Disease relevance of Mesenteric Arteries

• Using an in vivo mesenteric artery injury model and real-time continuous analysis of the thrombotic process, we observed that the time for appearance of first thrombus was delayed and that only small, unstable thrombi formed in P2Y12-/- mice without reaching occlusive size, in the absence of aspirin [1].
• These results indicate that selective increases in the reactivity of aortae and mesenteric arteries to NE occur in diabetic rats before the development of hypertension [2].
• By using mesenteric artery preparation, we showed that PAMP's ability to decrease norepinephrine overflow was significantly attenuated in pertussis toxin-treated rat (-18.5 +/- 6.9%; P<.05 versus control rats) [3].
• Large mesenteric arteries of rats treated with 100 ng . kg-1 . min-1 Ang II for 12 weeks were examined to distinguish hypertrophy from hyperplasia of vascular muscle [4].
• To assess the role of the sympathetic and central noradrenergic neurons in one- and two- kidney Goldblatt hypertension, we examined the concentration and turnover of norepinephrine (NE) in the aorta, mesenteric artery, left ventricle, hypothalamus, midbrain, and pons medulla of hypertensive and control rabbits [5].

Psychiatry related information on Mesenteric Arteries

• They found that spontaneous running increased aortic compliance and antioxidant capacity with decreased oxidative stress in mesenteric arteries, presenting support for the cardiovascular protective effects of physical activity [6].

High impact information on Mesenteric Arteries

• To examine the effects of RMCP-II more directly 1 mg of the highly purified chymase was introduced into the cranial mesenteric artery in ex vivo perfused normal rats [7].
• In mesenteric arteries, EDHF-mediated relaxations and hyperpolarizations were significantly reduced in Cu,Zn-SOD-/- mice with no inhibitory effect of catalase, while endothelium-independent relaxations and hyperpolarizations were preserved [8].
• EDHF-mediated relaxation and hyperpolarization in response to acetylcholine (ACh) were markedly attenuated in small mesenteric arteries from eNOS knockout (eNOS-KO) mice [9].
• We have undertaken this study to investigate the effect of the normalization of vascular NO production, as estimated by aortic cyclic guanosine monophosphate (cGMP) concentration and endothelial nitric oxide synthase (eNOS) protein expression in the aorta and mesenteric artery, on sodium and water excretion [10].
• Using perfused rat mesenteric arteries, PAMP (0, 1, 5, and 10 pmol/ml) decreased norepinephrine overflow by periarterial electrical nerve stimulation in a dose-dependent fashion (0.244 +/- 0.043, 0.231 +/- 0.048, 0.195 +/- 0.061 and 0.168 +/- 0.051 ng/gram tissue weigh: NS, P < 0.05, and P < 0.02, respectively) [11].

Chemical compound and disease context of Mesenteric Arteries

• Our previous finding that dexamethasone-induced hypertension in rats is associated with enhanced reactivity of mesenteric arteries to arginine vasopressin but not to angiotensin II (Ang II) or norepinephrine has led us to postulate that vasopressin contributes to the development or maintenance of glucocorticoid-induced hypertension [12].
• To clarify the pathophysiological role of vascular aldosterone in hypertension, we compared aldosterone production in the mesenteric arteries of stroke-prone spontaneously hypertensive rats (SHRSP) with that in Wistar-Kyoto rats (WKY) [13].
• 1. Hypoxia (PO2 < 5 mmHg) decreased vessel tone in isolated rat mesenteric arteries precontracted with either high [K+] or the thromboxane analogue U46619 [14].
• Adenosine A(2A) receptors in portal hypertension: their role in the abnormal response to adenosine of the cranial mesenteric artery in rabbits [15].
• In the chronic phase of 2K-1C hypertensive rats whose R-A system was within normal limits, increased incorporation rates of 3H-proline into noncollagenous protein or collagen of mesenteric arteries were decreased by splanchnicotomy or beta-aminopropionitrile and hypertension was lowered [16].

