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At least 19 recordsLinked to original sources
PubMed1996

Pharmacological characterization of the ETA receptor in the vascular smooth muscle comparing its analogous distribution in the rat mesenteric artery and in the arterial mesenteric bed.

The potency of ET-1, ET-2, and ET-3 to contract the isolated perfused rat arterial mesenteric bed was 2.73 +/- 0.57, 1.63 +/- 0.32, and 144 +/- 30 nM, respectively. The vasomotor effect of the ETs was slow in onset, persistent but reversible. Sarafotoxin S6b mimicked the ETs with a potency twofold lower than ET-1; sarafotoxin S6c and the C-terminal hexapeptide of ET-1 was inactive. ETH agonists such as IRL-1620 and AGETB-89 were inactive as vasoconstrictors within the range of concentrations examined. Minor chemical modifications of ET-1 amino acids residues in position 7 or 21 decreased significantly the peptide potency; ET-1 analogues with one or none of the disulfide bonds resulted inactive. The vasomotor effect of ETs was blocked in a competitive, reversible, and selective manner by FR 139317 and BQ-123, the latter being about threefold less potent than the former antagonist. The potency of FR 139317 was 20-fold higher to antagonize ET-3 than ET-1, and threefold higher to block ET-2 than ET-1. In strict analogy to FR 139317, BQ-123 was 12-fold more potent to antagonize ET-3 than ET-1, and fourfold more potent to antagonize ET-2 than ET-1. Upon removal of the endothelial cell layer, the vasomotor potency of ET-1 or the antagonist potency of FR 139317 remained unaltered, suggesting that the vasomotor receptors are localized in the arterial smooth muscles. The ET-1-induced vasomotor responses desensitized, an effect not crossed to noradrenaline (NA); perfusion with 10 microM indomethacin did not alter the vasomotor potency of ET-1, excluding the participation of eicosanoids in the arteriolar effects of ET-1. In isolated rings of the rat mesenteric artery, set to record isometric contractions of the circular muscular layer, the potency of the ETs and their structural analogues was as follows; ET-2 = ET-1 = sarafotoxin S6b > ET-3 > sarafotoxin S6c. The C-terminal hexapeptide of ET-1 and [Ala 1,3,11,15]ET-1 were inactive. The ET-1-induced vasoconstriction was antagonized in a concentration-dependent fashion by FR 139317. These results allow to conclude that the ETA receptors present in the arterial mesenteric circulation are localized in the vascular smooth muscle of the large-sized arteries as well as the smaller arterioles and precapillary vessels of the rat arterial mesenteric bed.

Animals↗
PubMed1991

[Effects of l-stepholidine on isolated rabbit basilar artery, mesenteric artery, and thoracic aorta].

l-Stepholidine (SPD) has been shown to be effective in treating migraine, but its mechanism is not clear. So the effects of SPD on isolated rabbit basilar artery (BA), mesenteric artery (MA) and thoracic aorta (TA) were studied. The contractions of BA and MA were induced by KCl (10-160 mmol.L-1) and the contraction of TA was caused by 5-HT (0.1-100 mumol.L-1). Ketanserin was used as reference. SPD (0.1-0.2 mmol.L-1) relaxed the contractions of BA and MA induced by KCl in a noncompetitive manner with pD'2 3.4 +/- 0.3 and 4.0 +/- 0.3, respectively. SPD had no selectivity in BA and MA. SPD also inhibited the contraction of TA induced by 5-HT with pA2 9.7 +/- 2.0 and pD'2 5.4 +/- 0.6, which showed a dual of both competitive and noncompetitive antagonisms. These results suggested that SPD had a blockade effect on the calcium channel and 5-HT2 receptors.

Animals↗
PubMed2003

Characterization of angiotensin-(1-7) receptor subtype in mesenteric arteries.

