The influence of the sympathetic nervous system on capillary permeability

Engel, D.

doi:10.1007/bf01851368

Cited by 20 publications

(6 citation statements)

References 28 publications

(7 reference statements)

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“…For example, sympathetic nerve stimulation increases vascular permeability, even though it also produces vasoconstriction (5). Consistent with these data, surgical (6, 7) or chemical (8)(9)(10) sympathectomy strongly inhibits noxious stimulus-evoked plasma extravasation (PE), a major sign of acute inflammation. Sympathectomy also markedly reduces inflammation and joint injury in rats with adjuvant-induced arthritis (11).…”

supporting

confidence: 62%

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Green

Basbaum

Helms

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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We assessed the contribution of ATP and adenosine (i) to a major sign of acute inflammation, plasma extravasation (PE), in the rat knee joint and (ii) to the severity of joint injury in adjuvant-induced experimental arthritis, a chronic inflammatory disease. PE induced by local infusion of bradykinin, which we have previously shown to depend on the sympathetic postganglionic neuron terminal, was markedly enhanced by coinfusion of either ATP or the adenosine A2-receptor agonist 2-[4-(2-carboxyethyl)phenylethylaminoJ-5'-Nethylcarboxamidoadenosine. Bradykinin-induced PE was inhibited by coinfusion of the ATP receptor antagonist adenosine 5'-[a,4-methyleneltripbosphate, the A2-receptor antagonist 3-(5H-thiozolo[2,3b]quinazolin-3-yl)phenol monohydrochloride, or the adenosine Al-receptor agonist N6-cyclopentyladenosine. The joint injury associated with experimental arthritis, which is reduced in severity in sympathectomized rats, was also markedly attenuated by daily administration of either ATP (40% reduction) or adenosine (55% reduction). These results demonstrate that the purines ATP and adenosine (acting at the A2 receptor), cotransmitters in the sympathetic postganglionic neuron terminal, enhance bradykinin-induced sympathetic postganglionic neuron terminal-dependent PE but inhibit the joint injury of arthritis. These opposing purinergic effects on PE and joint hijury suggest that enhanced PE protects against joint iury.A contribution of the peripheral limb of the sympathetic nervous system to inflammation has been demonstrated in a variety of animal models (1,2) and also in patients with inflammatory diseases, such as rheumatoid arthritis (3, 4). For example, sympathetic nerve stimulation increases vascular permeability, even though it also produces vasoconstriction (5). Consistent with these data, surgical (6, 7) or chemical (8-10) sympathectomy strongly inhibits noxious stimulus-evoked plasma extravasation (PE), a major sign of acute inflammation. Sympathectomy also markedly reduces inflammation and joint injury in rats with adjuvant-induced arthritis (11).We have recently shown that the PE produced by bradykinin (BK), a potent inflammatory agent, is mediated via an action on the sympathetic postganglionic neuron (SPGN) terminal (12). Specifically, sympathectomy significantly reduced PE evoked by infusion of BK into the knee joint of the rat. Although many SPGN neurotransmitters have been identified, our results suggested that release of the known sympathetic "cotransmitters" (i.e., norepinephrine, neuropeptide Y, and ATP) could not alone account for the PE produced by SPGN-terminal stimulation. Thus, norepinephrine inhibited PE, and neuropeptide Y had no effect on PE.Although ATP increased-PE, its effect, even at the highest doses, was smaller in amplitude and much shorter in duration than that produced by BK or by acute activation of SPGN terminals with 6-hydroxydopamine (12). Because indomethacin, a prostaglandin synthesis inhibitor, markedly reduced the PE produced by BK and because SPGNs synthesiz...

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supporting

confidence: 62%

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Green

Basbaum

Helms

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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“…The question as to whether the mechanism of decreased vascular permeability caused by sympathectomy (Engel, 1941(Engel, , 1978 and that caused by histamine injected i.a. are identical, could not be answered.…”

Section: Discussionmentioning

confidence: 99%

“…The influence of the sympathetic nervous system on capillary permeability was studied in previous experiments (Engel, 1941(Engel, , 1973(Engel, , 1978. The dye filtration through the articular barrier (synovial membrane + capillary endothelium) was tested by perfusing two knee joints, one of which was deprived of its sympathetic nerve supply by unilateral lumbosacral sympathectomy.…”

Section: Schliisselwiirter: Histamin -Vaskul~ire Permeabilit/itmentioning

confidence: 99%

“…For this purpose an Unitas perfusor (Braun) was used. See details of perfusion in my previous papers (Engel, 1978). The perfusates were Separately collected from the two knees every 15--20min and their dye content measured by a Leitz colorimeter or a spectrophotometer (Varian, 635 UV-visible), after adding 1--2 drops of 2% acetic acid to the perfusates.…”

Section: Measuring the Rate Of Dye Filtration Through The Articular Bmentioning

confidence: 99%

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The effects of intra-arterially administered histamine on vascular permeability

Engel

1979

Res. Exp. Med.

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The influence of intra-arterially administered histamine on the permeability of the articular barrier (synovial membrane plus vascular endothelium) was studied in cats. The dye penetration from the blood through the barrier was tested by perfusing the two knee joints with saline; the histamine solution was infused through one of the circumflex branches of the femoral artery. The dye content of the two perfusates was measured colorimetrically, the local blood supply of the two knee joints thermo-electrically. In the great majority of experiments it was found that the dye excretion was considerably reduced on the histamine-infused side, in spite of marked improvement of blood supply.

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“…Linde and colleagues (Linde et al, 1974) demonstrated an increase in vascular permeability following sympathetic nerve stimulation, and Engel (1941Engel ( , 1978 showed that lumbosacral sympathectomy substantially reduced baseline plasma extravasation. Chemical sympathectomy, with either 6-hydroxydopamine (Coderre et a]., 1989;Helme and Andrews, 198.5), reserpine (Gozsy and Kato, 1966), alpha-methylp-tyrosine, or guanethidine (Green, 1974), as wcll as surgical sympathectomy (Coderre et al, 1989), potently inhibit plasma extravasation evoked by thermal injury or intradermal or intra-articular injections of various irritant chcrnical and inflammatory mediators.…”

Section: Introductionmentioning

confidence: 98%

Neural influences on synovial mast cell density in rat

Levine

Coderre

Covinsky

et al. 1990

J of Neuroscience Research

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The mast cell, an immunocompetent cell that contributes to neurogenic inflammation in a variety of tissues, including synovium, is found in close proximity to peripheral terminals of unmyelinated primary afferents and sympathetic postganglionic nerve terminals. In this study we evaluated the hypothesis that the density of mast cells in synovial tissue is dependent on the neural innervation. In normal rats, we found that the density of mast cells in the ankle joint capsule, which is heavily innervated, is greater than in the capsule of the knee, which is less densely innervated. Selective lesions of unmyelinated primary afferents with capsaicin, or of sympathetic postganglionic neurons with guanethidine, produced a significant decrease in mast cells; surgical removal of the parasympathetic ganglia did not significantly affect mast cell density. Finally, the number of mast cells in the synovial joint of spontaneously hypertensive rats, which have increased sympathetic activity, was significantly greater than in normotensive control rats. These observations support the hypothesis that the innervation in the synovial joint of the rat, by unmyelinated afferents and sympathetic efferents, exerts a trophic effect on mast cell density.

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The influence of the sympathetic nervous system on capillary permeability

Cited by 20 publications

References 28 publications

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

Purinergic regulation of bradykinin-induced plasma extravasation and adjuvant-induced arthritis in the rat.

The effects of intra-arterially administered histamine on vascular permeability

Neural influences on synovial mast cell density in rat

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