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1 Department of Human Physiology, Centre for Neuroscience, Flinders University, Bedford Park, SA, Australia
* To whom correspondence should be addressed. E-mail: eugene.nalivaiko{at}flinders.edu.au.
The Current strategy for the prevention of excessive sympathetic neural traffic to the heart relies on the use of beta-blockers, drugs that act at the heart end of the brain-heart axis. In the present study, we attempted to suppress cardiac sympathetic nerve activity by affecting the relevant cardiomotor neurons in the brain using selective serotonin-1A receptor agonist 8-OH-DPAT. In conscious unrestrained rabbits, instrumented for recordings of heart rate, arterial pressure or cardiac output, we provoked increases in cardiac sympathetic activity by psychological (loud sound, pinprick and airjet) or inflammatory (lipopolysaccharide 0.5 µg/kg i.v.) stresses. Pinprick and airjet stresses elicited transient increases in heart rate (+50±7 and +38±4 BPM, respectively) and in mean arterial pressure (+16±2 and +15±3 mmHg, respectively). Lipopolysaccharide injection caused sustained increases in heart rate (from 210±3 to 268±10 BPM) and in arterial pressure (from 74±3 to 92±4 mmHg). Systemically administered 8-OH-DPAT (0.004-0.1 mg/kg) substantially attenuated these responses, in a dose-dependent manner. Drug effects were prevented by a selective serotonin-1A receptor antagonist WAY-100635 (0.1 mg/kg i.v.). Similarly to systemic administration, microinjection of 8-OH-DPAT (500 nl of 10 mM solution) into the medullary raphe/parapyramidal region caused anti-tachycardic effects during stressful stimulation and during LPS-elicited tachycardia. This is the first demonstration that activation of 5-HT1A receptors in the medullary raphe/parapyramidal area causes suppression of neurally mediated cardiovascular changes during acute psychological and immune stresses.
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