Functional evidence that balloon angioplasty results in transient nitric oxide synthase induction

Douglas, Stephen A.; Vickery-Clark, Lynne M.; Ohlstein, Eliot H.

doi:10.1016/0014-2999(94)90085-x

Cited by 26 publications

(8 citation statements)

References 23 publications

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“…The balloon injury did not interfere with the intrinsic contractility of muscle cells since the maximal responses to a high potassium concentration were not influenced by balloon catheter, as previously described by Douglas et al (1994) and Lemay et al (2000).…”

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjusupporting

confidence: 56%

“…This effect may be the consequence of an increased production of inducible nitric oxide in the ipsilateral vessel wall, as suggested by several studies (Major et al, 1985;Joly et al, 1992;Douglas et al, 1994;Hansson et al, 1994). The decreased response to Phe could also be related to the desensitisation to exogenous ligands (Candipan et al, 1994), to a decrease in a1-adrenoceptors from day 3 up to 10 weeks after injury (Bruijns et al, 1998) or increased production of inducible nitric oxide in injured vessel (Major et al, 1985;Joly et al, 1992;Douglas et al, 1994;Hansson et al, 1994;Yan & Hansson, 1998).…”

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjumentioning

confidence: 82%

“…However, the endothelium injury-induced balloon caused an immediate increase in the endothelin-1 contractile potency and it could be related to an increase in affinity for the endothelin-1 receptor subtype mediating vasoconstriction, an increase in agonist bio-availability at this smooth muscle cell receptor or the loss of some type of physiological antagonism, an intrinsic mechanism which normally exists to selectively oppose the contractile actions of this peptide (Douglas et al, 1994). Hill coefficients from all curves were similar to unity, suggesting a homogeneous response and the positive cooperative phenomenon does not affect the response (Kenakin, 1996).…”

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjumentioning

confidence: 99%

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The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

Accorsi‐Mendonça¹,

Corrêa²,

Paiva

et al. 2004

British J Pharmacology

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1 The effects of balloon injury on the reactivity of ipsilateral and contralateral carotid arteries were compared to those observed in arteries from intact animals (control arteries). 2 Carotid arteries were obtained from Wistar rats 2, 4, 7, 15, 30 or 45 days after injury and mounted in an isolated organ bath. Reactivity to angiotensin II (Ang II), phenylephrine (Phe) and bradykinin (BK) was studied. Curves were constructed in the absence or presence of endothelium or after incubation with 10 mM indomethacin, 500 mM valeryl salicylate or 0.1 mM celecoxib. 3 Phe, Ang II and BK maximum effects (Emax) were decreased in ipsilateral arteries when compared to control arteries. No differences were observed among pD2 or Hill coefficient. 4 Emax to Phe (4 and 7 days) and to Ang II (15 and 30 days) increased in the contralateral artery. In addition, Phe or Ang II reactivity was not significantly different in aorta rings from control or carotid-injured animals. 5 The increased responsiveness of contralateral artery was not due to changes in carotid blood flow or resting membrane potential. The endothelium-dependent inhibitory component is not present in the contraction of contralateral arteries and it is not related to superoxide anion production. 6 Indomethacin decreased contralateral artery responsiveness to Phe and Ang II. Valeryl salicylate reduced the Ang II response in contralateral and control arteries. Celecoxib decreased the Phe Emax of contralateral artery. 7 In conclusion, decreased endothelium-derived factors and increased prostanoids appear to be responsible for the increased reactivity of contralateral arteries after injury.

