1995
DOI: 10.1111/j.1476-5381.1995.tb14911.x
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Cytochrome P450‐dependent effects of bradykinin in the rat heart

Abstract: 1 Vasodilator responses to bradykinin (BK) in the rat heart are reported to be independent of NO and cyclo-oxygenase/lipoxygenase products of arachidonic acid (AA).2 We verified that inhibition of NO synthase with L-nitroarginine (50 [LM) and cyclo-oxygenase with indomethacin (2.8 AM) were without effect on vasodilator responses to BK (10-1000 ng) in the Langendorff rat heart preparation. 3 L-Nitroarginine elevated perfusion pressure, signifying a crucial role of NO in the maintenance of basal vasculature to… Show more

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Cited by 112 publications
(77 citation statements)
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References 19 publications
(25 reference statements)
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“…This finding contrasts, however, with observations made in other test systems. For example, in the rat isolated perfused heart, 17-ODYA (at a concentration of only 2 gM) inhibited the bradykinin-induced vasodilator responses, which were possibly mediated by EDHF (Fulton et al, 1995). Furthermore, EETs are reported to relax blood vessels from several vascular regions (Pfister et al, 1991;Gebremedhin et al, 1992;Rosolowsky & Campbell, 1993;Hecker et al, 1994).…”
Section: Discussionmentioning
confidence: 99%
“…This finding contrasts, however, with observations made in other test systems. For example, in the rat isolated perfused heart, 17-ODYA (at a concentration of only 2 gM) inhibited the bradykinin-induced vasodilator responses, which were possibly mediated by EDHF (Fulton et al, 1995). Furthermore, EETs are reported to relax blood vessels from several vascular regions (Pfister et al, 1991;Gebremedhin et al, 1992;Rosolowsky & Campbell, 1993;Hecker et al, 1994).…”
Section: Discussionmentioning
confidence: 99%
“…We have considerable evidence for a major cytochrome P450-dependent component to the response (Fulton et al, 1992), presumably via metabolism of arachidonic acid as bradykinin stimulates phospholipase C and A2. Indeed, in the rat perfused heart in which the vasodilator effect of bradykinin is independent of NO (Baydoun & Woodward, 1991;Fulton et al, 1995a) inhibitors of phospholipase C and A2 inhibit the effects of bradykinin (Fulton et al, 1995b) supporting a role for arachidonic acid metabolism. As inhibitors of cyclo-oxygenase and lipoxygenase did not affect the coronary vasodilator actions of bradykinin (Baydoun & Woodward, 1991), a role for cytochrome P450 was investigated (Fulton et al, 1995a).…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, in the rat perfused heart in which the vasodilator effect of bradykinin is independent of NO (Baydoun & Woodward, 1991;Fulton et al, 1995a) inhibitors of phospholipase C and A2 inhibit the effects of bradykinin (Fulton et al, 1995b) supporting a role for arachidonic acid metabolism. As inhibitors of cyclo-oxygenase and lipoxygenase did not affect the coronary vasodilator actions of bradykinin (Baydoun & Woodward, 1991), a role for cytochrome P450 was investigated (Fulton et al, 1995a). Thus, several inhibitors of cytochrome P450, including 17-ODYA, a mechanism based inhibitor of long chain fatty acid metabolism by cytochrome P450, all attenuated coronary vasodilatation to bradykinin (Fulton et al, 1995a).…”
Section: Discussionmentioning
confidence: 99%
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“…10). Several studies have implicated EETs in the EDHF-like response to bradykinin (12,13,19), and the vasodilator actions of 11,12 EET on the afferent arteriole are blocked by 1 mmol/l TEA (20,45). Thus a model in which bradykinin stimulates the release of an EET, whose formation can be prevented by 17-ODYA and whose smooth muscle vasodilator actions can be blocked by TEA, could explain the bradykinin response (see Ref.…”
Section: Discussionmentioning
confidence: 99%