Sympathetic innervation and beta‐adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint

Abstract

SUMMARYExperiments were performed to investigate the presence and nature of f-adrenoceptors in blood vessels supplying the posterior capsule of the rabbit knee joint. Electrical stimulation of the posterior articular nerve (PAN) and close intra-arterial injection of adrenaline produced vasoconstriction which reversed to vasodilatation with administration of the a-adrenoceptor antagonist phenoxybenzamine. In almost all animals close intra-arterial injection of the /,-adrenoceptor agonist isoprenaline resulted in vasodilatation. Injection of the more selective ,1-agonists dobutamine, salbutamol and terbutaline also produced vasodilatation with a rank potency order of isoprenaline > dobutamine > salbutamol > terbutaline. The /-adrenoceptor antagonist propranolol abolished the dilator responses to adrenaline and isoprenaline, and significantly reduced the dilator responses to PAN stimulation in phenoxybenzamine-treated animals. Nerve-mediated vasodilatation was also reduced by the substance P antagonist D-Pro4 D-Trp7'9'10 SP4 -1, suggesting that substance P contributes to this dilatation. Dobutamine, a selective /31-agonist, produced vasodilatation which was abolished by administration of the selective /ll-antagonist atenolol. Isoprenaline-induced vasodilatation was substantially reduced by atenolol. The dilator response to isoprenaline appeared to be unaffected by the selective I82-antagonist ICI1 18551, but the weak dilator responses to the selective fl2-agonists salbutamol and terbutaline were significantly reduced by this antagonist. The results of this study suggest that /-adrenoceptors appear to be involved in the sympathetic regulation of rabbit knee joint blood flow, and that this is predominantly mediated via fll-adrenoceptors.

Alteration in α- and β-adrenoceptor profile of rabbit knee joint blood vessels due to acute inflammation

“…Compared to the previous study on normal joint (Najafipour & Ferrell, 1993a) in which a predominant áµ_adrenoceptor response was shown, inflammation caused a shift from an áµ-towards an áÔ_adrenoceptor response. As it has been shown that the áÔ_adrenoceptor subtype is more dominant in resistance vessels and the áµ_subtype predominates in smaller branches (microcirculation), it seems that increasing the áÔ_response is an effort by the sympathetic nervous system to recover its reduced influence in joint blood flow regulation.…”

“…4B), indicating that atenolol at the dose used only blocked âÔ_subtypes. Therefore, compared to the previous study on normal joints, in which a predominant response of âÔ_adrenoceptors was seen (Najafipour & Ferrell, 1993c), the equal âÔ_ and âµ_adrenoceptor responses indicate that inflammation caused a shift from âÔ_ towards âµ_adrenoceptor response.…”

“…Previous investigations have revealed the role of the sympathetic nervous system in normal rabbit knee joint blood flow regulation (Ferrell & Najafipour, 1992;Najafipour & Ferrell, 1993a,c, 1995. In the present study, stimulation of the posterior articular nerve reduced the blood flow to the posterior capsule of the acutely inflamed knee by 9.9 ± 2.3% compared to a 36.5 ± 4% reduction in the normal joint recorded in a previous study (Ferrell & Najafipour, 1992).…”

Calcium channel blockers attenuate chronic inflammation in rat knee joints

“…Previous studies reported the inhibitory role of CCBs in acute (Najafipour and Ferrell, 1993) and chronic (McDougall et al, 1994) inflammation. One of the background causes leading to pathologic events is the increased blood flow in the inflamed joints (Khaksari et al, 2002), thus, in the present study, the effects of this inhibitions in blood flow, temperature, and the diameter of inflamed joints were evaluated.…”

“…These doses of drugs have shown inhibitory effect in previous studies (Najafipour and Ferrell, 1993). The drugs were dissolved in dimethyl sulfoxide (DMSO) (Merk, Germany) (Rawls et al, 2004a).…”