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Gewählte Publikation:

Holzer, P; Jocic, M; Peskar, BA.
Mediation by prostaglandins of the nitric oxide-induced neurogenic vasodilatation in rat skin.
BRIT J PHARMACOL 1995 116: 2365-2370. [OPEN ACCESS]
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Autor/innen der Med Uni Graz:
Holzer Peter
Peskar Bernhard
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Abstract:
1. Intraplantar administration of the nitric oxide (NO) donor, sodium nitroprusside (SNP), induces hyperaemia in the rat paw skin, which is in part due to release of calcitonin gene-related peptide (CGRP) from afferent nerve fibres. The present study examined whether prostaglandins or other inflammatory mediators participate in the neurogenic vasodilatation caused by SNP. Blood flow in the plantar hindpaw skin of urethane-anaesthetized rats was measured by laser Doppler flowmetry. 2. The hyperaemic responses to intraplantar administration of the NO donors SNP (150 pmol) and 3-morpholino-sydnonimine (SIN-1, 15 nmol) were attenuated by 45% and 61%, respectively, after injection of the CGRP antagonist, CGRP8-37 (50 nmol kg-1, i.v.) which did not significantly change baseline blood flow. 3. The NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 15 mg kg-1, i.v.), the bradykinin antagonist Hoc-140 (100 nmol kg-1, i.v.) and the histamine antagonists, pyrilamine (2 mg kg-1, i.v.) plus cimetidine (10 mg kg-1, i.p.) were without effect on baseline blood flow and the vasodilatation caused by SNP. 4. The cyclo-oxygenase inhibitors, indomethacin (10 mg kg-1, i.p.) and flurbiprofen (5 mg kg-1, i.p.) depressed the SNP-induced hyperaemia by 65% and 42%, respectively, without altering baseline blood flow. The ability of CGRP8-37 to inhibit the vasodilator response to SNP was lost in indomethacin-treated rats. 5. Intraplantar administration of prostaglandin E2 (PGE2, 15 pmol) evoked cutaneous vasodilatation which was attenuated by 66% after administration of CGRP8-37 but remained unaltered by indomethacin or L-NAME. 6. These data indicate that the neurogenic hyperaemia which in rat skin is induced by intraplantar administration of NO donors involves the formation of prostaglandins which in turn cause release of the vasodilator peptide, CGRP, from perivascular afferent nerve fibres.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Arginine - analogs and derivatives
Bradykinin - physiology
Calcitonin Gene-Related Peptide - physiology
Cyclooxygenase Inhibitors - pharmacology
Enzyme Inhibitors - pharmacology
Female - pharmacology
Histamine - physiology
Molsidomine - analogs and derivatives
NG-Nitroarginine Methyl Ester - analogs and derivatives
Nitric Oxide - pharmacology
Nitric Oxide Synthase - antagonists and inhibitors
Nitroprusside - pharmacology
Prostaglandins - physiology
Rats - physiology
Rats, Sprague-Dawley - physiology
Regional Blood Flow - drug effects
Research Support, Non-U.S. Gov't - drug effects
Skin - blood supply
Skin Physiology - blood supply
Vasodilation - drug effects
Vasodilator Agents - pharmacology

Find related publications in this database (Keywords)
Nitric Oxide
N-G-Nitro-L-Arginine Methyl Ester (L-Name)
Sodium Nitroprusside
3-Morpholine-Sydnonimine (Sin-1)
Prostaglandin E(2)
Indomethacin
Calcitonin Gene-Related Peptide (CGRP)
Afferent Nerve Fibers
Skin Blood How
Neurogenic Vasodilatation
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