Lymphatic Innervation

McHale, Noel G.

doi:10.1159/000158803

Cited by 31 publications

(22 citation statements)

References 17 publications

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“…However, the primary force that drives DC displacement is the lymphatic circulation. Lymph flow is regulated by spontaneous contraction of lymphatic vessel smooth muscle that in turn is stimulated by sympathetic nerves and adrenergic receptors (ARs) (7). The AR mediate the functional effects of epinephrine and norepinephrine (NE) by coupling to several of the major signaling pathways modulated by G proteins.…”

Section: Endritic Cells (Dc)mentioning

confidence: 99%

Dendritic Cell Migration Controlled by α1b-Adrenergic Receptors

Maestroni

2000

The Journal of Immunology

127

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Dendritic cells (DC) bring Ags into lymphoid organs via lymphatic vessels. In this study, we investigated the possibility that the sympathetic neurotransmitter norepinephrine (NE) influences DC migration. Murine epidermal Langerhans cells mobilization is enhanced by systemic treatment with the α2-adrenergic antagonist yohimbine and inhibited by local treatment with the specific α1-adrenergic antagonist prazosin (PRA). Consistently, NE enhances spontaneous emigration of DC from ear skin explants, and PRA inhibits this effect. In addition, local treatment with PRA during sensitization with FITC inhibits the contact hypersensitivity response 6 days later. In vitro, bone marrow-derived immature, but not CD40-stimulated mature DC migrate in response to NE, and this effect is neutralized by PRA. NE seems to exert both a chemotactic and chemokinetic activity on immature DC. Coherently, immature, but not mature DC, express mRNA coding for the α1b-adrenergic receptor subtype. Inactivation of this adrenergic receptor by the specific and irreversible antagonist chloroethylclonidine hinders the migration of injected DC from the footpad to regional lymph nodes. Thus, besides regulating lymph flow, the sympathetic innervation of lymphatic vessels may participate in directing DC migration from the site of inflammation to regional lymph nodes. Alternatively, the chemokinetic activity of NE may enhance the ability of DC to sample local Ags, and hence increase the number of DC migrating to the draining lymph nodes. This finding might improve our understanding of the biological basis of skin diseases and allergic reactions, and opens new pharmacological possibilities to modulate the immune response.

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Section: Endritic Cells (Dc)mentioning

confidence: 99%

Dendritic Cell Migration Controlled by α1b-Adrenergic Receptors

Maestroni

2000

The Journal of Immunology

127

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“…This mechanism is responsible for both the propulsion of lymph (each phasic constriction pumping lymph forward through unidirectional valves within lymphatic vessels; Mislin, 1983;Johnston & Elias, 1987;McHale, 1990), and for modulating the local vascular resistance and blood flow (see Haddock et al, 2002). Ranges of neurotransmitters and paracrine or hormonal substances including ET-1 modulate vasomotion.…”

Section: Introductionmentioning

confidence: 99%

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

Zhao

Helden

2003

British J Pharmacology

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1 In vitro experiments were performed to investigate the actions of endothelin-1 (ET-1) on vasomotion and vasospasm in guinea-pig mesenteric lymphatics. 2 ET-1 modulated lymphatic vasomotion independent of the endothelium, with lower concentrations (p10 nM) increasing lymphatic vasomotion and higher concentrations (X100 nM) causing vasospasm. 3 ET-1-induced increases in vasomotion were accompanied by an increase in tonic [Ca 2 þ ] i . 4 These actions were inhibited by the ET A receptor antagonist BQ-123 (1 mM), the phospholipase C (PLC) inhibitor U73122 (5 mM), removal of extracellular Ca 2 þ , chelation of intracellular Ca 2 þ with BAPTA/AM (10 mM), the store Ca 2 þ -ATPase inhibitor thapsigargin (1 mM), caffeine (10 mM) and the inositol 1,4,5-trisphosphate (IP 3 ) receptor blocker heparin and 2-APB (30 mM). In contrast, the ET B receptor antagonist BQ-788 (1 mM), ryanodine (1 & 20 mM), pertussis toxin (PTx) or Cs þ had no significant actions on vasomotion or the magnitude of increase in tonic [Ca 2 þ ] i . 5 ET-1-induced vasospasm was accompanied by a transient increase in smooth muscle [Ca 2 þ ] i followed by a sustained plateau, an action that was abolished by removal of extracellular Ca 2 þ , but only marginally inhibited by nifedipine (1 mM). 6 Caffeine (10 mM), SKF 96165 (30 mM) or U73122 (5 mM) together with nifedipine (1 mM) abolished ET-1-induced vasospasm and increase in [Ca 2 þ ] i . 7 These results indicate that ET-1 increases lymphatic vasomotion by acting on smooth muscle ET A receptors and activation of G-protein-PLC-IP 3 cascade, which is known to cause pacemaker Ca 2 þ release and resultant pacemaker potentials. High concentrations of ET-1 cause a failure in Ca 2 þ homeostasis causing vasospasm, triggered by excessive Ca 2 þ influx primarily through store-operated channels (SOCs) with L-Ca 2 þ voltage-operated channels (VOCs) also contributing, but to a much lesser extent.

