Role of prostaglandins in regulation of blood flow and modulation of sympathetic vasoconstriction in normal and acutely inflamed rabbit knee joints

Najafipour, Hamid; Ferrell, William R.

doi:10.1113/expphysiol.1994.sp003745

Cited by 12 publications

(10 citation statements)

References 18 publications

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“…This is supported by the fact that vascular resistance is increased by equimolar infusions (0.34 nmol min _1 ) of a non-selective COX inhibitor, but not a selective COX-2 inhibitor, and further by the detection of COX-1 but not COX-2 mRNA in joint tissue. These findings corroborate an earlier study on the rabbit knee by Najafipour & Ferrell (1994), and extend their work by using a more physiological preparation, more appropriate laser Doppler technology and by expanding the investigation to examine the roles of COX-1 and COX-2. The latter was achieved by using the novel selective COX-2 inhibitor, SC-236, and by investigating COX-1 and COX-2 expression using RT-PCR.…”

Section: Discussionsupporting

confidence: 87%

“…The LDI technique as used in the present study has many advantages over the laser Doppler flowmeter used by Najafipour & Ferrell (1994). Essentially it enables the sampling of an area of tissue in a relatively short time frame, thereby allowing the spatial distribution of tissue perfusion to be mapped.…”

Section: Discussionmentioning

confidence: 99%

“…The sympathetic nerves innervating the joint are important mediators of the vasoconstrictor 'tone' (Cobbold & Lewis, 1956), and this is partly offset by the release of vasodilating neuropeptides McMurdo et al 1997). PGs have also been shown to have a vasodilating role in maintaining articular blood flow (Najafipour & Ferrell, 1994) since intravenous infusion of indomethacin in the rabbit leads to a decrease in basal articular perfusion. However, this has not yet been corroborated in other species.…”

mentioning

confidence: 99%

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Expression of Constitutive but not Inducible Cyclooxygenase Maintains Articular Perfusion in the Rat Knee

Egan

Lockhart

McLean

et al. 2001

Experimental Physiology

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Experiments were performed in the normal rat knee joint to investigate the role of different isoforms of cyclooxygenase (COX) in the regulation of basal joint blood flow. Laser Doppler imaging (LDI) was used to measure articular perfusion, and reverse transcriptase polymerase chain reaction (RT‐PCR) for the detection of COX‐1 and COX‐2 mRNA in joint tissue. Intravenous infusion of indomethacin (a non‐selective inhibitor of COX; 0.34 nmol min−1) over 40 min produced a time dependent increase in articular vascular resistance (maximum 22.5% at 40 min; P < 0.0001, one‐way ANOVA) whereas vehicle over a similar time period had no effect in a control group. An equimolar concentration of a highly selective inhibitor for COX‐2, SC‐236, was administered in a further group of rats but this did not increase articular vascular resistance. While there was no significant difference between the response to vehicle and SC‐236 (two‐way ANOVA; P= 0.686, n= 6) the response to indomethacin was significantly greater than vehicle or SC‐236 (two‐way Anova; P < 0.0001, n= 6). COX‐1, but not COX‐2, was detectable by RT‐PCR in all joint tissue samples examined (n= 4). The results of this study indicate that prostaglandins (PGs) play an important role in the maintenance of basal perfusion in the rat knee joint, with COX‐1 being the physiologically relevant isoform.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Expression of Constitutive but not Inducible Cyclooxygenase Maintains Articular Perfusion in the Rat Knee

Egan

Lockhart

McLean

et al. 2001

Experimental Physiology

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“…Our previous study showed a significant reduction in the efficacy of the sympathetic nervous system in regulating blood flow to the inflamed joint (Najafipour & Ferrell, 1995), a possible explanation for the significantly higher blood flow observed in this condition. Further investigations revealed that although prostaglandins have a role to play in the regulation of basal blood flow to the inflamed joint but they do not appear to play a significant role in the modulation of sympathetic vasoconstriction responses (Najafipour & Ferrell, 1994). Also, nitric oxide (NO) production does not appear to be changed by the process of acute inflammation (Najafipour & Ferrell, 1993b).…”

mentioning

confidence: 99%

Alteration in α‐ and β‐Adrenoceptor Profile of Rabbit Knee Joint Blood Vessels due to Acute Inflammation

