Blood flow control in skeletal muscle achieves very close coupling between flow and the metabolism of the tissue. Integration of control is achieved by several means. There are differences in response capacity to many stimuli between large and small arterioles. Communication of signals among the cells of the arteriolar wall, both axially and between SMCs and ECs, enables the vessel and network to respond as a coordinated whole. Ascending flow-dependent dilation has also been identified as a mechanism supporting rapid modulation of the inflow to the tissue. Cellular signaling mechanisms underlying these responses are still being worked out: In addition to roles for such metabolically related substances as oxygen and adenosine, contributions from NO, and one or more EDHFs, have been identified. A role for KATP channels is strongly indicated, but where in the signaling cascade these channels contribute to the response is not clear.
Arcading arteriolar system: Arterioles that form a continuous loop from which smaller arterioles branch, in contrast to a bifurcating arteriolar system, in which an arteriole diverges into two smaller branches.
Gap-junction communication: Transfer of signals between the cytosols of two adjacent cells via a channel in their membranes.
NOS: Nitric oxide synthase, the enzyme responsible for production of nitric oxide. (eNOS is an isoform found in endothelial cells; nNOS, an isoform found in skeletal muscle.)
Transmural wall stress: The (normalized) tension in the vessel wall that resists the pressure exerted by the blood in the vessel lumen.
Bolz, S. S., Fissithaler, B., Pieperhoff, S., De Wit, C., Fleming, I., Busse, R., and Pohl, U. (2000). Antisense oligonucleotides against cytochrome P450 2C8 attenuate EDHF mediated Ca2+ changes and dilation in isolated resistance arteries. FASEB J. 14, 255-260.
Dora, K. A. (2001). Intercellular Ca2+ signalling: The artery wall. Semin. Cell. Dev. Biol. 12, 27-35. A good current source of how Ca2+ signaling is involved in communicated responses in the walls of larger arte-rioles and small arteries.
Gorczynski, R. J., and Duling, B. R. (1978). Role of oxygen in arteriolar functional vasodilation in hamster striated muscle. Am. J. Physiol. 235, H505-H515. This is included because it is a very elegant study showing direct coupling between skeletal muscle contraction and arteriolar responses.
Lash, J. M. (1996). Regulation of skeletal muscle blood flow during contractions. Proc. Soc. Exp. Biol. Med. 211, 218-235. A comprehensive review.
Laughlin, M. H., and Korzick, D. H. (2001). Vascular smooth muscle: Integrator of vasoactive signals during exercise hyperemia. Med. Sci. Sports. Exerc. 33, 81-91. Another comprehensive review with a different emphasis than the Lash review.
Murrant, C. L., and Sarelius, I. H. (2000). Coupling of muscle metabolism and muscle blood flow in capillary units during contraction. Acta Phys-iol. Scand. 168, 531-541.
Segal, S. S., Damon, D. N., and Duling, B. R. (1989). Propagation of vasomotor responses coordinates arteriolar resistances. Am. J. Physiol. 256, H832-H837.
Segal, S. S., and Jacobs, T. L. (2001). Role for endothelial cell conduction in ascending vasodilatation and exercise hyperaemia in hamster skeletal muscle. J. Physiol. (London) 536, 937-946.
Dr. Sarelius is a Professor of Pharmacology and Physiology and of Biomedical Engineering at the University of Rochester. Her laboratory focuses on cell communication in the arteriolar wall, and on signaling between blood cells (primarily leukocytes) and the microvessel wall. Her work is supported by grants from the National Institutes of Health.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...