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Articles in PresS, published online ahead of print August 22, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00634.2002
Submitted on July 22, 2002
Accepted on August 14, 2002
1 Department of Obstetrics and Gynecology, University of Vermont College of Medicine, Burlington, Vermont, USA
2 Department of Physiology, University of Bergen, Bergen, Norway
* To whom correspondence should be addressed. E-mail: gosol{at}zoo.uvm.edu.
Myogenic behavior, prevalent in resistance arteries and arterioles, involves the generation of force by vascular smooth muscle (VSM) in response to intravascular pressure. This process is often studied in vitro, using cannulated, pressurized arterial segments from different regional circulations. We propose a comprehensive model for myogenicity that consists of three interrelated but dissociable phases: (1) the initial development of myogenic tone [MT], (2) myogenic reactivity to subsequent changes in pressure [MR] and (3) forced dilatation at high transmural pressures [FD]. The three phases span the physiological range of transmural pressures (e.g., in cerebral arteries: MT: 40-60 mmHg; MR: 60-140 mmHg; FD: >140 mmHg), and are characterized by distinct changes in cytosolic calcium ([Ca2+]i) that do not parallel arterial diameter or wall tension, and therefore suggest the existence of additional regulatory mechanisms. Specifically, the development of MT is accompanied by a substantial (200%) elevation in [Ca2+]i concentrations and a reduction in lumen diameter and wall tension, whereas MR is associated with relatively small [Ca2+]i increments (<20% over the entire pressure range) in spite of considerable increases in wall tension and force production, but little or no change in diameter. FD is characterized by a significant additional elevation in [Ca2+]i (>50%), complete loss of force production and a rapid increase in wall tension. The utility of this model is that it provides a framework for comparing myogenic behavior of vessels of different size and anatomic origin, and for investigating the underlying cellular mechanisms that govern VSM mechanotransduction, and contribute to the regulation of peripheral resistance.
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