Electrical Excitability of the Fish Heart and Its Autonomic Regulation

Transcript expression of inward rectifier potassium channels of Kir2 subfamily in Arctic marine and freshwater fish species

“…Contraction of atrial and ventricular myocytes of the vertebrate heart are activated by a small depolarization of sarcolemmal from the resting membrane potential of about − 80 mV to the threshold (about − 65 mV) of the cardiac action potential (AP). Once generated, AP propagates in orderly manner through the cardiac syncytium and maintains pump function of the heart under changing physiological and environmental conditions including temperature changes (Harris 1941;Ramanathan et al 2006;Vornanen 2017). In working cardiac myocytes, electrical excitability, i.e., the ease with which cardiac myocytes are triggered to fire propagating (all-or-none) APs by the flow of transmembrane ion currents, critically depends on the balance between the inward (depolarizing) Na + current (I Na ) and the outward (repolarizing) K + current (I K1 ) (Milstein et al 2012, Varghese 2016.…”

“…At the threshold potential, the density of the depolarizing I Na exceeds the density of repolarizing I K1 (and I KAch ) and results in generation of propagating AP (Varghese 2016). Because I Na and I K1 have opposite effects on cardiac excitability, differences in heat-resistance between I Na and I K1 may result in thermal deterioration of electrical excitability (Vornanen 2016(Vornanen , 2017. Indeed, I Na is depressed at temperatures, where I K1 continues to increase generating a mismatch between I Na and I K1 : the diminished I Na may be unable to depolarize the membrane to action potential threshold, since the increased resting leakage of K + through I K1 channels effectively resist it.…”

Exploring the Relationship Between Physiological Performance and Reproductive Investment in Wild Fish Using Heart Rate Biologgers

“…Although fH was only monitored for up to 2.5 days during the egg developmental stage, fH fluctuated throughout the period (Figure 2.3). Previous research has shown that environmental factors, activity, and hormones can affect fish fH (discussed in Hoar et al 1992 andFarrell 1993;Vornanen 2017). For instance, cardiac output increases with temperature, where, in teleost fish, the pacemaker rate increases with acute temperature changes such that the Q10 for fH is ≥ 2.0 (Farrell 1992).…”

“…Hence, the more the heart expands the more blood volume can enter the heart, and with a greater central venous blood pressure, Vs will increase. In contrast, the intrinsic rate of the heart is determined by pacemaker cells and is driven by the balance between adrenergic and cholinergic tone (Farrell 1993;Vornanen 2017;Farrell and Smith 2017). The cardiac pacemaker cells contain cholinergic and adrenergic nerve endings, where adrenergic innervation occurs when epinephrine stimulates the ß-adrenoceptors on the heart, which in turn activate channels permitting the cycling of intracellular calcium that stimulate the nerve (Farrell 1993;Vornanen 2017).…”

“…Hence, a higher epinephrine concentration results in an increased fH and force of contraction (i.e., elevated adrenergic tone). However, if acetylcholine molecules bind to the muscarinic receptors on the pacemaker cells, the βadrenergic cascade is antagonized, reducing the parasympathetic drive of the pacemaker cells, and therefore the fH decreases (i.e., elevated cholinergic tone) (Altimiras et al 1997;Vornanen 2017).…”