PMID: 15272216Jul 24, 2004Paper

Captopril enhances cardiac vagal but not sympathetic neurotransmission in pithed rats

Journal of Pharmacological Sciences
Yoshinobu TakataH Kato

Abstract

The effect of captopril on neurally evoked bradycardia and tachycardia was investigated in pithed rats. Captopril enhanced the vagal nerve stimulation-evoked bradycardia. Angiotensin I reduced the vagal bradycardia, which was reversed by subsequent administration of captopril. Bradykinin did not affect the neurally evoked bradycardia. Captopril and angiotensin I affected neither the exogenous acetylcholine-evoked bradycardia nor the sympathetic nerve stimulation-evoked tachycardia. These results suggest that the interruption of angiotensin II formation by captopril causes less presynaptic inhibition of acetylcholine release via angiotensin II receptors without affecting cardiac sympathetic neurotransmission.

References

Mar 1, 1988·British Journal of Clinical Pharmacology·G B KondoweD W Harron
Jan 1, 1980·Neuroscience·I W ChubbG H White
Jan 1, 1982·Journal of Cardiovascular Pharmacology·R Hatton, D P Clough
Mar 25, 1983·European Journal of Pharmacology·A De JongeP A Van Zwieten

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Citations

Jul 2, 2016·Journal of Veterinary Cardiology : the Official Journal of the European Society of Veterinary Cardiology·A SakataniN Takemura
Apr 10, 2016·The Journal of Physiology·Beth A HabeckerCrystal M Ripplinger
Jul 24, 2007·American Journal of Physiology. Heart and Circulatory Physiology·Toru KawadaMasaru Sugimachi

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