Influence of l-type slow calcium channels blockers on cardiac, respiratory and motor activity at the intact and poisoned by physostigmine (eserine) of rats during the early ontogeny
- Authors: Kuznetsov S.V.1, Kuznetsova N.N.1,2, Gaydukova P.A.1
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Affiliations:
- Sechenov Institute of Evolutionary Physiology and Biochemistry Russian Academy of Sciences
- Institute of Experimental Medicine
- Issue: Vol 17, No 3 (2019)
- Pages: 39-49
- Section: Original study articles
- URL: https://journals.rcsi.science/RCF/article/view/16202
- DOI: https://doi.org/10.17816/RCF17339-49
- ID: 16202
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Abstract
The effects of calcium-channel blockers (CCBs) (verapamil, nifedipine) on heart rate, respiration rate and motor activity were studied in 3-30-day-old rats. The role of calcium channels in development of disturbances of a heart and respiratory rhythms after introduction to newborn rats of acetylcholinesterase (AChE) inhibitor of physostigmine was revealed. Parameters of functional activity of heart, respiratory and somatomotor systems in case of blockade of calcium channels were studied also under conditions of the activation of cholinoceptive structures caused by an injection to infant rats of AChE inhibitor after premedication by CCBs. It is shown that use of calcium channels blockers leads to development of bradycardia, and verapamil causes more expressed disturbance of a heart rhythm in rats of younger age, while blockade of dihydropyridinic receptors by nifedipine has no ontogenetic specifics. Similar ontogenetic dynamics concerns also reaction of respiratory system. Verapamil have a detrimental effect on respiration, up to a stop, in 3-7-day-old and to a lesser extent in 16-30-day-old infant rats. Nifedipine slightly reduces a respiration rate at younger infant rats, but raises it at the mature rats. The nifedipine injection more in comparison with verapamil changes the level and a pattern of motor activity. Preliminary blockade of calcium channels does not render significant change of reaction at the subsequent introduction of physostigmin.
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##article.viewOnOriginalSite##About the authors
Sergey V. Kuznetsov
Sechenov Institute of Evolutionary Physiology and Biochemistry Russian Academy of Sciences
Author for correspondence.
Email: ksv@iephb.ru
Dr. Biol. Sci. (Physiology), Chief Researcher, Head of Laboratory of Ontogenetic Development of Animals Nervous Activity
Russian Federation, Saint PetersburgNataliya N. Kuznetsova
Sechenov Institute of Evolutionary Physiology and Biochemistry Russian Academy of Sciences; Institute of Experimental Medicine
Email: nat.kuz@mail.ru
Dr. Biol. Sci. (Physiology), Laboratory of Ontogenetic Development of Animals Nervous Activity; Senior Researcher, S.V. Anichkov Department of Neuropharmacology
Russian Federation, Saint PetersburgPolina A. Gaydukova
Sechenov Institute of Evolutionary Physiology and Biochemistry Russian Academy of Sciences
Email: polina.gaydukova.95@mail.ru
Bachelor, Senior Research Assistant, Laboratory of Ontogenetic Development of Animals Nervous Activity
Russian Federation, Saint PetersburgReferences
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