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First published online May 1, 2006
Journal of Experimental Biology 209, 1956-1963 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02228

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

Gina L. J. Galli^1,2,3,*, Hans Gesser¹, Edwin W. Taylor², Holly A. Shiels³ and Tobias Wang¹

¹ Department of Zoophysiology, Aarhus University, Building 131, 8000 Aarhus C, Denmark
² School of Biosciences, The University of Birmingham, Edgbaston, Birmingham, B19 2TT, UK
³ Faculty of Life Sciences, The University of Manchester, 48 Grafton Street, Manchester, M13 9NT, UK

^* Author for correspondence at address 3 (e-mail: ginaljgalli{at}hotmail.com)

Accepted 21 March 2006

The functional significance of the sarcoplasmic reticulum (SR) in the generation of high heart rates and blood pressures was investigated in four species of reptile; the turtle, Trachemys scripta; the python, Python regius, the tegu lizard, Tupinanvis merianae, and the varanid lizard, Varanus exanthematicus. Force-frequency trials and imposed pauses were performed on ventricular and atrial tissue from each species with and without the SR inhibitor ryanodine, and in the absence and presence of adrenaline. In all species, an imposed pause of 1 or 5 min caused a post-rest decay of force, and a negative force-frequency response was observed in all species within their in vivo frequency range of heart rates. These relationships were not affected by either ryanodine or adrenaline. In ventricular strips from varanid lizards and pythons, ryanodine caused significant reductions in twitch force within their physiologically relevant frequency range. In atrial tissue from the tegu and varanid lizards, SR inhibition reduced twitch force across the whole of their physiological frequency range. In contrast, in the more sedentary species, the turtle and the python, SR inhibition only decreased twitch force at stimulation frequencies above maximal in vivo heart rates. Adrenaline caused an increase in twitch force in all species studied. In ventricular tissue, this positive inotropic effect was sufficient to overcome the negative effects of ryanodine. In atrial tissue however, adrenaline could only ameliorate the negative effects of ryanodine at the lower pacing frequencies. Our results indicate that reptiles recruit Ca²⁺ 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.

Key words: snake, lizard, turtle, trabeculae, ryanodine, adrenaline

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