scholarly journals Effects of propofol on rabbit mesenteric arteries and veins

1996 ◽  
Vol 76 (2) ◽  
pp. 333-334
Author(s):  
N Stratford
1995 ◽  
Vol 75 (4) ◽  
pp. 457-461 ◽  
Author(s):  
K Kamitani ◽  
M Yamazaki ◽  
M Yukitaka ◽  
Y Ito ◽  
Y Momose

SURG Journal ◽  
2008 ◽  
Vol 2 (1) ◽  
pp. 30-38
Author(s):  
Rebekah Carter ◽  
Nathan Ludwig

Norepinephrine (NE) and adenosine 5’-triphosphate (ATP) are neurotransmitters released from sympathetic neurons that act to alter net vascular tone in the mesentery via activation of adrenergic (α1 and α2) and purinergic (P2X and P2Y) receptors. This study was designed to identify adrenergic and purinergic receptors in third order mesenteric arteries and veins in male Sprague-Dawley rats. Agonists and antagonists of adrenergic and purinergic receptors were exogenously applied to vessels and contractile responses were measured using computer assisted video microscopy. NE and ATP both caused contractions of mesenteric arteries and veins. The selective α1 antagonist prazosin attenuated NE-derived constriction of the vessels. The selective α1 agonist phenylephrine was a more efficacious constrictor of both mesenteric arteries and veins than the selective α2 agonist clonidine. The P2X/P2Y1 receptor antagonist pyridoxal-phosphate-6-azophenyl-2’,4-disulfonic acid (PPADS) caused a rightward shift in the ATP dose response curve in mesenteric arteries but not veins. These data indicate that the α1 adrenergic receptors are the primary adrenoreceptors mediating contraction to NE in mesenteric vessels. Additionally, these data suggest that the P2X/P2Y1 receptors mediate substantial contractile responses to ATP in mesenteric arteries but not veins.


2000 ◽  
Vol 279 (3) ◽  
pp. H1185-H1193 ◽  
Author(s):  
Nancy J. Pelaez ◽  
Tracey R. Braun ◽  
Richard J. Paul ◽  
Richard A. Meiss ◽  
C. Subah Packer

One purpose of the current study was to establish whether vasoconstriction occurs in all vessel types in response to H2O2. Isometric force was measured in pulmonary venous and arterial rings, and isobaric contractions were measured in mesenteric arteries and veins in response to H2O2. A second purpose was to determine whether H2O2-induced contraction is calcium independent. The addition of H2O2 to calcium-depleted (using the Ca2+ ionophore ionomycin in zero calcium EGTA buffer) muscle caused contraction. Furthermore, permeabilized muscle contracted in response to H2O2 even in zero Ca2+. The final purpose was to determine whether the 20-kDa regulatory myosin light chain (MLC20) phosphorylation plays a role in H2O2-induced contraction. Pulmonary arterial strips were freeze-clamped at various time points during H2O2-induced contractions, and the relative amounts of phosphorylated MLC20 were measured. H2O2 caused dose-dependent contractions that were independent of MLC20 phosphorylation. ML-9, a myosin light chain kinase inhibitor, had no effect on the H2O2 contractile response. In conclusion, H2O2 induces Ca2+- and MLC20 phosphorylation-independent contraction in pulmonary and systemic arterial and venous smooth muscle.


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