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At least 1,207 records · Page 67Linked to original sources
PubMed2001

Angiotensin type 2 receptors: potential importance in the regulation of blood pressure.

The angiotensin type 2 receptor is one of two major angiotensin II receptors that has been identified, cloned and sequenced. The other major receptor, the angiotensin type 1 receptor, is thought to mediate most of the biological responses to the peptide. The angiotensin type 2 receptor is expressed heavily in fetal tissues, but only at a low level in the adult. Documented angiotensin type 2 receptor expression sites in the adult include kidney, heart and mesenteric blood vessels. The function of the angiotensin type 2 receptor is just beginning to be explored. Most of the evidence suggests that the angiotensin type 2 receptor mediates a vasodilator signalling cascade that includes bradykinin, nitric oxide and cyclic guanosine 5-monophosphate. At least some of the beneficial actions of angiotensin type 1 receptor blockade, such as hypotension, are mediated by stimulation of the angiotensin type 2 receptor. Several recent papers suggest that angiotensin type 2 receptors, presumably located in systemic blood vessels, mediate vasodilation and hypotension. The angiotensin type 2 receptor may be a new therapeutic target and candidate gene for the pathophysiology of hypertension.

Animals↗
PubMed2006

Schwann cells in rat vascular autonomic nerves activated via purinergic receptors.

Schwann cells at the somatic neuromuscular junction possess adenosine receptors that when activated by the release of endogenous transmitter modulate quantal transmitter release. Recently, purinergic receptors have been shown to exist on Schwann cells of axon varicosities in visceral smooth muscle where they are activated by endogenous transmitters to give a calcium transient, although adenosine receptors were not identified. In the present work, we show that Schwann cells associated with axon varicosities of vascular smooth muscle, namely that of mesenteric blood vessels, possess both adenosine and purinergic receptors that when activated give rise to calcium transients in these cells. Then qualitative differences exist in the extent of adenosine and purine receptors that give rise to calcium transients in Schwann cells located in these different muscles.

Adenosine↗
PubMed1996

Control of colonic variceal haemorrhage with a somatostatin analogue.

A 64 year old caucasian male with known alcoholic liver disease presented with rectal bleeding. The patient bled repeatedly despite resuscitation. A sigmoid colectomy was performed following an angiogram. Large colonic, rectal and mesenteric variceal vessels were noted at surgery. Further bleeding postoperatively was rapidly controlled with octreotide infusion. Octreotide may be as useful in the control of colonic variceal bleeding as it is in the control of oesophageal variceal bleeding.

Colon↗
PubMed1993

Protein-losing enteropathy due to secondary amyloidosis of the gastrointestinal tract.

A case of a 71 year old woman who experienced weight loss, diarrhea and edema due to protein-losing enteropathy caused by amyloidosis secondary to rheumatoid arthritis is described. Amyloid deposits were found in the systemic organs, specifically in the bowel. The arterioles were massively involved within the laminae propriae and many were narrowed considerably due to amyloid deposits. Ulcerative lesions, which were accompanied with the ruptured arterioles, were also found. Lymphangiectasia was present in the submucosa, subserosa and mesenterium. The mesenteric lymphatic vessels were deposited markedly with amyloid. The principal cause of the protein loss might be related to the increased capillary permeability to plasma proteins and the exudation through an inflamed mucosa. Functional disruption of the lymphatic flow in the bowel and mesenterium might also participate in the mechanisms of the protein loss. Evidence in this study supports the theory that lymphatic disorders in some patients with gastrointestinal amyloidosis are one of the important factors in the pathogenesis of protein-losing enteropathy.

Aged↗
PubMed1997

Tetrodotoxin-sensitive sodium current in sheep lymphatic smooth muscle.

1. Fast inward currents were elicited in freshly isolated sheep lymphatic smooth muscle cells by depolarization from a holding potential of -80 mV using the whole-cell patch-clamp technique. The currents activated at voltages positive to -40 mV and peaked at 0 mV. 2. When sodium chloride in the bathing solution was replaced isosmotically with choline chloride inward currents were abolished at all potentials. 3. These currents were very sensitive to tetrodotoxin (TTX). Peak current was almost abolished at 1 microM with half-maximal inhibition at 17 nM. 4. Examination of the voltage dependence of steady state inactivation showed that more than 90% of the current was available at the normal resting potential of these cells (-60 mV). 5. The time course of recovery from inactivation was studied using a double-pulse protocol and showed that recovery was complete within 100 ms with a time constant of recovery of 20 ms. 6. Under current clamp, action potentials were elicited by depolarizing current pulses. These had a rapid upstroke and a short duration and could be blocked with 1 microM TTX. 7. Spontaneous contractions of isolated rings of sheep mesenteric lymphatic vessels were abolished or significantly depressed by 1 microM TTX.

