PMID- 9853016
OWN - NLM
STAT- MEDLINE
DCOM- 19990218
LR  - 20131121
IS  - 0001-6772 (Print)
IS  - 0001-6772 (Linking)
VI  - 164
IP  - 3
DP  - 1998 Nov
TI  - Alpha 2-adrenoceptor activation may trigger the increased production of 
      endothelium-derived nitric oxide in skeletal muscle during acute haemorrhage.
PG  - 285-92
AB  - Our previous studies indicated that acute haemorrhage leads to a pronounced 
      increase in the release of endothelium-derived nitric oxide (EDNO) graded in 
      relation to the magnitude of the blood loss. The EDNO-induced vasodilatation, 
      confined selectively to the arterial 'feeder' vessels, attenuates the concomitant 
      reflex adrenergic constriction and thereby prevents deleterious reduction of 
      blood flow. The present study aimed at investigating whether the reflex release 
      of blood-borne catecholamines might trigger this EDNO release via activation of 
      endothelial alpha 2-adrenoceptors. The study was performed on the 
      sympathectomized vascular bed of cat skeletal muscle with a technique permitting 
      quantitative recordings of resistance (tone) in consecutive vascular sections. 
      Selection alpha 2-adrenoceptor blockade with idazoxan applied at steady state 
      vasoconstriction after a 35% blood loss evoked an initial generalized dilator 
      response (attributable to inhibition of post-synaptic smooth muscle alpha 
      2-adrenoceptors), followed by a constrictor response selectively in the arterial 
      feeder vessels, the latter compatible with the hypothesis of reduced EDNO release 
      by alpha 2-adrenoceptor blockade. More direct evidence for the hypothesis was 
      obtained from studies of the vascular response to EDNO blockade (L-NAME) after 
      haemorrhage in the presence and absence of alpha 2-adrenoceptor blockade. The 
      constrictor response to EDNO blockade, which is a measure of the pre-existing 
      EDNO dilator influence (EDNO production), was significantly smaller (P < 0.01) in 
      the presence than absence of alpha 2-adrenoceptor blockade. The results indicate 
      that blood-borne catecholamines, via activation of endothelial alpha 
      2-adrenoceptors, trigger the increase in the EDNO release in acute haemorrhage, 
      implying a functionally important negative feedback in the integrated control of 
      vascular tone in bleeding.
FAU - Ekelund, U
AU  - Ekelund U
AD  - Department of Physiology & Neuroscience, University of Lund, Sweden.
FAU - Bjornberg, J
AU  - Bjornberg J
FAU - Mellander, S
AU  - Mellander S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Acta Physiol Scand
JT  - Acta physiologica Scandinavica
JID - 0370362
RN  - 0 (Adrenergic alpha-2 Receptor Antagonists)
RN  - 0 (Adrenergic alpha-Antagonists)
RN  - 0 (Receptors, Adrenergic, alpha-2)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - MN3L5RMN02 (Clonidine)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
RN  - X4W3ENH1CV (Norepinephrine)
RN  - Y310PA316B (Idazoxan)
RN  - YKH834O4BH (Epinephrine)
SB  - IM
MH  - Acute Disease
MH  - Adrenergic alpha-2 Receptor Antagonists
MH  - Adrenergic alpha-Antagonists/pharmacology
MH  - Animals
MH  - Cats
MH  - Clonidine/pharmacology
MH  - Epinephrine/blood
MH  - Hemorrhage/*enzymology
MH  - Idazoxan/pharmacology
MH  - Male
MH  - Muscle, Skeletal/blood supply/*enzymology
MH  - Muscle, Smooth, Vascular/blood supply/drug effects/*enzymology
MH  - NG-Nitroarginine Methyl Ester/pharmacology
MH  - Nitric Oxide Synthase/antagonists & inhibitors/*metabolism
MH  - Nitric Oxide Synthase Type III
MH  - Norepinephrine/blood
MH  - Receptors, Adrenergic, alpha-2/*metabolism
MH  - Regional Blood Flow/drug effects/physiology
MH  - Vasodilation/drug effects/physiology
EDAT- 1998/12/16 00:00
MHDA- 1998/12/16 00:01
CRDT- 1998/12/16 00:00
PHST- 1998/12/16 00:00 [pubmed]
PHST- 1998/12/16 00:01 [medline]
PHST- 1998/12/16 00:00 [entrez]
AID - 10.1046/j.1365-201X.1998.00438.x [doi]
PST - ppublish
SO  - Acta Physiol Scand. 1998 Nov;164(3):285-92. doi: 
      10.1046/j.1365-201X.1998.00438.x.