BIOM 2011 Integrative Cell and Tissue Biology 2026/2027 Exam Effexts of Experiemental Drug Agents on Cardiac (9pages)

Course Code BIOM2011 Course Title Integrative Cell and Tissue Biology Course Coordinator Associate Professor Bradley Launikonis Due Date 10/05/2026 Assignment Title Effects of Experimental Drug Agents on Cardiac Function Word Count 1643 Date Submitted 11/05/2026 Extension applied for Yes / No Revised Date - Student Number Surname First Name 46500937 Arora Siddhant This study source was downloaded by 100000864769797 from CourseHero.com on 08-31-2026 07:48:39 GMT -05:00 https://www.coursehero.com/file/199512014/Cardiac-Prac-Report-Submission-Siddhant-Aroradocx/ 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).