scholarly journals Sampling the Rat Mesenteric Artery

2016 ◽  
Vol 44 (8) ◽  
pp. 1166-1169
Author(s):  
Marcia E. Pereira Bacares
Keyword(s):  
Vascular Injury ◽  
Cross Sections ◽  
Mesenteric Artery ◽  
Vascular System ◽  
Drug Candidates ◽  
Rat Mesenteric Artery ◽  
Histopathologic Evaluation ◽  
Mesenteric Vessels ◽  
Processing Techniques

Vascular injury can be induced by different classes of drug candidates, and it can affect the mesenteric vasculature. Sampling of the mesenteric vessels in the rat is crucial for proper assessment of potential adverse or pharmacologic effects of drugs in nonclinical rodent studies. To date, several sampling and processing techniques for the histopathologic evaluation of the mesenteric artery in rodents have been described and used in studies with candidate drugs that may affect the vascular system. However, most of those techniques require a significant amount of time and effort. A less labor-intensive, time-consuming, and expensive technique that allows examination of the mesentery vasculature with abundant longitudinal and cross sections of the vessels when examined microscopically was developed and presented here.

Effects of magnesium on the vasoconstrictor responses to norepinephrine and potassium chloride in the rat mesenteric artery.

1982 ◽  
Vol 23 (5) ◽  
pp. 783-789
Author(s):  
Hiromichi SUZUKI ◽  
Kazuoki KONDO ◽  
Michiko HANDA ◽  
Takao SARUTA
Keyword(s):  
Potassium Chloride ◽  
Mesenteric Artery ◽  
Rat Mesenteric Artery

Large-conductance Ca2+-activated K+ currents blocked and impaired by homocysteine in human and rat mesenteric artery smooth muscle cells

Life Sciences ◽  
2007 ◽  
Vol 80 (22) ◽  
pp. 2060-2066 ◽  
Author(s):  
Benzhi Cai ◽  
Dongmei Gong ◽  
Zhenwei Pan ◽  
Yu Liu ◽  
Hong Qian ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mesenteric Artery ◽  
Muscle Cells ◽  
Rat Mesenteric Artery ◽  
K Currents

Functional changes in adenylyl cyclases and associated decreases in relaxation responses in mesenteric arteries from diabetic rats

2005 ◽  
Vol 289 (5) ◽  
pp. H2234-H2243 ◽  
Author(s):  
Takayuki Matsumoto ◽  
Kentaro Wakabayashi ◽  
Tsuneo Kobayashi ◽  
Katsuo Kamata
Keyword(s):  
Mesenteric Artery ◽  
Diabetic Rats ◽  
Functional Change ◽  
Water Soluble ◽  
Mesenteric Arteries ◽  
Diabetic Rat ◽  
Adenylyl Cyclases ◽  
Camp Production ◽  
Functional Changes ◽  
Rat Mesenteric Artery

To assess the functional change in adenylyl cyclases (AC) associated with the diabetic state, we investigated AC-mediated relaxations and cAMP production in mesenteric arteries from rats with streptozotocin (STZ)-induced diabetes. The relaxations induced by the water-soluble forskolin (FSK) analog NKH477, which is a putative AC5 activator, but not by the β-adrenoceptor agonist isoproterenol (Iso) and the AC activator FSK, were reduced in intact diabetic mesenteric artery. In diabetic rats, however, Iso-, FSK-, and NKH477-induced relaxations were attenuated in the presence of inhibitors of nitric oxide synthase and cyclooxygenase. To exclude the influence of phosphodiesterase (PDE), we also examined the relaxations induced by several AC activators in the presence of 3-isobutyl-1-methylxanthine (IBMX; a PDE inhibitor). Under these conditions, the relaxation induced by Iso was greatly impaired in STZ-diabetic rats. This Iso-induced relaxation was significantly attenuated by pretreatment with SQ-22536, an AC inhibitor, in mesenteric rings from age-matched controls but not in those from STZ-diabetic rats. Under the same conditions, the relaxations induced by FSK or NKH477 were impaired in STZ-diabetic rats. Neither FSK- nor A-23187 (a Ca2+ ionophore)-induced cAMP production was significantly different between diabetics and controls. However, cAMP production induced by Iso or NKH477 was significantly impaired in diabetic mesenteric arteries. Expression of mRNAs and proteins for AC5/6 was lower in diabetic mesenteric arteries than in controls. These results suggest that AC-mediated relaxation is impaired in the STZ-diabetic rat mesenteric artery, perhaps reflecting a reduction in AC5/6 activity.

