Abstract:
:Paclitaxel is a chemotherapeutic agent used to treat solid tumours. However, it causes an acute and neuropathic pain syndrome that limits its use. Among the mechanisms involved in neuropathic pain caused by paclitaxel is activation of kinin receptors. Angiotensin converting enzyme (ACE) inhibitors can enhance kinin receptor signalling. The goal of this study was to evaluate the role of kinins on paclitaxel-associated acute pain syndromes (P-APS) and the effect of ACE inhibition on P-APS and paclitaxel-associated chronic peripheral neuropathy (P-CPN) in mice. Herein, we show that paclitaxel caused mechanical allodynia and spontaneous nociceptive behaviour that was reduced by antagonists of kinin receptors B1 (DALBk and SSR240612) and B2 (Hoe140 and FR173657). Moreover, enalapril (an ACE inhibitor) enhanced the mechanical allodynia induced by a low dose of paclitaxel. Likewise, paclitaxel injection inhibited ACE activity and increased the expressions of B1 and B2 receptors and bradykinin-related peptides levels in peripheral tissue. Together, our data support the involvement of kinin receptors in the P-APS and suggest kinin receptor antagonists to treat this syndrome. Because hypertension is the most frequent comorbidity affecting cancer patients, treatment of hypertension with ACE inhibitors in patients undergoing paclitaxel chemotherapy should be reviewed, since this could enhance the P-APS and P-CPN.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Brusco I,Silva CR,Trevisan G,de Campos Velho Gewehr C,Rigo FK,La Rocca Tamiozzo L,Rossato MF,Tonello R,Dalmolin GD,de Almeida Cabrini D,Gomez MV,Ferreira J,Oliveira SMdoi
10.1007/s12035-016-0275-7subject
Has Abstractpub_date
2017-12-01 00:00:00pages
7824-7837issue
10eissn
0893-7648issn
1559-1182pii
10.1007/s12035-016-0275-7journal_volume
54pub_type
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