Endothelin-1 and U46619 potentiate selectively the venous responses to nerve stimulation within the perfused superior mesenteric vascular bed of the rat

1990 ◽  
Vol 172 (2) ◽  
pp. 745-750 ◽  
Author(s):  
Timothy D. Warner ◽  
Pedro D'Orleans-Juste ◽  
John R. Vane
Keyword(s):  
Nerve Stimulation ◽  
Endothelin 1 ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

Direct evidence for the role of neuropeptide Y in sympathetic nerve stimulation-induced vasoconstriction

1998 ◽  
Vol 274 (1) ◽  
pp. H290-H294 ◽  
Author(s):  
Songping Han ◽  
Chun-Lian Yang ◽  
Xiaoli Chen ◽  
Linda Naes ◽  
Bryan F. Cox ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Biological Action ◽  
Sympathetic Nerve Stimulation ◽  
Low Frequencies ◽  
Vascular Bed ◽  
Potentiation Effect ◽  
Mesenteric Vascular Bed

Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter with norepinephrine (NE) in sympathetic nerve terminals and is thought to be involved in sympathetic nerve stimulation (SNS)-induced vasoconstriction. Using BIBP-3226, a Y1 receptor selective antagonist, we examined this hypothesis in the isolated and perfused mesenteric vascular bed. SNS produced a frequency-dependent increase in perfusion pressure and concomitant overflow of NPY immunoreactivity in the perfusate. [Leu31,Pro34]NPY potentiated NE-induced and ATP-induced vasoconstriction, indicating the presence and biological action of Y1 receptors in this vascular bed. The potentiation effect of [Leu31,Pro34]NPY of the increase in perfusion pressure by NE, ATP, or SNS was prevented by BIBP-3226. In addition, SNS-induced vasoconstriction at both high and low frequencies was significantly attenuated by BIBP-3226 at a concentration that completely blocked the [Leu31,Pro34]NPY-induced potentiation of the NE- or ATP-induced vasoconstrictor effect. These results suggest that ∼30% of vasoconstriction produced by SNS depends on NPY in the mesenteric vascular bed.

Analysis of adrenergic responses in the mesenteric vascular bed of the cat; evidence that vascular beta2-adrenoceptors are innervated

1984 ◽  
Vol 62 (12) ◽  
pp. 1470-1478 ◽  
Author(s):  
William M. Armstead ◽  
Howard L. Lippton ◽  
Albert L. Hyman ◽  
Philip J. Kadowitz
Keyword(s):  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Beta Adrenergic ◽  
Vascular Bed ◽  
Alpha Receptors ◽  
Mesenteric Vascular Bed ◽  
Dose Dependent ◽  
Mesenteric Vascular Resistance

Responses to sympathetic nerve stimulation and pressor hormones were investigated in the feline mesenteric vascular bed under conditions of controlled blood flow. Sympathetic nerve stimulation and norepinephrine produced frequency- and dose-dependent increases in mesenteric vascular resistance. However, when alpha-receptors were blocked with the non-equilibrium alpha-receptor antagonist, phenoxybenzamine, nerve stimulation and norepinephrine produced frequency- and dose-dependent decreases in mesenteric vascular resistance. These reductions in mesenteric vascular resistance were unchanged after indomethacin or atropine, whereas propranolol converted the mesenteric vasodilator responses to small vasoconstrictor responses. In these studies, responses to a variety of vasoconstrictor agents were enhanced after administration of propranolol. Sotalol, a nonselective beta blocker with little membrane stabilizing activity, also enhanced vasoconstrictor responses. The present data suggest that both alpha- and beta-adrenergic receptors are innervated in the feline mesenteric vascular bed, and that vasodilator responses to norepinephrine and sympathetic nerve stimulation are independent of activation of muscarinic receptors or formation of products in the cyclooxygenase pathway. These data also demonstrate that there is a nonspecific potentiation of intestinal vasoconstrictor responses after beta-adrenergic receptor blockade that is independent of a membrane-stabilizing or receptor-mediated mechanism.

Analysis of the Effects of Candesartan in the Mesenteric Vascular Bed of the Cat

Hypertension ◽  
1997 ◽  
Vol 30 (5) ◽  
pp. 1260-1266 ◽  
Author(s):  
Hunter C. Champion ◽  
Philip J. Kadowitz
Keyword(s):  
Vascular Bed ◽  
Mesenteric Vascular Bed

L-ARG/NO pathway contributes to LPS-induced hyporeactivity in rat mesenteric vascular bed: Effect of no-synthase inhibitors

1995 ◽  
Vol 31 ◽  
pp. 63 ◽  
Author(s):  
M. Potenza ◽  
M. Serio ◽  
M. Montagnani ◽  
G. Mansi ◽  
S. Pece ◽  
...  
Keyword(s):  
No Synthase ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

Losartan prevents mesenteric vascular bed alterations in high-fat diet fed rats

2020 ◽  
Author(s):  
Hyun J. Lee ◽  
Silvana M. Cantú ◽  
María Álvarez Primo ◽  
Horacio A. Peredo ◽  
Adriana S. Donoso ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

Analysis of responses to hAmylin, hCGRP, and hADM in isolated resistance arteries from the mesenteric vascular bed of the rat

Peptides ◽  
2001 ◽  
Vol 22 (9) ◽  
pp. 1427-1434 ◽  
Author(s):  
Hunter C. Champion ◽  
Robert L. Pierce ◽  
Trinity J. Bivalacqua ◽  
William A. Murphy ◽  
David H. Coy ◽  
...  
Keyword(s):  
Resistance Arteries ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

Comparison of acetylcholine-dependent relaxation in large and small arteries of rat mesenteric vascular bed

1994 ◽  
Vol 266 (3) ◽  
pp. H952-H958 ◽  
Author(s):  
J. J. Hwa ◽  
L. Ghibaudi ◽  
P. Williams ◽  
M. Chatterjee
Keyword(s):  
Methylene Blue ◽  
Channel Blocker ◽  
Mesenteric Arteries ◽  
K Channel ◽  
Resistance Arteries ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed ◽  
Relaxation Responses ◽  
Endothelium Dependent Relaxation

The relative contributions of nitric oxide (NO) to in vitro relaxation responses elicited by acetylcholine (ACh) were compared in vessels of different sizes from the rat mesenteric vascular bed. ACh elicited an endothelium-dependent relaxation in phenylephrine-contracted superior mesenteric arteries (SMA, unstretched luminal diam 650 microns), which was blocked by compounds that inhibited NO, such as hemoglobin (10 microM), methylene blue (10 microM), and NG-monomethyl-L-arginine (1 mM). In contrast, the endothelium-dependent relaxation induced by ACh in phenylephrine-contracted mesenteric resistance arteries (MRA, unstretched luminal diam 200 microns) was not blocked by hemoglobin, methylene blue, or NG-monomethyl-L-arginine. KCl (25 mM) partially inhibited the ACh-dependent relaxation in MRA. Furthermore, the ACh-dependent relaxation in MRA was selectively inhibited by the Ca(2+)-activated K+ channel blocker charybdotoxin (0.1 microM). In contrast, the ATP-sensitive K+ channel blocker glibenclamide (50 microM) did not block the ACh-dependent relaxation in MRA. We conclude that 1) NO is a major component of the ACh-dependent relaxation in SMA and 2) the ACh-dependent relaxation of MRA is resistant to NO inhibitors but sensitive to a Ca(2+)-activated K+ channel blocker. This suggests that an endothelium-derived hyperpolarization factor may be involved in the relaxation of MRA.

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