Action Potentials↗
PubMed1990

Responses of rat isolated intestinal segments to stimulation of perivascular mesenteric nerve fibres.

1. Isolated preparations of segments of rat jejunum were set up for isotonic recording of the activity of the longitudinal smooth muscle and the extrinsic nerve supply running with the mesenteric blood vessels was stimulated for 30-s periods at 0.5-20 Hz. 2. Contractions were regularly elicited during periods of stimulation at 0.5-2 Hz, and were usually elicited during stimulation at 5 Hz, but relaxations were usually elicited during stimulation at 10 and 20 Hz. On cessation of the period of stimulation, a secondary contraction occurred in most preparations regardless of whether the primary response during the period of stimulation had been a contraction or a relaxation. 3. Tetrodotoxin (0.9 microM) abolished responses during periods of stimulation and the secondary contraction. 4. The relaxations were mimicked by noradrenaline and were abolished by blockade of alpha- plus beta-adrenoceptors but were not affected by hexamethonium, indicating that they are attributable to stimulation of postganglionic noradrenergic fibres. 5. The contractions were mimicked by acetylcholine and were abolished by atropine and hexamethonium, suggesting that they are attributable to stimulation of preganglionic cholinergic nerves: they were also abolished in the presence of capsaicin, indicating that sensory neuropeptide-containing nerve fibres may be involved. 6. The secondary contraction that usually occurred on cessation of stimulation was still present after blockade by atropine or capsaicin of the contractions occurring during stimulation. It was also present after blockade by propranolol and phentolamine of the relaxations occurring during stimulation, and was not affected by indomethacin.

Animals↗
PubMed1977

The mode of action of tetrabenazine on peripheral noradrenergic nerves.

1. Tetrabenazine (100 mg/kg i.p. in rats) greatly decreased catecholamine-induced histofluorescence in the iris, hepatic portal vein, inferior vena cava and mesenteric blood vessels 4 h after injection. Fluorescence returned to normal by 24 h after injection. 2. The extent of this depletion (4 h after tetrabenazine) was similar to that seen 18 h after reserpine (0.5 mg/kg i.p.). 3. Incubation of tissues taken from rats 4 h after this dose of tetrabenazine with noradrenaline 5 X 10(-6)M restored the intraneuronal fluorescence as well as the electron density of noradrenergic vesicle cores viewed with the electron microscope. No such repletion was seen on incubation of tissues from reserpine-treated rats with noradrenaline under the same conditions. 4. Incubation of tetrabenazine-treated hepatic portal veins with noradrenaline also reinstated the normal response to electrical stimulation of the intramural nerves. This did not occur with reserpine-treated veins. 5. The interpretation that tetrabenazine exerts a reversible depleting effect on the noradrenergic vesicle is supported by the demonstration that it exerts no monoamine oxidase inhibiton.

Animals↗
PubMed1984

The inhibitory effect of aspirin on lymphatic contractility.

Spontaneous contractions and those elicited by two different methods of electrical stimulation were studied in isolated segments of bovine mesenteric lymphatic vessels. The effect of aspirin (a cyclo-oxygenase inhibitor) on spontaneous and evoked contractions of isolated lymphatic vessels was investigated. Aspirin at doses of 10(-6) M or greater depressed both spontaneous and action potential-dependent evoked contractions, but failed to inhibit contractions evoked by high current field stimulation. These latter contractions were rapidly depressed by the application of D600. When aspirin was applied for five minute periods, inhibition never occurred within the period of drug administration but was delayed, with maximum inhibition occurring approximately 10 min after washout of the drug. It is concluded that the inhibitory action of aspirin is unlikely to be a non-specific depression of the contractile mechanism, but rather a reduction in excitability probably as a result of cyclo-oxygenase inhibition.

Action Potentials↗
PubMedDate not supplied

Vascular injury associated with naturally occurring strangulating obstructions of the equine large colon.

Ten horses were euthanatized before, during, or after surgery to correct severe volvulus of the large colon. At surgery, the colonic serosa changed from blue-gray, blue or purple toward a more normal pink in seven horses after the volvulus was corrected. The mucosa consistently remained black or dark red. Results of postmortem colonic microangiography revealed perfusion of the serosa and the circular and longitudinal muscle layers, but mucosal perfusion was limited by thrombosis in the muscularis mucosae and submucosa. There was evidence of thrombosis of the mesenteric colic vessels in six horses. Damage to the colonic vascular system, especially thromboembolism in the submucosa, may be an important limitation to colonic viability after surgical correction of volvulus of the large colon.

Angiography↗
PubMed2005

Decreased prothrombotic effects of pegylated recombinant human megakaryocyte growth and development factor in thrombocytopenic state in a rat thrombosis model.

