Gender differences in the relative contribution of NO and EDHF on the regulation of vasomotor tone of rabbit mesenteric arteries

2006 ◽  
Vol 3 ◽  
pp. S49
Author(s):  
Paola Del Basso Orsini ◽  
Simona Calciano ◽  
Tiziana Coletta ◽  
Maria Zurlo ◽  
Fulvia Fabi
Keyword(s):  
Gender Differences ◽  
Mesenteric Arteries ◽  
Vasomotor Tone ◽  
Relative Contribution ◽  
Rabbit Mesenteric Arteries

Endothelium-independent vascular relaxation mediating ETB receptor in rabbit mesenteric arteries

1999 ◽  
Vol 276 (2) ◽  
pp. H383-H390 ◽  
Author(s):  
Takanori Iwasaki ◽  
Mitsuru Notoya ◽  
Yoko Hayasaki-Kajiwara ◽  
Toshitake Shimamura ◽  
Noriyuki Naya ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Radioligand Binding ◽  
Muscle Layer ◽  
Mesenteric Arteries ◽  
Binding Studies ◽  
Camp Content ◽  
Rabbit Mesenteric Artery ◽  
Etb Receptor ◽  
Radioligand Binding Studies ◽  
Rabbit Mesenteric Arteries

Vascular response mediating endothelin (ET)Breceptor was studied using isolated rabbit mesenteric arteries. ET-1 (0.1–30 nM) caused a concentration-dependent contraction, whereas ET-3 >100 nM caused only weak contraction. Up to 1 μM of sarafotoxin S6c showed no contraction. In arteries precontracted with phenylephrine, ET-3 (0.03–1 nM) caused a concentration-dependent relaxation, which was not affected by endothelium denudation. The ET-3-induced relaxation was antagonized by BQ-788 and PD-142893 but not by BQ-123 in the endothelium-denuded arteries. Treatment with indomethacin but not with N G-nitro-l-arginine methyl ester completely inhibited the relaxation. ET-3 stimulated the release of 6-keto-PGF1α and PGE2 from the endothelium-denuded arteries. ET-3 also significantly increased cAMP content but not cGMP content in the arteries. Radioligand-binding studies using serial sections of the artery revealed the expression of not only ETA but also ETB receptors in the smooth muscle layer of the arteries. These results suggest that ET-3 activates ETB receptor in smooth muscle cells of rabbit mesenteric artery, producing vasodilator prostaglandins from arachidonic acid probably via a catalysis of cyclooxygenase, which accumulates cAMP in subendothelial tissues and produces relaxations.

EDRF-mediated shear-induced dilation opposes myogenic vasoconstriction in small rabbit arteries

1991 ◽  
Vol 261 (6) ◽  
pp. H2016-H2023 ◽  
Author(s):  
U. Pohl ◽  
K. Herlan ◽  
A. Huang ◽  
E. Bassenge
Keyword(s):  
Shear Stress ◽  
Tissue Perfusion ◽  
Vessel Diameter ◽  
Mesenteric Arteries ◽  
Major Mechanism ◽  
Exercise Hyperemia ◽  
Myogenic Activity ◽  
Adequate Tissue ◽  
Rabbit Mesenteric Arteries

In small saline-perfused rabbit mesenteric arteries (diam 221 +/- 4 microns, means +/- SE; n = 48) in situ, the interactions of endothelium-derived relaxing factor (EDRF)-mediated flow-dependent dilation and myogenic constriction were studied. When pump flow was increased two- to fivefold (2.8 +/- 0.1-fold), input perfusion pressure rose by 133 +/- 17%. Vessel diameter first increased passively by 9 +/- 1% and then decreased to or below control values reflecting the vascular myogenic activity. This was followed by a 16 +/- 3% increase in diameter, which was flow dependent, because nonperfused vessels exposed to the same intravascular pressures did not dilate. When the perfusate viscosity was increased with dextran solutions, both the basal diameters and the flow-induced dilator responses were significantly augmented, indicating that the increase in shear stress was the stimulus. The flow-dependent dilation was abolished by inhibition of EDRF with either hemoglobin (10 microM) or NG-nitro-L-arginine (0.3 mM) and also after preincubation with neuraminidase (0.2 U/ml, 30 min), which removes part of the membrane glycocalyx. Thus, myogenic responses in small mesenteric arteries can be effectively opposed by shear-induced release of EDRF. This might be a major mechanism for maintaining adequate tissue perfusion when pressure and shear stress increase simultaneously (e.g., exercise hyperemia, autoregulation) and otherwise myogenic activity would reduce vascular conductivity.

scholarly journals Mechanism of endothelin-3-induced relaxation in isolated rabbit mesenteric arteries

1998 ◽  
Vol 76 ◽  
pp. 125
Author(s):  
Takanori Iwasaki ◽  
Toshitake Shimamura ◽  
Yoko Hayasaki ◽  
Noriyuki Naya ◽  
Masatoshi Nakajima
Keyword(s):  
Mesenteric Arteries ◽  
Endothelin 3 ◽  
Rabbit Mesenteric Arteries

Elucidation of the temporal relationship between endothelial-derived NO and EDHF in mesenteric vessels

2007 ◽  
Vol 293 (3) ◽  
pp. H1682-H1688 ◽  
Author(s):  
Louise S. Harrington ◽  
Martin J. Carrier ◽  
Nicola Gallagher ◽  
Derek Gilroy ◽  
Chris J. Garland ◽  
...  
Keyword(s):  
Time Course ◽  
Temporal Relationship ◽  
Mesenteric Arteries ◽  
Third Order ◽  
Physiological Importance ◽  
Relative Contribution ◽  
Mesenteric Vessels ◽  
Lipid Metabolites ◽  
First Time ◽  
Subsequent Addition

Although the endothelium co-generates both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), the relative contribution from each vasodilator is not clear. In studies where the endothelium is stimulated acutely, EDHF responses predominate in small arteries. However, the temporal relationship between endothelial-derived NO and EDHF over more prolonged periods is unclear but of major physiological importance. Here we have used a classical pharmacological approach to show that EDHF is released transiently compared with NO. Acetylcholine (3 × 10−6 mol/l) dilated second- and/or third-order mesenteric arteries for prolonged periods of up to 1 h, an effect that was reversed fully and immediately by the subsequent addition of l-NAME (10−3 mol/l) but not TRAM-34 (10−6 mol/l) plus apamin (5 × 10−7 mol/l). When vessels were pretreated with l-NAME, acetylcholine induced relatively transient dilator responses (declining over ∼5 min), and vessels were sensitive to TRAM-34 plus apamin. When measured in parallel, the dilator effects of acetylcholine outlasted the smooth muscle hyperpolarization. However, in the presence of l-NAME, vasodilatation and hyperpolarization followed an identical time course. In vessels from NOSIII−/− mice, acetylcholine induced small but detectable dilator responses that were transient in duration and blocked by TRAM-34 plus apamin. EDHF responses in these mouse arteries were inhibited by an intracellular calcium blocker, TMB-8, and the phospholipase A2 inhibitor AACOCF3, suggesting a role for lipid metabolites. These data show for the first time that EDHF is released transiently, whereas endothelial-derived NO is released in a sustained manner.

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