Course Code BIOM2011
Course Title Integrative Cell and Tissue Biology
Course Coordinator Associate Professor Bradley Launikonis
Due Date 10/05/2022
Assignment Title Effects of Experimental Drug Agents on Cardiac
Function
Word Count 1643
Date Submitted 11/05/2022
Extension applied for Yes / No Revised Date -
Student Number Surname First Name
46500937 Arora Siddhant
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Introduction
The sympathetic nervous system plays an integral role in stress-induced cardiac
activity, first garnered and expressed by Walter Branford Cannon in his literature titled "Fight
or Flight" Response (Craft, J et al., 2019). The sympathetic response is monitored across
numerous species, with primary reference made to cane toad species (Bufo marinus) in this
report. Regarded for its administered positive chronotropic and inotropic effects, inducing the
sympathetic response triggers multiple physiological adaptations, including but not limited
to; accelerated heart rate (HR), increased ventricular contractile force (VCF) and cardiac
contractility (Lakkatta EG, 2004).
Following inducement of the flight or flight response, activation of the autonomic
nervous system (ANS) is initiated, releasing specific neurotransmitters, noradrenaline and
adrenaline (O’Donnel SR; Wanstall JC, 1982). Part of the triggered response via the ANS is
the subsequent binding process by which the neurotransmitters bind to β1 and 2-adrenergic
receptors (β1/2-AR) present on cardiac cells (Madamanchi A, 2007). A variety of
physiological processes, including nervous system functionality, is regulated by the hormone
adrenaline, a primary agonist of all β-ARs within the G-protein coupled receptor family
(GCPR) (Pavoine C; Defer N, 2005). Adrenaline binds specifically to GCPR-ligands and
induces structural changes in the G-protein by coupling to heterotrimeric G-proteins,
facilitating the conversion of G-protein-bound GDP to GTP (Madamanchi A, 2007).
Undergoing detachment of the G-protein leaves active Gα and Gβ subunits to mediate
downstream nervous signalling and action potential propagation, yielding an increase in
blood flow and HR (Madamanchi A, 2007).
A representation of the effects of adrenaline is thoroughly catalogued in the
pharmacological study conducted by O'Donnel et al. (1982) in cane toads, which distinctively
demonstrated the antagonistic effects of propanol and agonistic effects of adrenaline
subsequent to binding with β-adrenergic receptors. The author's findings further observed a
correlation between drug administration and an influx in the availability of calcium ions
within the nervous system (O'Donnel et al., 1982). This increased availability of calcium ions
infused into cardiac cells through multiple pathways, specifically L-type channels, facilitates
cardiac depolarisation, coupled with a subsequent increase in VCF (De Ruijter W et al.,
2002). This study, coupled with substantial evidence from other sources, suggests that cane
toads are a viable experimental option applicable when accurately characterising the effects
of drugs on cardiac conduction, specifically HR and VCF (De Ruijter W et al., 2002).
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