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The involvement of norepinephrine, neuropeptide Y and nitric oxide in the cutaneous vasodilator response to slow local heating
Author(s) -
Hodges Gary J,
Kosiba Wojciech A,
Zhao Kun,
Johnson John M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.967.12
Subject(s) - yohimbine , vasodilation , medicine , endocrinology , neuropeptide y receptor , chemistry , prazosin , nitric oxide , norepinephrine , propranolol , microdialysis , nitric oxide synthase , antagonist , axon reflex , adrenergic , neuropeptide , receptor , biology , dopamine
Adrenergic blockade abolishes the axon reflex (AR) during slow local heating and reduces the final vasodilator response. We tested whether the neurotransmitters, norepinephrine (NE) and/or neuropeptide Y (NPY) were involved and whether they acted via nitric oxide synthase (NOS). In 7 subjects, 4 forearm sites were instrumented with microdialysis fibers, local heaters and laser‐Doppler probes. Part 1: treatments were untreated control, propranolol (PRO) and yohimbine (YOH) to antagonize a‐ and ß‐adrenergic receptors, BIBP to antagonize Y 1 ‐receptors and combined PRO, YOH and BIBP. Sites were locally heated from 33 to 40°C over 70 min. PRO+YOH or BIBP raised the temperature at which AR occurred or abolished it. The combination treatment consistently eliminated it. Overall vasodilation at the PRO+YOH and BIBP sites was less than at the control site. To test whether NE and NPY were acting via NOS, treatments were: untreated control, bretylium (BT) to stop neurotransmitter release, L‐NAME to inhibit NOS and BT+L‐NAME. The AR was absent at all treated sites. The decrease of the final vasodilation was not different among sites. These data suggest that NE and NPY are important for the AR and achieving complete vasodilation. Additionally, vasoconstrictor nerve and NOS blockade does not have an increased inhibition, suggesting that NE and NPY promote vasodilation via an NO‐dependent mechanism. Supported by NIH, HL‐059166