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(Circulation Research. 2003;93:9.)
© 2003 American Heart Association, Inc.

Editorials

Bobbing Along on the Crest of a Wave

NO Ascends Hamster Cheek Pouch Arterioles

Ingrid Fleming

From the Institut für Kardiovaskuläre Physiologie, Klinikum der J.W.Goethe-Universität, Frankfurt am Main, Germany.

Correspondence to Ingrid Fleming, Institut für Kardiovaskuläre Physiologie, Klinikum der J.W.Goethe-Universität, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany. E-mail fleming@em.uni-frankfurt.de

Key Words: gap junctional communication • microcirculation • endothelium-derived hyperpolarizing factor • Ca²⁺ signaling

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The resistance network that controls blood flow to skeletal muscle comprises terminal arterioles, as well as larger arterioles and the small (feeder) arteries from which they derive. For example, in a contracting skeletal muscle, low PO₂ and vasoactive metabolites elicit a local response and initiate a conducted vasodilatation that "ascends" the vascular tree to induce the simultaneous vasodilatation of the feed arteries as well as branch arteries and thus increase blood flow. This coordinated longitudinal transmission of vasomotor responses is essential to achieve optimal organ perfusion.¹

Experimentally, ascending dilatation can be studied in vivo and in vitro by assessing the response to a vasoactive substance at the point of application (local response) as well as at a remote site, usually 0.5 to 2 mm upstream of the local site. This conducted vasodilatation can travel bidirectionally, but upstream sites are generally chosen since the vasoactive compounds applied in superfused systems are unable to directly affect upstream sites. The amplitude of the conducted vasodilatation is generally smaller than that of the local response and although there is a gradual decline in the conducted vasodilatation along some arterioles, there is no obvious decay of the conducted response along feed arteries.

Conducted responses have been intensively investigated and although the exact mechanism remains to be clarified, most researchers agree that nitric oxide (NO) does not play a major role in this response. Indeed, conducted vasodilatation in response to a number of stimuli is not affected by NO synthase (NOS) inhibitors,^2–4 and the response . . . [Full Text of this Article]

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