Mesenteric arteries from male Sprague-Dawley rats were mounted in a pressurized myograph system. Ang-(1-7) concentration-dependent responses were determined in arteries preconstricted with endothelin-1 (10(-7)M). The receptor(s) mediating the Ang-(1-7) evoked dilation were investigated by pretreating the mesenteric arteries with specific antagonists of Ang-(1-7), AT(1) or AT(2) receptors. The effects of Ang-(3-8) and Ang-(3-7) were also determined. Ang-(1-7) caused a concentration-dependent dilation (EC(50): 0.95 nM) that was blocked by the selective Ang-(1-7) receptor antagonist D-[Ala(7)]-Ang-(1-7). Administration of a specific antagonist to the AT(2) receptor (PD123319) had no effect. On the other hand, losartan and CV-11974 attenuated the Ang-(1-7) effect. These results demonstrate that Ang-(1-7) elicits potent dilation of mesenteric resistance vessels mediated by a D-[Ala(7)]-Ang-(1-7) sensitive site that is also sensitive to losartan and CV-11974.

Angiotensin I↗
PubMedDate not supplied

Long-term sensory denervation does not modify endothelial function or endothelial substance P and nitric oxide synthase in rat mesenteric arteries.

Mesenteric endothelial cell function and immunoreactivity for substance P and nitric oxide synthase (NOS) were examined in control rats and rats treated with capsaicin as neonates to destroy primary afferent nerves. Endothelial vasodilator function was examined pharmacologically in the methoxamine raised-tone isolated perfused mesenteric arterial bed. Endothelial immunoreactivity for substance P and NOS was examined at the ultrastructural level by electron-microscopic immunocytochemistry. The endothelium-dependent vasodilators acetylcholine and adenosine 5'-triphosphate elicited dose-dependent relaxations which were not different between control and capsaicin-treated rats. Dose-dependent relaxations to endothelium-independent vasodilators, calcitonin gene-related peptide and sodium nitroprusside, were also unchanged by capsaicin treatment. Positive staining for substance P was detected in 25% of endothelial cells in both control and capsaicin-treated rats. Positive staining for NOS was detected in 50% of endothelial cells in control rats, and this was not changed by capsaicin treatment. These results confirm that endothelial substance P is independent of substance P contained in sensory nerves. Long-term sensory denervation does not produce changes in endothelium-dependent or -independent relaxation, or in the number of endothelial cells showing positive labelling for substance P and NOS in rat mesenteric arteries.

Animals↗
PubMed2000

Ultrastructure of substance P-immunoreactive terminals and their relation to vascular smooth muscle cells of rat small mesenteric arteries.

Mesenteric arteries of the rat are surrounded by a plexus of primary afferent nerve terminals which contain both substance P (SP) and calcitonin gene-related peptide (CGRP). The ultrastructural arrangement of the innervation was studied in second-order branches of the rat mesenteric artery using immunohistochemical labelling with antibodies against SP. The structure and distribution of SP-immunoreactive (SP+) and SP-negative (SP-, i.e., virtually all noradrenergic) axons and their terminals within the adventitia of the artery have been determined. Sixteen percent of axons and 22% of varicosities in the perivascular plexus were SP+. Most of the SP+ varicosities lay between 0.4 and 2 microm from the smooth muscle cells, whereas most SP- varicosities lay much closer to the vessel (i.e., <1 microm). SP+ varicosities typically contained the same number and size of small synaptic vesicles and mitochondria as SP- varicosities, but there were more large dense-cored vesicles in the SP+ varicosities. Unlike SP- varicosities, the peptidergic varicosities did not show clustering of synaptic vesicles toward one part of the axon membrane, and none of them formed junctions with the smooth muscle cells. Close relationships between SP+ and SP- varicosities lacked any detectable structural specialization. The arrangement of SP+ (primary afferent) terminals and their association with vascular smooth muscle cells indicates that peptide released from afferent terminals must diffuse further than noradrenaline from sympathetic terminals to reach the vascular smooth muscle.

Animals↗
PubMed1977

Celiac axis, superior mesenteric artery, and inferior mesenteric artery occlusion: surgical considerations.