Previous in vitro studies demonstrated that thrombopoietin (TPO) acts on platelets to activate a variety of intracellular signaling pathways and to enhance platelet sensitivity to multiple agonists. Little is known, however, about whether TPO exerts prothrombotic effects in vivo. The aim of this study was to examine the effects of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF), a pegylated N-terminal domain of human TPO, in a rat model of venous thrombosis. A microthrombus was photochemically induced on the vessel wall of a mesenteric venule, but the vessel was not occluded by it. A single intravenous injection of PEG-rHuMGDF (3 microg kg(-1)) after the thrombus generation into normal rats enhanced the thrombus size, resulting in transient thrombotic occlusion in the majority of rats. Stimulatory effects on thrombus growth were also observed following administration of glycosylated recombinant human full-length TPO (6 microg kg(-1)). In rats rendered thrombocytopenic by total body irradiation, however, PEG-rHuMGDF, even at 300 microg kg(-1), did not induce a significant increase in thrombus size or thrombotic occlusion. Platelets from thrombocytopenic rats had decreased surface levels of c-Mpl and decreased sensitivity to PEG-rHuMGDF in an in vitro aggregation response. Thus, decreased prothrombotic effects of PEG-rHuMGDF in thrombocytopenic rats might be the result not only of low platelet counts but also of decreased platelet reactivity to PEG-rHuMGDF. These results indicate that PEG-rHuMGDF has little effect on venous thrombus formation in thrombocytopenic states associated with high endogenous TPO levels.

Animals↗
PubMed1998

Intestinal cryptococcosis in a common marmoset (Callithrix jacchus).

A five-year-old female common marmoset (Callithrix jacchus) died after a one-month clinical course of nonspecific signs. Pathologic findings were acute diffuse fibrinonecrotizing enteritis and granulomatous endolymphangitis of intestinal and mesenteric lymphatic vessels. Both lesions were associated with a marked proliferation of Mayer's mucicarmine-positive, 4 to 15 microm yeasts that were surrounded by a wide clear halo. The infection was probably acquired by oral route. Other findings included moderate multifocal granulomatous and necrotizing hepatitis and mesangial nephropathy. Although the immunological status of this marmoset was unknown, cryptococcosis might induce primary lethal intestinal infections in callitrichids.

Animals↗
PubMedDate not supplied

Comparison of radiographic and computed tomography lymphangiography for identification of the canine thoracic duct.

Standard radiographic lymphangiograms and computed tomography (CT) lymphangiograms were performed on 10 female dogs without intrathoracic disease. Positive contrast lymphagiography was performed by injection into a catheterized mesenteric lymphatic vessel, and lateral thoracic radiographs, ventrodorsal thoracic radiographs, and thoracic CTs were obtained. The number of visible ducts was recorded for each image at the midbody of the ninth thoracic vertebra (T9) through the first lumbar vertebra (L1). Data were combined for all dogs at each data acquisition point. Data were analyzed by comparing data from all three images independently, and then by combining data for the radiographs and comparing the study with the highest number of visible duct branches to the CT. Significant differences in numbers of branches were found at T11 and L1. This study suggests that CT may be able to quantify branches of the thoracic duct more accurately than standard radiographic lymphangiography.

Animals↗
PubMed2004

Cyclooxygenase-2 inhibition improves vascular endothelial dysfunction in a rat model of endotoxic shock: role of inducible nitric-oxide synthase and oxidative stress.

We investigated whether cyclooxygenase (COX) isoforms (COX-1 and COX-2) and decreased NO availability contribute to endothelial dysfunction in endotoxemic rats. The involvement of reactive oxygen species (ROS) was also evaluated. Rats were injected with Salmonella-derived lipopolysaccharide or saline. After 6 h, endothelial function of mesenteric resistance arteries was evaluated. In controls, acetylcholine (ACh)-induced relaxation was inhibited by the nitric-oxide synthase inhibitor N(G)-monomethyl-l-arginine (l-NMMA) and unaffected by 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl)-phenyl-2(5H)-furanone (DFU) (COX-2 inhibitor). In lipopolysaccharide (LPS)-treated rats, the response to ACh was blunted compared with controls, less sensitive to l-NMMA, and enhanced by DFU. COX-2 blockade also improved the inhibitory effect of l-NMMA on cholinergic relaxation. SC-560 [5-(4-clorophenyl)-1-(4-metoxyphenyl)-3-trifluoromethylpirazole] (COX-1 inhibitor) did not modify the response to ACh in both groups. LPS-induced endothelial dysfunction was unaffected by the thromboxane A(2) (TxA(2)) receptor antagonist SQ-29548 (7-[3-[[2-[(phenylamino)carbonyl]hydrazino]methyl]-7-oxabicyclo[2.2.1] hept-2-yl]-[1S(1alpha,2alpha(Z),3alpha,4alpha)]-5-heptenoic acid). In vivo inducible nitric-oxide synthase (iNOS) inhibition by S-methylisothiourea partly attenuated LPS-induced endothelial dysfunction. The antioxidants ascorbic acid and superoxide dismutase normalized endothelium-dependent relaxation and restored the inhibitory action of l-NMMA on ACh. Responses to sodium nitroprusside were similar in both groups. In LPS-treated rats, reverse transcription-polymerase chain reaction showed a marked increase in mesenteric iNOS and COX-2 expressions, whereas endothelial nitric-oxide synthase and COX-1 were unchanged. LPS-induced COX-2 overexpression was reduced but not abrogated by S-methylisothiourea. LPS-induced COX-2 up-regulation was also documented by immunohistochemistry. In conclusion, mesenteric resistance vessels from endotoxemic rats show impaired endothelial function due to reduced NO availability, a condition that is partly ascribable to an iNOS-dependent enhanced COX-2 expression, whereas TxA(2) does not seem to be involved. Oxidative stress is the main mechanism responsible for reduced NO availability, and COX-2 might act as a source of ROS.

