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

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 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.

Aging and total stenosis triggers differential responses of carotid and basilar arteries to endothelin-1 and phenylephrine

“…Our findings are in agreement with previous studies describing reduced contraction for several agonists such as endothelin-1, phenylephrine and angiotensin II in injured arteries (Milner et al, 1997;Accorsi-Mendonça et al, 2004;Fukada et al, 2004a;2004b).…”

“…The increased response of the right carotid artery is in accordance with previous observations from our laboratory showing that vascular injury caused by balloon catheter increased phenylephrineinduced contraction in the contralateral arteries (Accorsi-Mendonça et al, 2004). These results indicate that there may be compensatory mechanisms in the contralateral artery that are activated after vascular injury.…”

“…Animal models of vascular occlusive diseases (Kennedy et al, 2006), as well as models of vascular injury (Milner et al, 1997;Accorsi-Mendonça et al, 2004;Fukada et al, 2004a;2004b), are associated with reduced contractility of the injured artery to catecholamines and angiotensin II. Interestingly, the effects of stenosis on the vascular responses to KCl were reported to be tissue and age-dependent (Asano et al, 1993).…”

Rosiglitazona e lesão vascular em coelhos hipercolesterolêmicos: avaliação da formação neointimal

“…Therefore, a more thorough understanding of all mechanisms implicated in the metabolism of RGZ is essential. Local and systemic changes in the vascular bed after catheter balloon injury have been widely described in the literature 7,8 . There have been reports that vascular injury can cause changes in healthy tissues at locations distant from the injury site.…”

Mecanismos celulares que influenciam a sinalização por receptores 1-adrenérgicos na carótida contra-lateral à lesão por cateter balão

“…As alterações celulares que interferem na sinalização por receptores adrenérgicos na carótida contra-lateral à lesão não estão relacionadas a fatores humorais, mas são decorrentes da resposta neurocompensatória ativada pela lesão por cateter balão (ACCORSI-MENDONÇA et al, 2004).…”