Cotransmission from sympathetic vasoconstrictor neurons to small cutaneousarteries in vivo

Authors
Citation
Jl. Morris, Cotransmission from sympathetic vasoconstrictor neurons to small cutaneousarteries in vivo, AM J P-HEAR, 46(1), 1999, pp. H58-H64
Citations number
29
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
46
Issue
1
Year of publication
1999
Pages
H58 - H64
Database
ISI
SICI code
0363-6135(199907)46:1<H58:CFSVNT>2.0.ZU;2-K
Abstract
This study has characterized constrictions of small cutaneous arteries in t he guinea pig ear in response to electrical stimulation of the cervical sym pathetic nerve (SNS) in vivo. Video microscopy and on-line image analysis w ere used to examine diameter changes of ear arteries (80-140 mu m resting d iameter) in anesthetized guinea pigs. Trains of 50-300 impulses, but not si ngle pulses or short trains, produced frequency-dependent (2-20 Hz) constri ctions. The purinoceptor antagonist suramin (30 mu M) greatly reduced const rictions produced by exogenous ATP but did not affect constrictions produce d by SNS at 10 Hz or exogenous norepinephrine. The az-adrenoceptor antagoni st yohimbine (1 mu M) enhanced the peak amplitude of sympathetic constricti ons at lower stimulation frequencies (1-5 Hz). The amplitude of constrictio ns to SNS at 10 Hz was reduced, and the latency of constrictions was increa sed by the al-adrenoceptor antagonist prazosin (1 mu M). Constrictions to S NS at 10 Hz remaining after prazosin treatment were reduced in amplitude by dihydroergotamine (2 mu M) and were attenuated further by the neuropeptide Y Y-1-receptor antagonist 1229U91 (0.3 mu M). Thus norepinephrine and neur opeptide Y act as cotransmitters to mediate sympathetic constriction of sma ll ear arteries at higher stimulation frequencies (10 Hz), but ATP does not seem to contribute directly to these constrictions.