We showed that chronic but not acute treatment with the beta-adrenoceptor agonists, bambuterol, isoprenaline, fenoterol, salbutamol, salmeterol, terbutaline or ritodrine suppressed mechanical allodynia. We confirmed that the action of these beta-adrenoceptor agonists was mediated through beta(2)-adrenoceptors by blocking it with intraperitoneal or intrathecal, but not intracerebroventricular or intraplantar, injections of the antagonist ICI118551. We also showed that chronic treatments with the beta-adrenoceptor antagonists, propranolol or ICI118551 did not suppress the allodynia. ^[1]

In een andere publicatie wordt datzelfde effect op de beta-receptoren nog eens beklemtoond:

Using a murine model of neuropathy, we demonstrated that the stimulation of beta2-adrenergic receptors (beta2-AR) is not only necessary for antidepressant drugs to exert their antiallodynic action but that it is in fact sufficient to alleviate neuropathic allodynia.^[2]

Er zijn daarom onderzoekers die menen dat in de toekomst de beta-agonisten de rol van anti-derpessiva als pijnstillers bij neuropathische pijn zou kunnen overnemen, zoals de titel luidt van een recent artikel hierover: From antidepressant drugs to Beta-mimetics: preclinical insights on potential new treatments for neuropathic pain.^[2]

Referenties

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