Occlusion of the celiac, superior mesenteric, and inferior mesenteric artery has been studied in 46 patients treated by operation. The condition was acute and was caused by embolic obstruction of the superior mesenteric artery in four cardiac patients and detachment of the inferior mesenteric artery in two patients during removal of infrarenal abdominal aortic aneurysms. The condition was chronic and involved two or all three of the vessels in 40 patient. Embolic obstruction caused severe abdominal pain but few physical signs early in the process,, but the picture of an acute abdomen indicating bowel gangrene developed in a few hours. Ischemia from inferior mesenteric detachment was observed at operation. Patients with chronic obstruction had abdominal pain, weight loss, and diarrhea. Patients with embolic obstruction were treated successfully by embolectomy, and patients developing intraoperative sigmoid ischemia were treated by reattachment of inferior mesenteric arteries to aortic graft. Various procedures were employed in patients with chronic multiple obstruction. However, graft bypass using Dacron tubing was preferable because of its simplicity and because the frequently (48%) associated occlusive disease and aneurysm of the distal aorta were treated at the same time. Confining operation to the abdomen significantly reduced the magnitude of operation and eliminated risks in this age group. Of the 46 patients, 91% survived and were relieved of their symptoms despite associated disease. The 5-year survival rate in this group of patients was 62%.

Adult↗
PubMed2000

Vanilloid receptors on capsaicin-sensitive sensory nerves mediate relaxation to methanandamide in the rat isolated mesenteric arterial bed and small mesenteric arteries.

In the present study, the vasodilator actions of methanandamide and capsaicin in the rat isolated mesenteric arterial bed and small mesenteric arterial segments were investigated. Methanandamide elicited concentration-dependent relaxations of preconstricted mesenteric arterial beds (pEC(50)=6.0+/-0.1, E(max)=87+/-3%) and arterial segments (pEC(50)=6.4+/-0.1, E(max)=93+/-3%). In arterial beds, in vitro capsaicin pre-treatment blocked vasorelaxation to 1 and 3 microM methanandamide, and reduced to 12+/-7% vasorelaxation to 10 microM methanandamide. Methanandamide failed to relax arterial segments pre-treated in vitro with capsaicin. In arterial beds from rats treated as neonates with capsaicin to cause destruction of primary afferent nerves, methanandamide at 1 and 3 microM did not evoke vasorelaxation, and relaxation at 10 microM methanandamide was reduced to 26+/-4%. Ruthenium red (0.1 microM), an inhibitor of vanilloid responses, attenuated vasorelaxation to methanandamide in arterial beds (pEC(50)=5.6+/-0.1, E(max)=89+/-1%). Ruthenium red at 1 microM abolished the response to 1 microM methanandamide, and greatly attenuated relaxation at 3 and 10 microM methanandamide in arterial beds. In arterial segments, ruthenium red (0.15 microM) blocked vasorelaxation to methanandamide, but not to CGRP. In arterial segments, the vanilloid receptor antagonist capsazepine (1 microM) inhibited, and the calcitonin gene-related peptide (CGRP) receptor antagonist CGRP(8 - 37) (3 microM) abolished, methanandamide-induced relaxations. CGRP(8 - 37), but not capsazepine, attenuated significantly relaxation to exogenous CGRP. These data show that capsaicin and ruthenium red attenuate vasorelaxation to methanandamide in the rat isolated mesenteric arterial bed and small mesenteric arterial segments. In addition, CGRP(8 - 37) and capsazepine antagonize responses to methanandamide in mesenteric arterial segments. In conclusion, vanilloid receptors on capsaicin-sensitive sensory nerves play an important role in the vasorelaxant action of methanandamide in the rat isolated mesenteric arterial bed and small mesenteric arterial segments.

Animals↗
PubMed1995

Enhanced contractile responses mediated by different 5-HT receptor subtypes in basilar arteries, superior mesenteric arteries and thoracic aortas from stroke-prone spontaneously hypertensive rats.

