Tachycardia releases atrial natriuretic peptide in the anesthetized rabbit |
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| Authors: | A J Rankin C A Courneya N Wilson J R Ledsome |
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| Affiliation: | 1. University of Bristol, School of Veterinary Sciences, Regenerative Medicine Laboratory, Biomedical Science Building, University Walk, Bristol BS8 1TD, United Kingdom;2. University of Bristol, School of Clinical Sciences, Regenerative Medicine Laboratory, Biomedical Science Building, University Walk, Bristol BS8 1TD, United Kingdom;3. University of Cambridge, Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, E.D. Adrian Building, Forvie Site, Robinson Way, Cambridge CB2 0PY, United Kingdom;4. University of Cambridge, Department of Physiology Development and Neuroscience, Anatomy Building, Downing St, Cambridge CB2 3DY, United Kingdom;5. University of Bristol, School of Veterinary Sciences, Langford House, Langford, North Somerset BS40 5DU, United Kingdom |
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| Abstract: | In anesthetized, vagotomized rabbits the plasma concentration of immunoreactive atrial natriuretic peptide (IR-ANP) was found to be 58.5 +/- 3.4 pg/mL (n = 18) when measured using a radio-immunoassay. Tachycardia, induced by electrical pacing of the right atrium, resulted in increased plasma levels of IR-ANP. The size of the increase in IR-ANP appeared to be related to the degree of tachycardia induced. The release of IR-ANP with tachycardia was unaffected by beta-adrenergic blockade with atenolol (2 mg/kg), muscarinic blockade with atropine (2 mg/kg) or ganglionic blockade with hexamethonium (10 mg/kg). The results show that IR-ANP is released in response to tachycardia and that this does not involve a neuronal reflex. |
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