scholarly journals Sources of Ca2+ in relation to generation of acetylcholine-induced endothelium-dependent hyperpolarization in rat mesenteric artery

1997 ◽  
Vol 120 (7) ◽  
pp. 1328-1334 ◽  
Author(s):  
Mitsuhiro Fukao ◽  
Yuichi Hattori ◽  
Morio Kanno ◽  
Ichiro Sakuma ◽  
Akira Kitabatake
Keyword(s):  
Mesenteric Artery ◽  
Rat Mesenteric Artery

Orchidectomy Modulates α2-Adrenoceptor Reactivity in Rat Mesenteric Artery through Increased Thromboxane A2 Formation

2005 ◽  
Vol 43 (1) ◽  
pp. 101-108 ◽  
Author(s):  
Javier Blanco-Rivero ◽  
Gloria Balfagón ◽  
Mercedes Ferrer
Keyword(s):  
Mesenteric Artery ◽  
Rat Mesenteric Artery

Abstract 13: P2X7 Receptor Knockout Attenuates Angiotensin II-Induced Hypertension, Vascular Injury And CD8 + T Cell Infiltration

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Brandon G Shokoples ◽  
Kevin Comeau ◽  
Akinori Higaki ◽  
Antoine Caillon ◽  
Pierre Paradis ◽  
...  
Keyword(s):  
T Cells ◽  
Vascular Injury ◽  
Mesenteric Artery ◽  
P2x7 Receptor ◽  
Ang Ii ◽  
Perivascular Adipose Tissue ◽  
T Cell Infiltration ◽  
Induced Hypertension ◽  
Post Menopausal ◽  
Aortic Stiffening

Background: The P2X7 receptor (P2RX7) recognizes damage associated molecule patterns such as adenosine triphosphate (ATP), and triggers the activation of immune cells. Elevated plasma ATP levels have been observed in hypertensive patients, providing a potential mechanism for P2RX7 activation. Additionally, a hypomorphic polymorphism for P2X7 is correlated with a decreased risk for essential hypertension in Chinese post-menopausal women. However, it is unknown whether P2RX7 activation contributes to angiotensin (Ang) II-induced blood pressure (BP) elevation and vascular damage. We hypothesized that P2rx7 knockout would blunt Ang II-induced BP elevation, vascular injury, and infiltration of activated immune T cells into perivascular adipose tissue (PVAT). Methods: Ten-to-12-week-old male C57BL/6J male wild-type (WT) and P2rx7 -/- mice were infused or not with Ang II (1000ng/kg/min) for 14 days. BP was determined by telemetry, mesenteric artery function and remodeling using pressurized myography, aortic stiffening by ultrasound and infiltration of activated immune T cells in aortic PVAT by flow cytometry. Results: Ang II-infused P2rx7 -/- mice display a reduced systolic BP (164±3 vs. 176±2 mm Hg, P <0.05) and pulse pressure (37±4 vs. 53±3 mm Hg, P <0.001) in comparison to WT mice. Aortic stiffening occurred in WT mice treated with Ang II, demonstrated by an increased pulse wave velocity (7.7±0.7 vs. 5.9±0.3 m/s, P <0.05), accompanied by a 3.8-fold increased infiltration of activated CD8 + T cells in aortic PVAT (60±16 vs 16±3 cells/aortic PVAT, P <0.001), which were both absent in P2rx7 -/- mice (6.4±1.4 vs 5.5±1.1 m/s and 27±7 vs 16±3 cells/aortic PVAT). In addition, the frequency of IFN-γ producing CD8 + T cells in the spleen of Ang II-treated WT mice increased (2.6±0.2% vs 1.2±0.2%), which did not occur in P2rx7 -/- mice (1.7±0.3% vs 1.7±0.2%). Ang II-infusion induced mesenteric artery endothelial dysfunction in WT mice (61±7 vs 83±4% relaxation response to acetylcholine, P <0.05), which was absent in P2rx7 -/- mice (89±3 vs 90±3%). Conclusion: P2rx7 knockout attenuates Ang II-induced hypertension, vascular injury, and infiltration of activated CD8 + T cells into aortic PVAT.

