The Interaction between Flow-Induced Vasoconstriction and Vasodilation: A Mechanism for Setting the Level of Vascular Tone

Bevan, John A.

doi:10.1007/978-1-4615-2397-0_22

Cited by 1 publication

(3 citation statements)

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“…Most previous studies have demonstrated that intralumenal flow causes vasodilatation by increasing the production of endothelium‐derived prostacyclin and NO (Holtz et al , 1984; Frangos et al , 1985; Roller & Kaley, 1990; Kanai et al , 1995). However, vasoconstrictor responses to flow have also been observed in several arteries of the rabbit including ear, pial and pulmonary arteries (Bevan & Joyce, 1988; Garcia‐Rolden & Bevan, 1990; Bevan, 1993). Because flowinduced contraction in ear arteries was still observed following endothelial removal, it has been assumed that flow‐induced contraction is an endothelium‐independent event (Bevan, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…However, vasoconstrictor responses to flow have also been observed in several arteries of the rabbit including ear, pial and pulmonary arteries (Bevan & Joyce, 1988; Garcia‐Rolden & Bevan, 1990; Bevan, 1993). Because flowinduced contraction in ear arteries was still observed following endothelial removal, it has been assumed that flow‐induced contraction is an endothelium‐independent event (Bevan, 1993). However, at least for porcine isolated small pulmonary arteries, this constriction is endotheliumdependent and is mediated by increased production of superoxide radicals.…”

Section: Discussionmentioning

confidence: 99%

“…Gaine et al , 1997). Indeed, a previous preliminary study demonstrated that intralumenal flow caused vasoconstriction, not vasodilatation, of small pulmonary arteries (Bevan, 1993). The present experiments were, therefore, performed to assess the response of small porcine pulmonary arteries to flow and to determine the cellular mechanisms and potential mediators involved in the response.…”

Section: Introductionmentioning

confidence: 99%

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Superoxide and endothelium‐dependent constriction to flow in porcine small pulmonary arteries

Wiener

Flavahan

1998

British J Pharmacology

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1 The aim of this study was to determine the response of porcine small pulmonary arteries to intralumenal ow and to identify the cellular mechanisms and potential mediators involved in the response. 2 Porcine small pulmonary arteries were isolated from a branch of the main intrapulmonary artery of the lower lung lobe and studied in a perfusion myograph system that allowed independent control of transmural pressure and intralumenal¯ow. At a transmural pressure of 20 mmHg, the baseline internal diameter (BID) of the arteries was 251.2+16.1 mm (n=16). 3 Under quiescent conditions or during constriction with U46619 to *60% of BID, intralumenal¯ow caused reversible constriction in arteries with endothelium (in the presence of U46619,¯ow decreased diameter from 60.0+2.5% to 49.5+3.0% BID at 10 ml min 71 , n=16, P50.05) but no change in diameter of arteries without endothelium. 4 In the presence of superoxide dismutase (SOD, 150 u ml 71 ), the response to¯ow was converted from constriction to vasodilatation (in presence of U46619 and SOD,¯ow increased diameter from 54.2+3.4% to 76.7+4.5% BID at 10 ml min 71 , n=10, P50.05). Inhibition of NO synthase with L-NAME (3610 75 M) abolished the¯ow-induced vasodilatation occurring in the presence of SOD and thē ow-induced constriction occurring in the absence of SOD. In arteries with endothelium, L-NAME (3610 75 M) caused signi®cant vasoconstriction, whereas SOD did not alter vasomotor tone. 5 Acetylcholine (10 78 to 10 76 M) caused endothelium-dependent relaxation of small pulmonary arteries that was not signi®cantly a ected by SOD (150 u ml 71 ) but was inhibited by L-NAME (3610 75 M).6 These results suggest that in small, porcine, isolated pulmonary arteries, intralumenal¯ow increases the production of NO but this is obscured by the generation of superoxide which causes vasoconstriction.

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