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Coronary chemoreflex evoked by intrapericardial nicotine has a somatic component
1Department of Anatomy and Physiology, College of Veterinary Medicine, Kansas State University, Manhattan 66506, USA.
The American Journal of Physiology
|February 1, 1997
Summary
The coronary chemoreflex, triggered by cardiac receptor stimulation, can attenuate the knee-jerk reflex via vagal nerves. This somatic response may contribute to fainting during exertion.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Autonomic Nervous System Regulation
Background:
- Vagally innervated cardiac and pulmonary receptors trigger reflexes affecting blood pressure.
- The pulmonary depressor reflex includes a somatic component that attenuates muscle reflexes.
Purpose of the Study:
- To investigate if the coronary chemoreflex also attenuates somatic reflexes, specifically the knee-jerk reflex.
- To elucidate the neural pathways involved in this potential somatic reflex.
Main Methods:
- Cardiac receptors in anesthetized cats were stimulated using nicotine and bradykinin injected into the pericardial sac.
- The knee-jerk reflex was measured by eliciting it via patellar tendon tapping.
- Vagotomy and procaine blockade were used to determine the neural mediation of observed effects.
Main Results:
- Intrapericardial nicotine significantly attenuated the knee-jerk reflex (-26.2%).
- This attenuation was vagally mediated and dependent on cardiac receptor stimulation.
- Intrapericardial bradykinin augmented the knee-jerk reflex (17.5%), an effect not mediated by vagal nerves.
Conclusions:
- The coronary chemoreflex, a vagally mediated response, includes a somatomotor component that attenuates the knee-jerk reflex.
- This somatic response may play a role in exertional syncope and vasovagal syncope.
- Bradykinin's effect on the knee-jerk reflex is independent of vagal pathways.