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Comparative Study
. 2004 May;142(1):79-88.
doi: 10.1038/sj.bjp.0705732. Epub 2004 Mar 22.

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

D Accorsi-Mendonça  1 , F M A Corrêa, T B Paiva, H P de Souza, F R M Laurindo, A M de Oliveira
Affiliations
Comparative Study

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

D Accorsi-Mendonça et al. Br J Pharmacol. 2004 May.

Abstract

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 microm indomethacin, 500 microm valeryl salicylate or 0.1 microm 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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Figures

Figure 1
Figure 1
(a) Phe concentration–effect curves from control carotid arteries and contralateral and ipsilateral arteries 4 and 7 days after the injury; (b) Emax values (g) for Phe obtained in control, contralateral and ipsilateral carotid arteries (2, 4, 7, 15, 30 and 45 days after the injury). One-way ANOVA followed by Bonferroni's post test, P<0.05, *significantly different from control group.
Figure 2
Figure 2
(a) Ang II concentration–effect curves from control carotid arteries and contralateral and ipsilateral carotid arteries taken 15 and 30 days after the injury; (b) Ang II Emax values (g) from control, contralateral and ipsilateral arteries (2, 4, 7, 15, 30 and 45 days after the injury). One-way ANOVA followed by Bonferroni's post test, P<0.05, *significantly different from control group.
Figure 3
Figure 3
KCL-induced contraction (90 mM) in isolated carotid from control or injured animals killed 15 days after the injury. One-way ANOVA (not significant).
Figure 4
Figure 4
(a) Phe Emax (g) in aorta rings from control or operated rats 4 and 7 days after the injury in carotid artery. One-way ANOVA: not significant. (b) Ang II Emax (g) in aorta rings from control or operated rats 15 and 30 days after the injury in carotid artery. One-way ANOVA: not significant.
Figure 5
Figure 5
Carotid blood flow (ml min−1) in control, contralateral or ipsilateral arteries (2, 4, 7, 15, 30 and 45 days after the injury). One-way ANOVA followed by Bonferroni's post test, P<0.05, * significantly different from control group.
Figure 6
Figure 6
Resting potential membrane (mV) of control, contralateral or ipsilateral arteries (2, 4, 7, 15, 30 and 45 days after the injury). One-way ANOVA followed by Bonferroni's post test, P<0.05, * significantly different from control group.
Figure 7
Figure 7
(a) Phe Emax (g) of control or contralateral (4 and 7 days after the injury) arteries with or without endothelium; (b): Ang II Emax (g) of control or contralateral (15 and 30 days after the injury) arteries with or without endothelium. Unpaired ‘t' test, P<0.05, *significantly different from respective group with endothelium.
Figure 8
Figure 8
Coelenterazine chemiluminescence's response (cpm mg.dry weight−1 min−1) in control or contralateral carotid arteries 4, 7, 15 or 30 days after the injury. One-way ANOVA: not significant.
Figure 9
Figure 9
Effect of indomethacin (10 μM) on Emax of Phe (a) or Ang II (b) in control or contralateral arteries. Unpaired ‘t' test, P<0.05, *significantly different from respective group in the absence of inhibitor.
Figure 10
Figure 10
Effect of valeryl salicylate (500 μM) or celecoxib (0.1 μM) on Emax of Phe(a) or Ang II (b) in control or contralateral arteries. Unpaired ‘t' test, P<0.05, *significantly different from respective group in the absence of inhibitor.
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