1. The contractile effects of 5-hydroxytryptamine (5-HT) in isolated ring preparations of basilar arteries (BA) thoracic aortas (TA) and superior mesenteric arteries (SMA) from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats were investigated pharmacologically. 2. The pD2 values (expressed as a negative logarithm of of EC50) for 5-HT in BA of SHRSP were greater than those of WKY. Increased pD2 values for 5-HT were also found in SMA and TA of SHRSP when compared to WKY. 3. Ketanserin (a 5-HT2 antagonist) produced a biphasic displacement of the concentration-response curves for 5-HT in BA of WKY and SHRSP but elicited a parallel rightward shift of the 5-HT curve in SMA and TA of the two groups. 4. 5-CT (a 5-HT1 agonist)-induced contractions and their pD2 values in the presence of ketanserin were larger in BA of SHRSP than in those of WKY, while 5-CT did not contract SMA or TA in either group. 5. No significant difference was found in the contractile response induced by alpha-methyl-5-HT (a 5-HT2 agonist) in BA from SHRSP and WKY, while the pD2 values for alpha-methyl-5-HT were increased in SMA and TA from SHRSP when compared to WKY. 6. These results suggest that the hyperresponsiveness to 5-HT found in SHRSP arteries may be mediated by different 5-HT receptor subtypes, that is, by 5-HT1 in BA and by 5-HT2 in SMA and TA.

Animals↗
PubMed1997

BIBP 3226, suramin and prazosin identify neuropeptide Y, adenosine 5'-triphosphate and noradrenaline as sympathetic cotransmitters in the rat arterial mesenteric bed.

The physiological role of neuropeptide Y (NPY) and extracellular adenosine 5'-triphosphate (ATP) in sympathetic neurotransmission is becoming increasingly clear. To assess whether NPY and ATP act as cotransmitters together with noradrenaline (NA) in the sympathetic nerves of the superior mesenteric artery, the changes in perfusion pressure of the arterial mesenteric bed caused by nerve stimulation were recorded. Depolarization of the perivascular superior mesenteric arterial nerves caused frequency- and time-dependent increases in the perfusion pressure that were abolished by guanethidine, which implied the sympathetic origin of these responses. Independent perfusion with either 500 nM BIBP 3226, an NPY Y1 antagonist; 3 microM suramin, a competitive purinoceptor antagonist; or 0.1 nM prazosin, a competitive alpha-1 adrenoceptor antagonist, evoked approximately a 30% reduction in the rise in perfusion pressure caused by the 20- to 30-Hz electrical depolarization of the perimesenteric arterial nerves. Prazosin (0.1 nM) blocked the increases in perfusion pressure caused by electrical stimulation of the perimesenteric nerves but did not significantly reduce the vasomotor effect of exogenous NA. Likewise, 5-methyl urapidil and chloroethylclonidine, alpha-1 adrenoceptor antagonists with selectivity for the alpha-1A and alpha-1B receptor subtypes, respectively, concentration-dependently decreased the increase in perfusion pressure elicited by electrical stimulation of the perimesenteric nerves at concentrations lower than that required to block the vasoconstriction elicited by exogenous NA. The combined perfusion of 3 microM suramin plus 0.1 nM prazosin did not result in a complete inhibition of the physiological response. Only upon the simultaneous application of BIBP plus suramin plus prazosin was the rise in perfusion pressure abolished. These results support the working hypothesis that the sympathetic nerves of the rat mesenteric bed release NPY, ATP and NA that act as postjunctional cotransmitters in this neuroeffector junction.

Adenosine Triphosphate↗
PubMed2001

Colonic necrosis subsequent to catheter-directed thrombin embolization of the inferior mesenteric artery via the superior mesenteric artery: a complication in the management of a type II endoleak.

The optimal management of endoleaks after endovascular repair of abdominal aortic aneurysms remains to be established. In this report, we describe a persistent side-branch, or type II, endoleak 1 year after endograft implantation treated with catheter-directed embolization of the aneurysm sac and the inferior mesenteric artery via the superior mesenteric artery, with embolization agents including thrombin, lipiodol, and gelfoam powder. Shortly after the embolization procedure, colonic necrosis developed in the patient, manifested by peritonitis, which necessitated a partial colectomy. This case underscores the devastating complication of colonic ischemia as a result of catheter-directed embolization of the inferior mesenteric artery in the management of an endoleak.

Aged↗
PubMed1987

Rare case of the inferior mesenteric artery arising from the superior mesenteric artery.

