Force frequency relation in the myocardium of rainbow trout

The purpose of this study was to determine whether steroid hormones modulate cardiac function in rainbow trout (Oncorhynchus mykiss Walbaum). We assessed the effects of exogenously administered steroids on isolated ventricle strips and report that physiological concentrations of androgens, 17β-estradiol and cortisol rapidly (<10·min) enhance inotropism (30-40%) in a sexspecific manner. These effects were specific to the hormones studied, absent if animals were anesthetized chemically and dependent upon steroid concentration and contraction frequency. Based on the use of specific steroid receptor antagonists and key enzyme inhibitors, it appears that testosterone, 11-ketotestosterone and cortisol each act through specific intracellular receptors in males and that the positive inotropism requires the synthesis of polyamines and nitric oxide. Cortisol and 17β-estradiol, but not androgens, had similar effects in females and also involved similar signaling pathways. Androgen and cortisol effects were additive in males but cortisol and 17β-estradiol were not additive in females, suggesting sex differences in the pathways through which these hormones stimulate inotropism. In summary, gonadal steroids and cortisol promote ventricular contractility in a sexdependent manner through mechanisms that appear multifaceted. Ultimately, steroid-mediated improvements in cardiac performance might involve non-genomic pathways and be physiologically important during migration, spawning or stressful periods.

Section: Discussionsupporting

confidence: 87%

Sex-dependent effects of gonadal steroids and cortisol on cardiac contractility in rainbow trout

Farrar

Rodnick

2004

“…For example, while the decline of heart rate and cardiac contractility has previously been attributed to altered ionic trans-membrane ion conductance across the sarcolemma [owing to failing Na + channel function or a denaturation of Na + /K + -ATPase (Lennard and Huddart, 1991;Vornanen et al, 2014)], this may instead reflect an ATP limitation of Na + /K + -ATPase at high temperatures. Furthermore, impaired Na + /K + -ATPase activity may also lead to a reduced influx of K + , causing extracellular hyperkalemia, which further impairs myocardial conductivity, rhythmicity and contractility of hearts from fish and other ectotherms (Chapman and Rodrigo, 1987;Hove-Madsen and Gesser, 1989;Kalinin and Gesser, 2002;Nielsen and Gesser, 2001).…”

Section: Physiological Implications Of Reduced Oxidative Capacity In mentioning

confidence: 99%

Thermal sensitivity and phenotypic plasticity of cardiac mitochondrial metabolism in European perch, Perca fluviatilis

Ekström

Sandblom

Blier

et al. 2016

Cellular and mitochondrial metabolic capacity of the heart has been suggested to limit performance of fish at warm temperatures. We investigated this hypothesis by studying the effects of acute temperature increases (16, 23, 30, 32.5 and 36°C) on the thermal sensitivity of 10 key enzymes governing cardiac oxidative and glycolytic metabolism in two populations of European perch (Perca fluviatilis) field-acclimated to 15.5 and 22.5°C, as well as the effects of acclimation on cardiac lipid composition. In both populations of perch, the activity of glycolytic ( pyruvate kinase and lactate dehydrogenase) and tricarboxylic acid cycle ( pyruvate dehydrogenase and citrate synthase) enzymes increased with acute warming. However, at temperatures exceeding 30°C, a drastic thermally induced decline in citrate synthase activity was observed in the cold-and warmacclimated populations, respectively, indicating a bottleneck for producing the reducing equivalents required for oxidative phosphorylation. Yet, the increase in aspartate aminotransferase and malate dehydrogenase activities occurring in both populations at temperatures exceeding 30°C suggests that the malate-aspartate shuttle may help to maintain cardiac oxidative capacities at high temperatures. Warm acclimation resulted in a reorganization of the lipid profile, a general depression of enzymatic activity and an increased fatty acid metabolism and oxidative capacity. Although these compensatory mechanisms may help to maintain cardiac energy production at high temperatures, the activity of the electron transport system enzymes, such as complexes I and IV, declined at 36°C in both populations, indicating a thermal limit of oxidative phosphorylation capacity in the heart of European perch.

“…In Series II, twitch force and maximal rate of contraction were determined as previously described (Hove-Madsen and Gesser, 1989).…”

Section: Calculations and Statisticsmentioning

confidence: 99%

Intrinsic autoregulation of cardiac output in rainbow trout(Oncorhynchus mykiss) at different heart rates

Altimiras

Axelsson

2004

SUMMARYIntrinsic regulation of the heart in teleosts is partly driven by central venous pressure, which exerts a modulatory role on stroke volume according to the well-known Frank-Starling mechanism. Although this mechanism is well understood from heart perfusion studies, less is known about how this mechanism operates in vivo, where heart rate varies markedly. We used zatebradine, a bradycardic agent, to attain resting heart rates in surgically instrumented animals. A dose of zatebradine of 2.79±0.47 mg l-1 decreased heart rate by half, from 44.4±4.19 beats min-1 to 22.1±1.9 beats min-1. Zatebradine had no significant effect on the peripheral vasculature and no inotropic effects, so was a suitable pharmacological agent with which to manipulate heart rate. When heart rate halved, cardiac output dropped to 87.5±4.6% of the control value, due to the concomitant increase in stroke volume to 165±13%. In vivo recordings of venous pressure at varying heart rates indicated that the partial compensation in cardiac output was possible through an increase in pressure in the sinus venosus, from -0.06±0.04 kPa at a control heart rate of 58.3±3.5 beats min-1 (N=10)to 0.07±0.05 kPa after injection of zatebradine (4 mg kg-1). The operation of the so-called time-dependent autoregulatory mechanism was further demonstrated in perfused hearts. The positive pressures recorded in the sinus venosus at low heart rates coincident with non-invasive measurements in trout suggest that atrial filling in trout is more dependent on the build-up of pressure in the venous circulation (vis-à-tergofilling) than a suction mechanism during ventricular contraction(vis-à-fronte filling).