Picture of sea vessel plough through rough maritime conditions

Innovations in marine technology, pioneered through Open Access research...

Strathprints makes available scholarly Open Access content by researchers in the Department of Naval Architecture, Ocean & Marine Engineering based within the Faculty of Engineering.

Research here explores the potential of marine renewables, such as offshore wind, current and wave energy devices to promote the delivery of diverse energy sources. Expertise in offshore hydrodynamics in offshore structures also informs innovations within the oil and gas industries. But as a world-leading centre of marine technology, the Department is recognised as the leading authority in all areas related to maritime safety, such as resilience engineering, collision avoidance and risk-based ship design. Techniques to support sustainability vessel life cycle management is a key research focus.

Explore the Open Access research of the Department of Naval Architecture, Ocean & Marine Engineering. Or explore all of Strathclyde's Open Access research...

Agonist-evoked Ca2+ wave progression requires Ca2+ and IP3

McCarron, J.G. and Chalmers, S. and MacMillan, D. and Olson, M.L. (2010) Agonist-evoked Ca2+ wave progression requires Ca2+ and IP3. Journal of Cellular Physiology, 224 (2). pp. 334-344. ISSN 0021-9541

Full text not available in this repository. Request a copy from the Strathclyde author

Abstract

Smooth muscle responds to IP3-generating agonists by producing Ca2+ waves. Here, the mechanism of wave progression has been investigated in voltage-clamped single smooth muscle cells using localized photolysis of caged IP3 and the caged Ca2+ buffer diazo-2. Waves, evoked by the IP3-generating agonist carbachol (CCh), initiated as a uniform rise in cytoplasmic Ca2+ concentration ([Ca2+]c) over a single though substantial length (∼30 µm) of the cell. During regenerative propagation, the wave-front was about 1/3 the length (∼9 µm) of the initiation site. The wave-front progressed at a relatively constant velocity although amplitude varied through the cell; differences in sensitivity to IP3 may explain the amplitude changes. Ca2+ was required for IP3-mediated wave progression to occur. Increasing the Ca2+ buffer capacity in a small (2 µm) region immediately in front of a CCh-evoked Ca2+ wave halted progression at the site. However, the wave front does not progress by Ca2+-dependent positive feedback alone. In support, colliding [Ca2+]c increases from locally released IP3 did not annihilate but approximately doubled in amplitude. This result suggests that local IP3-evoked [Ca2+]c increases diffused passively. Failure of local increases in IP3 to evoke waves appears to arise from the restricted nature of the IP3 increase. When IP3 was elevated throughout the cell, a localized increase in Ca2+ now propagated as a wave. Together, these results suggest that waves initiate over a surprisingly large length of the cell and that both IP3 and Ca2+ are required for active propagation of the wave front to occur.