Biological context of Mesenteric Arteries

• Perfusion myography of mesenteric arteries from tTA+/RVCH+ mice also revealed increased vasoconstriction in response to phenylephrine and impaired metacholine-induced vasodilatation when compared with littermate controls or with the doxycyline-treated group [17].
• Saralasin-resistant rats exhibited a decreased number of vascular ANF binding sites in both mesenteric arteries and aorta [18].
• Perfusion of rat mesenteric arteries with insulin, IGF-I, or IGF-II resulted in the potentiation of arginine vasopressin (AVP)-induced vasoconstriction [19].
• These data, therefore, do not support a role for oxidative stress or dyslipidaemia in mediating the impaired ACh-induced endothelium-dependent relaxation of small mesenteric arteries from the streptozotocin-diabetic rat [20].
• The kinetics of the release of rat mast cell protease-II (RMCP-II) from mucosal mast cells in the jejunum of Nippostrongylus brasiliensis primed (immune) rats was investigated using ex vivo perfusion of a segment of jejunum through the cranial mesenteric artery [21].

Anatomical context of Mesenteric Arteries

• Since the pressor response to AII involves angiotensin interaction with its vascular receptor, binding studies of mesenteric artery and uterine smooth muscle AII receptors were performed [22].
• In the lungs, aorta, mesenteric arteries, and adrenal medulla, ACE labeling was highest in the 2K-1C group, intermediate in the 1K-1C and control groups, and lowest in the DOCA-salt group [23].
• The lowering of BP was associated with the expression of AT1R-AS transcript and decreases in AT1-receptor in many peripheral angiotensin II target tissues such as mesenteric artery, adrenal gland, heart, and kidney [24].
• Calcium channels in muscle cells isolated from rat mesenteric arteries: modulation by dihydropyridine drugs [25].
• In adipocytes, ANF and CNP stimulated cGMP generation. cGMP production by mesenteric arteries was stimulated by sodium nitroprusside but not by ANF or CNP [26].

Associations of Mesenteric Arteries with chemical compounds

• In parallel studies of mesenteric arteries, PGI2 synthesis and cAMP production were enhanced at low O2 [27].
• Rat mesenteric artery resistance vessels (MARV, n = 9) were incubated for 48 h with either L, M, L + M, or vehicle (V) and tested for reactivity to NE, serotonin, acetylcholine, atrial natriuretic peptide, and sodium nitroprusside (SNP) [28].
• These results indicate that H(2)O(2) is an EDHF in mouse small mesenteric arteries and that eNOS is a major source of the reactive oxygen species [9].
• The histamine content in the intestinal wall did not fall significantly at any time after mesenteric artery occlusion and reperfusion [29].
• The vasoconstrictor action of endothelin-1 was examined on ring segments of human mesenteric arteries [30].

Gene context of Mesenteric Arteries

• Differential effects of endothelin receptor activation on cyclic flow variations in rat mesenteric arteries [31].
• Role of AT2 receptors in angiotensin II-stimulated contraction of small mesenteric arteries in young SHR [32].
• OBJECTIVE: The aim of this study was to investigate the relative role of the angiotensin type 1 (AT1) and type 2 (AT2) receptors in mediating angiotensin II-induced regulation of AT2 receptor in mesenteric artery [33].
• Increased collagen type I/III accumulation and decreased elastin content in the media of mesenteric arteries was noted in Mthfr compared to Mthfr mice [34].
• We conclude that ETA and ETB receptor protein and mRNA expression is developmentally regulated in the postnatal swine mesenteric artery, being expressed to a greater degree in younger animals [35].

Analytical, diagnostic and therapeutic context of Mesenteric Arteries

• In isolated perfused rabbit mesenteric arteries, prostaglandin (PG) E1 and E2, 1-5NG/ML, did not alter the basal perfusion pressure, but reduced the vasoconstrictor responses to sympathetic nerve stimulation; the responses to injected norepinephrine were reduced by PGE1 and variably affected by PGE2 [36].
• Acetylcholine (ACh) induced hyperpolarization and relaxation in rat mesenteric arteries contracted with norepinephrine, as indicated from studies with simultaneous microelectrode and tension recordings [37].
• Regulation of the postsynaptic alpha-adrenergic receptor in rat mesenteric artery. Effects of chemical sympathectomy and epinephrine treatment [38].
• Naloxone (3 X 10(-5)M) augmented the epinephrine-induced constriction of both feline and monkey mesenteric artery at epinephrine concentrations of 10(-7) to 10(-5) M [39].
• Northern blot analysis using a specific 32P-labeled complementary RNA probe for rat preproendothelin-1 of 319 base pairs revealed a fourfold to fivefold increase in abundance of preproendothelin-1 messenger RNA transcripts in both aorta and mesenteric arteries from DOCA-salt hypertensive rats [40].

References