average BP rise following the first stimulus was +25 mmHg and the average HR change was +17 bpm. The responses after autonomic blockades were affected as follows: atropine increased the HR rise (+45.1 +/- 1.7 bpm), atenolol reversed the HR changes to a bradycardic response (-21.4 +/- 9.1 bpm), after prazosin treatment the BP rise was reversed into a BP decrease (-11.3 +/- 3.2 mmHg) and the HR increase was amplified (+/-76.0 +/- 10.0 bpm). Finally, the delay for obtaining the maximal BP change was increased from 1.9 to 2.6 s following prazosin pretreatment, 4 These results indicate that the BP rise resulting from an acute loud noise depends on a vascular sympathetic activation (prevented with prazosin), which is partly blunted by vasodilation (revealed with prazosin). The evoked HR changes combine a sympathetic activation (fully expressed following atropine) and a vagal activation (unmasked with atenolol). Further experiments are necessary to document the vasodilatory component unmasked with prazosin.