Tachykinin-induced vasodilatation in rat skin measured with a laser-Doppler flowmeter: evidence for receptor-mediated effects

Andrews, Paul V.; Helme, Robert D.

doi:10.1016/0167-0115(89)90175-4

Cited by 14 publications

(3 citation statements)

References 29 publications

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“…plasma extravasation und vasodilation. seem to occur via activation ofthe NK-1 tachykinin receptor [2][3][4], whereas studies in human mast cells, as well as in those from rodent, have shown that histamine release oeeurs independently of tachykinin receptor activation [111. It is likely that the discrepancy between human and rodent data on neurogenic skin inflammation are due to mast cell heterogeneity in response to neurogenic stimuli as described for other mast cell secretagogues as well [11.46].…”

Section: Discussionmentioning

confidence: 99%

No release of histamine and substance P in capsaicin‐induced neurogenic inflammation in intact human skin in vivo: a microdialysis study

Petersen

Winge

Brodin

et al. 1997

Clin Experimental Allergy

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Section: Discussionmentioning

confidence: 99%

No release of histamine and substance P in capsaicin‐induced neurogenic inflammation in intact human skin in vivo: a microdialysis study

Petersen

Winge

Brodin

et al. 1997

Clin Experimental Allergy

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“…A role for tachykinins as arteriolar dilators in the microvasculature, however, is not well documented. Substance P has been found by intravital microscopy (Persson et al, 1991;Raud et al, 1991) and laser-Doppler flowmetry (Andrews & Helme, 1989;Kerezoudis et al, 1993;Lam & Ferrell, 1993) to cause transient arteriolar dilatation, and the higher activity of substance P as compared to neurokinins A and B has led to the suggestion that arteriolar dilatation results, at least in part, from NKI receptor stimulation (see Lam & Ferrell, 1993). Confirmation of NK,-receptor evoked arteriolar dilatation, however, requires evidence from studies with receptor-selective antagonists.…”

Section: Introductionmentioning

confidence: 99%

Inhibition by SR140333 of NK₁ tachykinin receptor‐evoked, nitric oxide‐dependent vasodilatation in the hamster cheek pouch microvasculature in vivo

Hall

Brain

1994

British J Pharmacology

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1 This study investigated tachykinin-evoked vasodilatation in the microvasculature of the hamster cheek pouch in vivo. Arterioles and venules were observed by intravital microscopy with video recording, and vasodilatation and constriction, defined as changes in blood vessel diameter, measured by image analysis. All agents were applied topically by superfusion. None of the agents tested had a significant effect on venule diameter. 2 When arterioles were preconstricted (by ca. 50%) with endothelin-1 present in the superfusing medium, substance P (0.3-30 nM) was a potent vasodilator, being 10 fold more active than both neurokinin A and the NK, receptor-selective agonist, substance P methyl ester. The NK2 receptorselective agonist, [P-Ala8]-NKA(4-10)(0.1-10 M) was active only at high concentrations, and the NK3 receptor-selective agonist senktide (O.1 -10 gM) was virtually inactive (n = 8 hamsters). Dilatation evoked by tachykinins and analogues was rapid in onset (<0.5min) and readily reversible. 3 At low concentrations (1-10nM), the non-peptide tachykinin NK, receptor antagonist SR140333.2]octone, chloride) had no effect on the diameter of preconstricted arterioles per se, but potently inhibited dilator responses to substance P methyl ester (apparent pKB 9.9 ± 0.2; n = 5 hamsters, n = 10 estimates). SR140333 (10 nM) did not inhibit submaximal dilator responses evoked by human alpha calcitonin gene-related peptide (aCGRPh; 1.0 nM; P> 0.05; n = 5). 4 The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 gM) caused a 51.3 ± 5.4% arteriolar constriction. In the presence of L-NAME, submaximal vasodilator responses to substance P (10-I00 nM) and carbachol (0.1-1.0 fiM) were significantly attenuated (n = 5 hamsters; P< 0.05) as compared to responses obtained in preparations that were preconstricted to a similar extent by endothelin-l (48.0 ± 5.6%). L-NAME (10 M) was without effect on submaximal vasodilator responses to aCGRPh (0.1 nM) or sodium nitroprusside (1O nM) (n = 5 hamsters; P> 0.05). 5 We conclude that tachykinin-evoked arteriolar vasodilatation in the hamster cheek pouch is mediated via NK, receptor activation and depends, at least in part, on the release of nitric oxide. The NKI receptors mediating vasodilatation can be blocked by topical application of SR140333; which may therefore be useful in the investigation of the role of NK, receptors in neurogenic inflammation in the microvasculature.

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“…The actions of SP are for the most part vasoconstrictive (endothelial cell contraction giving rise to plasma extravasation). Nonetheless there are reports that SP can act as a vasodilator in part by stimulating the release of histamine from mast cells [75][76][77][78] or by direct action that does not involve the release of histamine. Antagonists for the NK-1 receptor can also abolish the SP-produced vasodilation [79,80] .…”

Section: Neurogenic Infl Ammationmentioning

confidence: 99%

Role of Neurogenic Inflammation in Pancreatitis and Pancreatic Pain

Vera–Portocarrero¹,

Westlund²

2005

Neurosignals

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Pain arising from pancreatic diseases can become chronic and difficult to treat. There is a paucity of knowledge regarding the mechanisms that sensitize neural pathways that transmit noxious information from visceral organs. In this review, neurogenic inflammation is presented as a possible amplifier of the noxious signal from peripheral organs including the pancreas. The nerve pathways that transmit pancreatic pain are also reviewed as a conduit of the amplified signals. It is likely that components of these visceral pain pathways can also be sensitized after neurogenic inflammation.

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Tachykinin-induced vasodilatation in rat skin measured with a laser-Doppler flowmeter: evidence for receptor-mediated effects

Cited by 14 publications

References 29 publications

No release of histamine and substance P in capsaicin‐induced neurogenic inflammation in intact human skin in vivo: a microdialysis study

No release of histamine and substance P in capsaicin‐induced neurogenic inflammation in intact human skin in vivo: a microdialysis study

Inhibition by SR140333 of NK₁ tachykinin receptor‐evoked, nitric oxide‐dependent vasodilatation in the hamster cheek pouch microvasculature in vivo

Role of Neurogenic Inflammation in Pancreatitis and Pancreatic Pain

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Tachykinin-induced vasodilatation in rat skin measured with a laser-Doppler flowmeter: evidence for receptor-mediated effects

Cited by 14 publications

References 29 publications

No release of histamine and substance P in capsaicin‐induced neurogenic inflammation in intact human skin in vivo: a microdialysis study

No release of histamine and substance P in capsaicin‐induced neurogenic inflammation in intact human skin in vivo: a microdialysis study

Inhibition by SR140333 of NK1 tachykinin receptor‐evoked, nitric oxide‐dependent vasodilatation in the hamster cheek pouch microvasculature in vivo

Role of Neurogenic Inflammation in Pancreatitis and Pancreatic Pain

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Inhibition by SR140333 of NK₁ tachykinin receptor‐evoked, nitric oxide‐dependent vasodilatation in the hamster cheek pouch microvasculature in vivo