scholarly journals Inhibition of Ras-GTPase Improves Diabetes-Induced Abnormal Vascular Reactivity in the Rat Perfused Mesenteric Vascular Bed

2004 ◽  
Vol 13 (2) ◽  
pp. 57-62 ◽  
Author(s):  
Mariam H.M. Yousif ◽  
Ibrahim F. Benter ◽  
Saju Abraham ◽  
Saghir Akhtar
Keyword(s):  
Vascular Reactivity ◽  
Ras Gtpase ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

Effects of potassium and ouabain on the vascular reactivity to norepinephrine in the rat mesenteric artery

1979 ◽  
Vol 57 (8) ◽  
pp. 908-912 ◽  
Author(s):  
Kazuoki Kondo ◽  
Tetsuji Okuno ◽  
Konosuke Konishi ◽  
Takao Saruta ◽  
Eiichi Kato
Keyword(s):  
Prostaglandin E2 ◽  
Mesenteric Artery ◽  
Vascular Reactivity ◽  
Potassium Concentration ◽  
Vascular Wall ◽  
Vascular Response ◽  
Vascular Bed ◽  
Rat Mesenteric Artery ◽  
Low Potassium ◽  
Mesenteric Vascular Bed

In the perfused rat mesenteric vascular bed, the effects of potassium and ouabain on the vascular response to norepinephrine were studied. Neither changing the concentration of potassium (1.9 to 7.9 mM) nor adding ouabain (8.6 × 10−7 to 2.2 × 10−4 M) to the perfusate changed the basal pressure. A slight increase in the potassium concentration in the perfusate attenuated the vascular response to norepinephrine, and a slight decrease in the potassium concentration potentiated this response. Ouabain in the perfusate potentiated the vascular response to norepinephrine in a dose-related manner. The effect of potassium on the vascular response was inhibited in the presence of ouabain. In preparations in which vascular reactivity had been abolished by indomethacin and then restored by prostaglandin E2, the effects of potassium and ouabain on the vascular reactivity to norepinephrine were similar to those found in the untreated preparations. These results indicate that a slight change in potassium concentration in the perfusate can affect the vascular response to norepinephrine by changing the activity of a Na+–K+-dependent ATPase. It is also suggested that the potentiating effect of low potassium concentration on the norepinephrine response is, at least in the rat mesenteric vascular bed, not mediated by the synthesis of prostaglandin E2 in the vascular wall.

Effects of estrogens and selective estrogen receptor modulators on vascular reactivity in the perfused mesenteric vascular bed

2007 ◽  
Vol 293 (5) ◽  
pp. R1969-R1975 ◽  
Author(s):  
Connie J. Mark ◽  
Rabelais Tatchum-Talom ◽  
Douglas S. Martin ◽  
Kathleen M. Eyster
Keyword(s):  
Estrogen Receptor ◽  
Vascular Reactivity ◽  
Ethinyl Estradiol ◽  
Selective Estrogen Receptor Modulators ◽  
Estradiol Benzoate ◽  
Estrogen Receptor Modulators ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed ◽  
Receptor Modulators

Estrogens and selective estrogen receptor modulators (SERMs), such as raloxifene (RAL) and tamoxifen (TAM), acutely relax arteries, but the long-term effects of estrogens and SERMs on vascular reactivity in the mesenteric vasculature have not been well defined. In this study, we used an isolated, perfused mesenteric vascular bed technique to investigate the effect of chronic treatment of estrogens and SERMs on vascular reactivity of the mesenteric bed. Ovariectomized female Sprague-Dawley rats were treated by gavage with vehicle (control, 2-hydroxypropyl-β-cyclodextrin), ethinyl estradiol, estradiol benzoate, equilin (EQ), TAM, or RAL for 3 wk. EQ and TAM increased vasoconstriction in response to all three vasoconstrictors tested (KCl, norepinephrine, and 5-HT). Ethinyl estradiol increased vasoconstriction in response to KCl and 5-HT, whereas responses to estradiol benzoate and RAL were less consistent. Only EQ (134 ± 4 mmHg) and TAM (104 ± 4 mmHg) changed mean arterial blood pressure compared with control (117 ± 4 mmHg). These data demonstrate that 3-wk gavage treatment with estrogens and SERMs affects vascular reactivity in the mesenteric vascular bed. However, the three formulations of estrogen did not produce equivalent effects, and the effects of the SERMs were different from those of the estrogens.

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.

Sign in / Sign up

Export Citation Format

Share Document