Abstract 244: Increased Expression and Enhanced Vasorelaxation Activity of Specific Estrogen Receptor Subtypes in the Aorta and Mesenteric Vessels during Pregnancy

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Karina M Mata ◽  
Wei Li ◽  
Ossama M Reslan ◽  
Waleed T Siddiqui ◽  
Lauren A Opsasnick ◽  
...  
Keyword(s):  
Renal Artery ◽  
Mesenteric Artery ◽  
Receptor Subtypes ◽  
Vascular Effects ◽  
Western Blots ◽  
Expression Activity ◽  
Mesenteric Vessels ◽  
Nos Inhibitor ◽  
Dependent Mechanism

Pregnancy (Preg) is associated with hormonal and vascular changes, and estrogen (E2) may promote systemic vasodilation during Preg; however, the specific E2 receptor (ER), post-ER signaling mechanisms and vascular bed involved are unclear. To test if Preg is associated with distinct expression/activity of ERs in different blood vessels, BP and plasma E2 were measured in virgin and day-19 Preg rats, and the aorta, carotid, mesenteric and renal artery were isolated for measurement of ERα, ERβ and GPR30 expression, and the responses to E2 and specific ER agonists PPT (ERα), DPN (ERβ) and G1 (GPR30). BP was in Preg (89±6) < virgin (98±4mmHg), and plasma E2 was in Preg (120.5±5.8) > virgin (94.3±7.5pg/ml). Western blots revealed increased ERα and ERβ in aorta and mesenteric artery and GPR30 in aorta of Preg vs virgin. Immunohistochemistry revealed that the increases in ERs were mainly in intima and media. E2 and PPT caused greater relaxation of aorta of Preg (52.8±5.5, 49.3±11.4) than virgin (30.0±3.9, 19.3±3.8%) and of mesenteric artery of Preg (77.9±4.7, 75.4±4.5) than virgin (57.4±5.9, 46.5±9.5%), but similar relaxation in carotid and renal artery of Preg vs virgin. DPN and G1 caused greater relaxation in mesenteric and renal artery (15 to 30%) than aorta and carotid artery (<10%), but only aortic relaxation to G1 was in Preg (26.2±4.4) > virgin (5.3±6.7%). The NOS inhibitor L-NAME ± EDHF blocker tetraethylammonium or endothelium removal reduced PPT relaxation in aorta, suggesting an endothelium-dependent mechanism, but did not affect E2, PPT, DPN or G1-induced relaxation in other vessels, suggesting endothelium-independent mechanisms. PPT caused relaxation of Ca 2+ entry-dependent KCl contraction of mesenteric artery that was in Preg (69.7±5.5) > virgin rats (52.9±8.11%). Thus, during pregnancy, an increased ERα expression in endothelial and smooth muscle layers of aorta and mesenteric artery is associated with increased ERα-mediated relaxation via endothelium-derived vasodilators and direct inhibition of Ca 2+ entry pathways, supporting a role of aortic and mesenteric arterial ERα in pregnancy-associated systemic vasodilation. GPR30 may contribute to aortic dilation while the enhanced ERβ may mediate other genomic vascular effects during pregnancy.

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