The role of the sarcoplasmic reticulum in the generation of high heart rates and blood pressures in reptiles

Galli, Gina L. J.; Gesser, H.; Taylor, E. W.; Shiels, Holly A.; Wang, Tobias

doi:10.1242/jeb.02228

Cited by 45 publications

(46 citation statements)

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“…Recently, we have shown isolated turtle ventricular muscle to be relatively insensitive to ryanodine, a compound that inhibits the SR Ca 2ϩ release channel. These results suggest that, similar to fish, the SR contributes little Ca 2ϩ to turtle heart contraction and relaxation (12). In the absence of a functional SR, we would hypothesize that sarcolemmal Ca 2ϩ transport is the primary source of Ca 2ϩ and that the NCX is the primary Ca 2ϩ efflux pathway.…”

Section: ϩmentioning

confidence: 80%

“…The cardiac muscle of many ectothermic species, including the turtle, are ryanodine insensitive and exhibit a postrest decay of force, suggesting SR independence, at least under normal physiological conditions (10,12,17,41). In the present study, we tested SR involvement in cellular Ca 2ϩ flux directly, and we show that inhibition of SR function with a combination of ryanodine and thapsigargin had little effect on [Ca 2ϩ ] i in turtle ventricular myocytes, supporting earlier findings on isolated muscle preparations (12). Thus, in the absence of a functional SR, the turtle heart will depend strongly on transsarcolemmal Ca 2ϩ cycling for both the contraction and relaxation of the myocyte.…”

Section: Discussionmentioning

confidence: 99%

“…The majority of this extracellular Ca 2ϩ enters the cell through L-type Ca 2ϩ channels, although in some species, the NCX may also contribute significant amounts of activator Ca 2ϩ (19,34,42). The contribution of intracellular Ca 2ϩ cycling through the sarcoplasmic reticulum (SR) is minimal in most ectothermic vertebrates and varies subject to experimental conditions (6,12,13,21,31). In contrast, activation of the myofilaments in most adult mammalian hearts occurs mainly through the mobilization of the intracellular Ca 2ϩ stores of the SR, with sarcolemmal Ca 2ϩ influx primarily acting as a trigger for SR Ca 2ϩ release (6).…”

Section: ϩmentioning

confidence: 99%

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Calcium flux in turtle ventricular myocytes

Galli

Taylor²,

Shiels³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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The relative contribution of the sarcoplasmic reticulum (SR), the L-type Ca2+ channel and the Na+/Ca2+ exchanger (NCX) were assessed in turtle ventricular myocytes using epifluorescent microscopy and electrophysiology. Confocal microscopy images of turtle myocytes revealed spindle-shaped cells, which lacked T-tubules and had a large surface area-to-volume ratio. Myocytes loaded with the fluorescent Ca2+-sensitive dye Fura-2 elicited Ca2+ transients, which were insensitive to ryanodine and thapsigargin, indicating the SR plays a small role in the regulation of contraction and relaxation in the turtle ventricle. Sarcolemmal Ca2+ currents were measured using the perforated-patch voltage-clamp technique. Depolarizing voltage steps to 0 mV elicited an inward current that could be blocked by nifedipine, indicating the presence of Ca2+ currents originating from L-type Ca2+ channels (ICa). The density of ICa was 3.2 ± 0.5 pA/pF, which led to an overall total Ca2+ influx of 64.1 ± 9.3 μM/l. NCX activity was measured as the Ni+-sensitive current at two concentrations of intracellular Na+ (7 and 14 mM). Total Ca2+ influx through the NCX during depolarizing voltage steps to 0 mV was 58.5 ± 7.7 μmol/l and 26.7 ± 3.2 μmol/l at 14 and 7 mM intracellular Na+, respectively. In the absence of the SR and L-type Ca2+ channels, the NCX is able to support myocyte contraction independently. Our results indicate turtle ventricular myocytes are primed for sarcolemmal Ca2+ transport, and most of the Ca2+ used for contraction originates from the L-type Ca2+ channel.

