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Jiao JH, Baertschi AJ. Neural control of the endocrine rat heart. Proc Natl Acad Sci U S A. 1993;90(16):7799-803doi: 10.1073/pnas.90.16.7799.
Jiao, J. H., & Baertschi, A. J. (1993). Neural control of the endocrine rat heart. Proceedings of the National Academy of Sciences of the United States of America, 90(16), 7799-803. https://doi.org/10.1073/pnas.90.16.7799
Jiao, J H, and Baertschi, A J. "Neural control of the endocrine rat heart." Proceedings of the National Academy of Sciences of the United States of America vol. 90,16 (1993): 7799-803. doi: https://doi.org/10.1073/pnas.90.16.7799
Jiao JH, Baertschi AJ. Neural control of the endocrine rat heart. Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7799-803. doi: 10.1073/pnas.90.16.7799. PMID: 8356087; PMCID: PMC47230.
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Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7799-803. doi: 10.1073/pnas.90.16.7799.

Neural control of the endocrine rat heart.

Proceedings of the National Academy of Sciences of the United States of America

J H Jiao, A J Baertschi

Affiliations

  1. Department of Molecular Physiology and Biological Physics, University of Virginia Health Sciences Center, Charlottesville 22908.

PMID: 8356087 PMCID: PMC47230 DOI: 10.1073/pnas.90.16.7799
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Abstract

Although atrial stretch is the accepted stimulus for atrial natriuretic factor (ANF), in vivo studies suggest a stretch-independent, neurally induced ANF release mechanism. Thus the hypothesis that cardiac nerves can stimulate ANF secretion was tested in the Langendorff-perfused, paced rat heart. Venom from the scorpion Centruroides sculpturatus was used to activate neuronal sodium channels, veratridine was added to activate sodium channels (predominantly in myocytes), and electrical stimulation was applied to the right atrial appendage. The efficacy of nerve stimulation was verified by measurements of increased neuropeptide Y in the effluent. ANF levels in the effluent increased by 120% over baseline with 0.5 microM scorpion venom and by 88% with 0.5 microM veratridine (P < 0.01). Cardiac mechanics did not explain the large, concentration-dependent ANF response to the scorpion venom, since changes in the left ventricular developed pressure were small, opposite to those induced by veratridine, and unaffected by sympathectomy or adrenergic receptor blockade. Prior chemical sympathectomy and adrenergic receptor blockade almost abolished the ANF response to scorpion venom but hardly affected the ANF response to veratridine. Addition of 1 microM tetrodotoxin abolished all ANF responses. Electrical stimulation of the atrial appendage increased the ANF secretion by 60.2% (P < 0.02), in conjunction with neuropeptide Y, whereas control stimulations were ineffective. These studies unequivocally demonstrate that stimulation of cardiac sympathetic nerves potently stimulates ANF secretion.

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