Najafipour

2000

Experimental Physiology

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Experiments were performed to investigate the nature of α‐ and β‐adrenoceptors in blood vessels supplying the posterior capsule of the acutely inflamed rabbit knee joint, and results were compared to findings from previous experiments on the normal joint, to assess any alteration which may occur in the adrenoceptor profile due to the inflammation process. Electrical stimulation of the posterior articular nerve resulted in vasoconstriction which was reversed to vasodilatation by phentolamine and yohimbine. The dose‐response curves to close intra‐arterial injection of α‐adrenoceptor agonists showed a rank‐order potency of: adrenaline = phenylephrine = clonidine. The adrenaline dose‐response curve was shifted to the right by administration of antagonists with a rank‐order potency of: phentolamine = yohimbine = prazosin. At this stage of the experiments there was an equal response of α1‐ and α2‐adrenoceptors in blood vessels of the acutely inflamed rabbit knee joint. In another group of animals the neurally mediated vasodilatation, which appeared after administration of phentolamine, was completely blocked by propranolol, and was reduced by about 50% by atenolol. The dose‐response curves to close intra‐arterial injection of β‐adrenoceptor agonists showed a rank‐order potency of: isoprenaline > salbutamol = dobutamine. The isoprenaline dose‐response curve was shifted to the right by administration of antagonists with a rank‐order potency of: propranolol > atenolol. These experiments also showed an almost equal response of β1‐ and β2‐adrenoceptors in blood vessels of the acutely inflamed rabbit knee joint. Overall, compared to previous experiments on the normal joint in which α2‐ and β1‐adrenoceptor responses predominated, acute inflammation resulted in a shift from α2‐ towards α1‐ and from β1‐ towards β2‐adrenoceptor responses.

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“…Blood-vessel response to saphenous nerve stimulation was also shown to be reduced in chronically inflamed rat knee joints [15]. Further investigation revealed that although prostaglandins have a role to play in the regulation of basal blood flow to the inflamed joint, they do not appear to play a significant role in the modulation of sympathetic vasoconstriction response [21]. Also, nitric oxide (NO) production did not appear to be changed by the process of acute inflammation in the joint [18].…”

Section: Introductionmentioning

confidence: 97%

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

Najafipour

Niazmand

2006

Pflugers Arch - Eur J Physiol

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Experiments were performed to investigate the nature of alpha- and beta-adrenoceptors in blood vessels supplying the posterior capsule of the chronically inflamed rabbit knee joint, and results were compared to the finding from previous experiments on the normal and acutely inflamed joint to assess any alteration which may occur in the adrenoceptor profile due to the chronic inflammation process. Electrical stimulation of the posterior articular nerve resulted in vasoconstriction that was completely blocked by phentolamine. This constrictor response was almost equally inhibited by prazosin and yohimbine. The dose-response curves to close intraarterial injection of alpha-adrenoceptor agonists showed a rank-order potency of adrenaline = clonidine = phenylephrine. The adrenaline dose-response curve was shifted to the right by administration of alpha-antagonists with a rank-order potency of phentolamine = prazosin = yohimbine. At this stage of experiments, there was an equal response of alpha(1)- and alpha(2)- adrenoceptors in blood vessels of the chronically inflamed rabbit knee joint. In another group of animals, the neurally mediated vasodilatation, which appeared after administration of phentolamine, was completely blocked by propranolol and was reduced significantly by ICI118551, but the effect of atenolol was not significant. The dose-response curve to close intraarterial injection of beta-adrenoceptor agonists showed a rank-order potency of: isoprenaline > salbutamol > dobutamine. The isoprenaline dose-response curve was shifted to the right by administration of beta-antagonists with rank-order potency of propranolol > ICI118551 > atenolol. These experiments showed a greater beta(2)-adrenoceptor response than beta(1)-adrenoceptor response in chronically inflamed rabbit-knee-joint blood vessels. Overall, compared to previous experiments on normal joint in which alpha(2)- and beta(1)-adrenoceptor responses predominated, and in acutely inflamed joint in which an equal alpha(1)/alpha(2) and beta(1)/beta(2) response was shown, in chronically inflamed joint the sympathetic constriction response was returned toward normal. No more alpha-adrenoceptor shift had happened, and the shift of beta(1) to beta(2) response continued.

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Role of prostaglandins in regulation of blood flow and modulation of sympathetic vasoconstriction in normal and acutely inflamed rabbit knee joints

Cited by 12 publications

References 18 publications

Expression of Constitutive but not Inducible Cyclooxygenase Maintains Articular Perfusion in the Rat Knee

Expression of Constitutive but not Inducible Cyclooxygenase Maintains Articular Perfusion in the Rat Knee

Alteration in α‐ and β‐Adrenoceptor Profile of Rabbit Knee Joint Blood Vessels due to Acute Inflammation

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

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