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Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjusupporting

confidence: 56%

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjumentioning

confidence: 82%

Section: Accorsi-mendonc¸a Et Al Vascular Change In Distant Uninjumentioning

confidence: 99%

See 1 more Smart Citation

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

Accorsi‐Mendonça¹,

Corrêa²,

Paiva

et al. 2004

British J Pharmacology

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“…An individual ring preparation was used once to construct a single concentration-response curve. Concentration-response curves were analysed by fitting the experimental data to one of the following logistic equations by nonlinear least squares regression (Douglas et al, 1994c):…”

Section: Methodsmentioning

confidence: 99%

Pharmacological evidence for the presence of three distinct functional endothelin receptor subtypes in the rabbit lateral saphenous vein

Douglas

Beck

Elliott

et al. 1995

British J Pharmacology

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1 Contraction of the rabbit isolated saphenous vein is mediated by a heterogeneous endothelin (ET) receptor population. This study has characterized these receptor subtypes by use of several pharmacologically distinct ET receptor agonists and antagonists.2 ET-1, ET-3, sarafotoxin S6c (STXc) and [Ala3"']ET-1 produced biphasic, concentration-dependent contractions of the saphenous vein, responses which were best fitted by a two-site model comprised of a high (pM) and a low (nM) affinity site. In contrast, IRL 1620 only recognized one of these sites. ET(1621) was devoid of contractile activity. ET-1, ET-3 and STXc were equipotent at the high affinity site (pD2s of 12.0 ± 0.2, 12.2 ± 0.2 and 12.3 ± 0.3) indicating that this site had the characteristics of an ETB receptor. In contrast, the low affinity site had the functional characteristics of an ETc receptor since the pD2s for ET-3 (10.2 ± 0.3) and STXc (10.6 ± 0.3) were significantly greater than that for ET-l (9.1 ± 0.1). These contractile responses were insensitive to BQ-123, confirming that ETA receptors were not involved in mediating this effect.

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“…For example, in atherosclerosis ( vide supra ), the loss of endothelial cell NO production may be somewhat compensated for by the induction of novel isoforms of NOS within the vascular smooth muscle 64 . This is due to the local production of cytokines, as has been suggested to occur following destruction of the endothelium by balloon angioplasty 65 . Interestingly, exposure of the endothelium and vascular smooth muscle to the same cytokines increases the expression of ET‐1 66 , 67 .…”

Section: Nitric Oxide and Et‐1 Interactions In Disease Statesmentioning

confidence: 97%

Relationships Between the Endothelin and Nitric Oxide Pathways

Warner

1999

Clin Exp Pharma Physio

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1. In the normal blood vessel, the vascular endothelium regulates the tone of the underlying smooth muscle and the reactivity of blood elements, such as platelets and neutrophils, by the release of mediators, in particular nitric oxide (NO) and endothelin-1 (ET-1). 2. Nitric oxide is a potent vasodilator that also inhibits platelet and neutrophil aggregation and adhesion; ET-1 is the most potent mammalian vasoconstrictor peptide yet found. Recently, much research effort has focused on examining the interactions between these two important mediators. At a simple level, ET-1 acts on specific receptors on the endothelium to increase the release of NO, while NO depresses the production and/or release of ET-1 from endothelial cells. 3. While ET-1 appears to have a relatively small influence on the basal regulation of blood pressure, NO appears central. For example, inhibition of NO production in normotensive animals produces a marked elevation in blood pressure. 4. Conversely, numerous vascular disease states have been associated with elevations in the production and/or release of ET-1 and it has been implicated in the deleterious changes associated with ischaemia-reperfusion injury, subarachnoid haemorrhage and hypertension. In these conditions, NO production may also be increased by the induction of NO synthetic pathways within the vascular smooth muscle. Endothelin-1 may also be produced by the vascular smooth muscle under similar circumstances. 5. Therefore, in pathological states, a new balance between NO and ET-1 production may be central to changes in blood vessel reactivity, smooth muscle proliferation and blood coagulability.

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Functional evidence that balloon angioplasty results in transient nitric oxide synthase induction

Cited by 26 publications

References 23 publications

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine

Pharmacological evidence for the presence of three distinct functional endothelin receptor subtypes in the rabbit lateral saphenous vein

Relationships Between the Endothelin and Nitric Oxide Pathways

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