The authors observed a variation of the inferior mesenteric artery, which arose from the superior mesenteric artery, in a 69-year-old Japanese male cadaver during dissection in 1984. In this case, no rudiment of the ordinary inferior mesenteric artery could be found on the abdominal aorta. There are few reports of this variation, and an extensive search of the available literature revealed only four cases, including two in Japan. Such a variation had been somewhat inadequately described as an "absence of the inferior mesenteric artery" in the previous reports, but we avoided this terminology, because all of the cases possessed an artery, which, though arising from the superior mesenteric artery instead of the abdominal aorta, had the same branches as a normal inferior mesenteric artery. Consistent with findings observed in the previous cases, the unusual inferior mesenteric artery arose as the first branch of the superior mesenteric artery, with the common trunk of both mesenteric arteries originating from the abdominal aorta at a level at which an ordinary superior mesenteric artery would arise. It is for this reason that we did not adopt another acceptable name, that is, "the common mesenteric artery," for this variation. The variation can be explained as the result of an unusual development of the embryonic artery system, which comprises a number of ventral splanchnic arteries interconnected by longitudinal anastomotic channels to supply the primitive digestive tube.

Aged↗
PubMed2000

Embolization of type II endoleaks fed by the inferior mesenteric artery: using the superior mesenteric artery approach.

PURPOSE: To evaluate the use of a superior mesenteric artery (SMA) approach to embolize type II endoleaks arising from the inferior mesenteric artery (IMA). TECHNIQUE: When reperfusion of the aneurysmal sac via the SMA occurs through the IMA, as shown by computed tomography (CT) and angiography, the IMA origin can be accessed via the marginal artery or the anastomosis of Riolan. The SMA is catheterized with a 5-F catheter, and a coaxial catheter is advanced to the leak to deliver 2- to 8-mm-diameter minicoils to embolize the IMA origin and entire aneurysmal sac. Embolization usually requires from 1 to 2 hours to complete. In our experience with this technique in 11 cases, complications have not occurred, and there has been only one very small residual leak that sealed the next day. Over a 24.5-month follow-up (range 12-39), the endoleaks have remained sealed according to serial color duplex scans. CONCLUSIONS: Successful percutaneous treatment of type II endoleak due to IMA inflow can be accomplished using an SMA access via the Riolan anastomosis or marginal artery. The procedure appears to be safe and has no adverse effects.

Aged↗
PubMed1986

Action and metabolism of des(Arg)kinins in mesenteric arteries.

Kallidin and bradykinin can be hydrolyzed at their C-termini to produce des(Arg10)kallidin and des(Arg9)bradykinin respectively. These des(Arg)kinins, previously thought to be biologically inactive, are now known to have potent effects on B1 receptors. Although stimulation of B1 receptors has been reported to produce peripheral vasodepressor responses in certain experimental states, only constriction has been reported in isolated vessels (i.e., rabbit aorta, basilar artery, mesenteric vein). In the present study, we have investigated the biologic activity of des(Arg) kinins on a peripheral resistance vessel (rabbit mesenteric artery). We found that des(Arg)bradykinin relaxes mesenteric arteries, and that its potency relative to kallidin and bradykinin is consistent with the presence of B1 receptors. Further, intact mesenteric arteries, and a plasma membrane fraction purified from these arteries, contained a carboxypeptidase activity which was capable of producing des(Arg)kinins from both kallidin and bradykinin. Thus, these data demonstrate that the vasculature has the enzymatic capacity to form B1 kinins, and that stimulation of B1 receptors in resistance vessels can be associated with peripheral vasodilation.

Animals↗
PubMed2004

Rare case of the inferior mesenteric artery and the common hepatic artery arising from the superior mesenteric artery.

We found a case in which inferior mesenteric artery and the common hepatic artery arose from the superior mesenteric artery, forming the common hepatomesenteric trunk, during a routine dissection carried out at Iwate Medical University in 2002. This variation is rare, but can be embryonically explained. A change in the positions of the disappearance of the ventral splanchnic arteries and the longitudinal anastomotic channel results in variations in the system of arteries distributed to the digestive organs. In the present case, the longitudinal anastomotic channel between the superior and the inferior mesenteric arteries survived to form the common mesenteric artery, which was joined by the common hepatic artery, forming the common hepatomesenteric trunk.

Aged↗