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Section: ϩmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: ϩmentioning

confidence: 99%

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Calcium flux in turtle ventricular myocytes

Galli

Taylor²,

Shiels³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Adrenergic stimulation increases Ca 2+ currents through L-type Ca 2+ -channels in the sarcolemma and thereby exerts a positive inotropic effect (Bers, 1991;Bers, 2002). Indeed, adrenergic stimulation increases the duration of the action potential in turtles, although this was only significant when the action potential had previously been compromised by hyperkalemia (Nielsen and Gesser, 2001), and adrenaline increases twitch force in ventricular strips from Trachemys (Ball and Hicks, 1996;Nielsen and Gesser, 2001;Overgaard et al, 2005;Galli et al, 2006a). These effects are consistent with the rise in stroke volume, which occur upon adrenergic stimulation in vivo (Overgaard et al, 2002;Hicks and Wang, 1998).…”

Section: +mentioning

confidence: 99%

Tribute to P. L. Lutz: cardiac performance and cardiovascular regulation during anoxia/hypoxia in freshwater turtles

Overgaard

Gesser

Wang

2007

Journal of Experimental Biology

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SUMMARY Freshwater turtles overwintering in ice-covered ponds in North America may be exposed to prolonged anoxia, and survive this hostile environment by metabolic depression. Here, we review their cardiovascular function and regulation, with particular emphasis on the factors limiting cardiac performance. The pronounced anoxia tolerance of the turtle heart is based on the ability to match energy consumption with the low anaerobic ATP production during anoxia. Together with a well-developed temporal and spatial energy buffering by creatine kinase, this allows for cellular energy charge to remain high during anoxia. Furthermore, the turtle heart is well adapted to handle the adverse effects of free phosphate arising when phosphocreatine stores are used. Anoxia causes tenfold reductions in heart rate and blood flows that match the metabolic depression, and blood pressure is largely maintained through increased systemic vascular resistance. Depression of the heart rate is not driven by the autonomic nervous system and seems to arise from direct effects of oxygen lack and the associated hyperkalaemia and acidosis on the cardiac pacemaker. These intra- and extracellular changes also affect cardiac contractility, and both acidosis and hyperkalaemia severely depress cardiac contractility. However, increased levels of adrenaline and calcium may, at least partially, salvage cardiac function under prolonged periods of anoxia.

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“…The phenomenon is primarily attributed to reduced cardiac filling time and pressure (preload pressure) at high contraction frequencies (Markwalder and Starling, 1914;Altimiras and Axelsson, 2004). Heart rate is further entwined with myocardial contractility through the 'force-frequency' effect, which describes the rate-dependent change in myocardial force production that may be negative, positive or flat, and varies between species (Shiels et al, 2002;Galli et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Autoregulation of cardiac output is overcome by adrenergic stimulation in the anaconda heart

Joyce

Axelsson

Wang

2016

Journal of Experimental Biology

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Most vertebrates increase cardiac output during activity by elevating heart rate with relatively stable stroke volume. However, several studies have demonstrated 'intrinsic autoregulation' of cardiac output where artificially increased heart rate is associated with decreased stroke volume, leaving cardiac output unchanged. We explored the capacity of noradrenaline to overcome autoregulation in the anaconda heart. Electrically pacing in situ perfused hearts from the intrinsic heart rate to the maximum attainable resulted in a proportional decrease in stroke volume. However, noradrenaline, which increased heart rate to the same frequency as pacing, maintained stroke volume and thus increased cardiac output. In atrial and ventricular preparations, noradrenaline significantly increased the force of contraction and contraction kinetics. Thus, the increased contractility associated with adrenergic stimulation ameliorates filling limitations at high heart rates. Although heart rate appears the primary regulated variable during activity, this may only be achieved with compensatory amendments in myocardial contractility provided by adrenergic stimulation.

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The role of the sarcoplasmic reticulum in the generation of high heart rates and blood pressures in reptiles

Abstract: 2+from the SR for force development in a frequency and tissue dependent manner. This is discussed in the context of the development of high reptilian heart rates and blood pressures.

Cited by 45 publications

References 45 publications

Calcium flux in turtle ventricular myocytes

Calcium flux in turtle ventricular myocytes

Tribute to P. L. Lutz: cardiac performance and cardiovascular regulation during anoxia/hypoxia in freshwater turtles

Autoregulation of cardiac output is overcome by adrenergic stimulation in the anaconda heart

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