Norepinephrine, but not neuropeptide Y, is involved in the cutaneous vasodilator response in young human females

Ann B Collins; Stephen J Carter; Andrew T Del Pozzi; Gary J Hodges

doi:10.1096/fasebj.26.1_supplement.lb751

Norepinephrine, but not neuropeptide Y, is involved in the cutaneous vasodilator response in young human females

The FASEB Journal ◽

10.1096/fasebj.26.1_supplement.lb751 ◽

2012 ◽

Vol 26 (S1) ◽

Author(s):

Ann B Collins ◽

Stephen J Carter ◽

Andrew T Del Pozzi ◽

Gary J Hodges

Keyword(s):

Neuropeptide Y ◽

Human Females ◽

Vasodilator Response

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The involvement of norepinephrine, neuropeptide Y, and nitric oxide in the cutaneous vasodilator response to local heating in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.90412.2008 ◽

2008 ◽

Vol 105 (1) ◽

pp. 233-240 ◽

Cited By ~ 74

Author(s):

Gary J. Hodges ◽

Wojciech A. Kosiba ◽

Kun Zhao ◽

John M. Johnson

Keyword(s):

Nitric Oxide ◽

Neuropeptide Y ◽

Neurotransmitter Release ◽

Local Heating ◽

Axon Reflex ◽

Laser Doppler Flow ◽

Doppler Flow ◽

Vasodilator Response ◽

Oxide Synthase ◽

Dependent Mechanism

Presynaptic blockade of cutaneous vasoconstrictor nerves (VCN) abolishes the axon reflex (AR) during slow local heating (SLH) and reduces the vasodilator response. In a two-part study, forearm sites were instrumented with microdialysis fibers, local heaters, and laser-Doppler flow probes. Sites were locally heated from 33 to 40°C over 70 min. In part 1, we tested whether this effect of VCN acted via nitric oxide synthase (NOS). In five subjects, treatments were as follows: 1) untreated; 2) bretylium, preventing neurotransmitter release; 3) NG-nitro-l-arginine methyl ester (l-NAME) to inhibit NOS; and 4) combined bretylium + l-NAME. At treated sites, the AR was absent, and there was an attenuation of the ultimate vasodilation ( P < 0.05), which was not different among those sites ( P > 0.05). In part 2, we tested whether norepinephrine and/or neuropeptide Y is involved in the cutaneous vasodilator response to SLH. In seven subjects, treatments were as follows: 1) untreated; 2) propranolol and yohimbine to antagonize α- and β-receptors; 3) BIBP-3226 to antagonize Y1 receptors; and 4) combined propranolol + yohimbine + BIBP-3226. Treatment with propranolol + yohimbine or BIBP-3226 significantly increased the temperature at which AR occurred ( n = 4) or abolished it ( n = 3). The combination treatment consistently eliminated it. Importantly, ultimate vasodilation with SLH at the treated sites was significantly ( P < 0.05) less than at the control. These data suggest that norepinephrine and neuropeptide Y are important in the initiation of the AR and for achieving a complete vasodilator response. Since VCN and NOS blockade in combination do not have an inhibition greater than either alone, these data suggest that VCN promote heat-induced vasodilation via a nitric oxide-dependent mechanism.

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NPY modulates neurotransmission of CGRP-containing vasodilator nerves in rat mesenteric arteries

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1991.261.3.h683 ◽

1991 ◽

Vol 261 (3) ◽

pp. H683-H690 ◽

Cited By ~ 14

Author(s):

H. Kawasaki ◽

C. Nuki ◽

A. Saito ◽

K. Takasaki

Keyword(s):

Neuropeptide Y ◽

Cold Storage ◽

Nerve Stimulation ◽

Calcitonin Gene Related Peptide ◽

Mesenteric Arteries ◽

Related Peptide ◽

Vasodilator Response ◽

Calcitonin Gene ◽

Vascular Beds ◽

Distinct Distribution

The effect of neuropeptide Y (NPY) in neurotransmission of calcitonin gene-related peptide (CGRP)-containing vasodilator nerves was investigated in rats. In perfused mesenteric vascular beds with active tone, perivascular nerve stimulation (PNS; 1-8 Hz) caused a frequency-dependent vasodilator response, which was abolished by 300 nM tetrodotoxin (TTX), 500 nM capsaicin, 1 microM human CGRP-(8-37), or cold storage denervation (4 degrees C for 72 h). NPY (5, 10, and 50 nM) concentration dependently inhibited the vasodilator response to PNS, whereas NPY had little effect on vasodilation induced by exogenous CGRP (10 and 100 pmol) or 1 nmol acetylcholine (ACh). NPY (10 nM) inhibited the neurogenic release of CGRP-like immunoreactivity induced by PNS (4 and 8 Hz), which was abolished by 300 nM TTX and the removal of Ca2+ from the medium. Combined perfusion with 5 nM NPY and 10 nM norepinephrine additively inhibited the vasodilator response to PNS but not to exogenous CGRP and ACh. Immunohistochemistry showed the distinct distribution of CGRP- and NPY-like immunoreactivity-containing fibers in rat mesenteric arteries. These results suggest that NPY modulates presynaptically the release of CGRP from CGRP-containing vasodilator nerves in rat mesenteric arteries.

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