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“…The active driving forces, resulting from intrinsic pump activity of lymph vessels, play a pivotal role in the centripetal propulsion of lymph (1,31,39). Neural (21), humoral (30), and mechanical factors (8,22,23) modify the rhythm and amplitude of lymphatic intrinsic pump activity. Recently, it has become clear that lymphatic endothelium-derived nitric oxide (NO) strongly contributes to regulation of lymphatic intrinsic pump activity.…”

mentioning

confidence: 99%

ATP inhibits pump activity of lymph vessels via adenosine A₁ receptor-mediated involvement of NO- and ATP-sensitive K⁺ channels

Kousai¹,

Mizuno²,

Ikomi³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Kousai, Akira, Risuke Mizuno, Fumitaka Ikomi, and Toshio Ohhashi. ATP inhibits pump activity of lymph vessels via adenosine A 1 receptor-mediated involvement of NO-and ATP-sensitive K ϩ channels. Am J Physiol Heart Circ Physiol 287: H2585-H2597, 2004. First published August 12, 2004 doi:10.1152/ajpheart.01080. 2003.-We examined the effects of ATP on intrinsic pump activity in lymph vessels isolated from the rat. ATP caused significant dilation with a cessation of lymphatic pump activity. Removal of the endothelium or pretreatment with N -nitro-L-arginine methyl ester (L-NAME) significantly reduced ATP-induced inhibitory responses of lymphatic pump activity, whereas reduction was not suppressed completely by 10 Ϫ6 M ATP. L-Arginine significantly restored ATPinduced inhibitory responses in the presence of L-NAME. ATPinduced inhibitory responses in lymph vessels with endothelium were also significantly, but not completely, suppressed by pretreatment with glibenclamide. 8-Cyclopentyl-1,3-dipropylxanthine (a selective adenosine A 1 receptor antagonist), but not suramine (a P2X and P2Y receptor antagonist) or 3,7-dimethyl-1-proparglyxanthine (a selective adenosine A 2 receptor antagonist), significantly decreased ATP-induced inhibitory responses. ␣,␤-Methylene ATP (a selective P2X and P2Y receptor agonist) had no significant effect on lymphatic pump activity. In some lymph vessels with endothelium (24 of 30 preparations), adenosine also caused dose-dependent dilation with a cessation of lymphatic pump activity. L-NAME significantly reduced the inhibitory responses induced by the lower (3 ϫ 10 Ϫ8 -3 ϫ 10 Ϫ7 M) concentrations of adenosine. Glibenclamide or 8-cyclopentyl-1,3-dipropylxanthine also significantly suppressed adenosine-induced inhibitory responses. These findings suggest that ATP-induced dilation and inhibition of pump activity of isolated rat lymph vessels are endothelium-dependent and -independent responses. ATP-mediated inhibitory responses may be, in part, related to production of endogenous nitric oxide, involvement of ATP-sensitive K ϩ channels, or activation of adenosine A 1 receptors in lymphatic smooth muscle and endothelium.rat; endothelium; smooth muscle; nitric oxide THE TRANSPORT OF LYMPH depends on passive and active driving forces as well as the rate of lymph production in organs and tissues. The active driving forces, resulting from intrinsic pump activity of lymph vessels, play a pivotal role in the centripetal propulsion of lymph (1,31,39). Neural (21), humoral (30), and mechanical factors (8,22,23) modify the rhythm and amplitude of lymphatic intrinsic pump activity. Recently, it has become clear that lymphatic endothelium-derived nitric oxide (NO) strongly contributes to regulation of lymphatic intrinsic pump activity. Thus NO causes relaxation of lymphatic smooth muscles and reduces lymphatic intrinsic pump activity (24,26,27,35,40,45,48). ATP-sensitive K ϩ (K ATP ) channels have been found in the plasma membrane of cells, including vascular and nonvascular smooth muscles, and then beca...

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Lymphatic Innervation

Cited by 31 publications

References 17 publications

Dendritic Cell Migration Controlled by α1b-Adrenergic Receptors

Dendritic Cell Migration Controlled by α1b-Adrenergic Receptors

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

ATP inhibits pump activity of lymph vessels via adenosine A₁ receptor-mediated involvement of NO- and ATP-sensitive K⁺ channels

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Lymphatic Innervation

Cited by 31 publications

References 17 publications

Dendritic Cell Migration Controlled by α1b-Adrenergic Receptors

Dendritic Cell Migration Controlled by α1b-Adrenergic Receptors

ET‐1‐associated vasomotion and vasospasm in lymphatic vessels of the guinea‐pig mesentery

ATP inhibits pump activity of lymph vessels via adenosine A1 receptor-mediated involvement of NO- and ATP-sensitive K+ channels

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ATP inhibits pump activity of lymph vessels via adenosine A₁ receptor-mediated involvement of NO- and ATP-sensitive K⁺ channels