Acetylcholine↗
PubMed1987

Differential intestinal absorption of two fatty acid isomers: elaidic and oleic acids.

The absorption of 14C-labeled oleic acid and 14C-labeled elaidic acid was studied in bile- and pancreatic juice-diverted adult rats. In some cases these acids were compared with 14C-labeled palmitic acid absorption. Sodium taurocholate-emulsified test infusates containing an equimolar mixture of monopalmitin and two fatty acids (oleic and elaidic or palmitic), one of which was 14C labeled, were infused through a duodenal canula. The chyle was collected from the mesenteric lymphatic vessel by plastic tubing. Among the three fatty acids studied, oleic acid exhibited the highest lymphatic recovery rate (43-50%). Elaidic and palmitic acids appeared more slowly and in lesser amounts (10-17%). Simultaneously, the highest amount of chylomicrons was observed when the lipid emulsion contained oleic acid alone; the lowest was observed when elaidic acid was the only unsaturated fatty acid. Experimental data have also shown that compared with elaidic acid, oleic acid is preferentially incorporated into the lymph triglycerides. We can conclude from the data presented that the enterocytic enzymes involved in the absorption of lipids show a high degree of specificity related to the fatty acid isomery, since the absorption of elaidic acid differs markedly from its isomer oleic acid.

Animals↗
PubMed2000

Physiological roles of endogenous nitric oxide in lymphatic pump activity of rat mesentery in vivo.

Physiological roles of endogenous nitric oxide (NO) in the lymphatic pump activity of rat mesenteries in vivo were evaluated using an intravital video microscope system. Changes in the pumping frequency (F), the end diastolic diameter (EDD), and the end systolic diameter (ESD) of the mesenteric lymph microvessels were measured with the microscope system and then the pump flow index (PFI) was calculated. A 15-min superfusion of 30 microM N(omega)-nitro-L-arginine methyl ester (L-NAME) in the mesenteries caused significant increases of F and PFI and a significant decrease of the EDD and ESD. Simultaneous superfusion of 1 mM L-arginine with 30 microM L-NAME produced a significant reversal of the L-NAME-mediated increase of F and decrease of ESD. A 15-min superfusion of 100 microM aminoguanidine caused no significant effects on F, EDD, and ESD of the mesenteric lymph vessels in vivo. These findings suggest that endogenous NO has physiologically modulated the lymphatic pump activity in rat mesentery in vivo and that the production and release of NO may be mediated by constitutive NO synthase but not by inducible NO synthase.

Animals↗
PubMed2003

Increased calcium intake reduces plasma cholesterol and improves vasorelaxation in experimental renal failure.

Chronic renal failure (CRF) is associated with abnormal lipid metabolism and high prevalence of vascular complications. Calcium salts are commonly used in CRF as phosphate binders. Increased calcium intake may also lower plasma cholesterol and beneficially influence vascular tone. Therefore, we investigated the influence of increasing dietary calcium from 0.3% to 3.0% for 8 wk after 5/6 nephrectomy (NTX) on plasma cholesterol and mesenteric resistance vessel tone in male Sprague-Dawley rats. The groups were Sham, Sham-Calcium, NTX, and NTX-Calcium (n = 10-11). Blood pressure was modestly elevated after NTX, whereas the plasma creatinine, urea nitrogen, phosphate, and parathyroid hormone levels were clearly increased. The high-calcium diet suppressed plasma phosphate and parathyroid hormone but was without effect on blood pressure. The NTX resulted in 1.6-fold elevation in plasma total cholesterol and 40% reduction in high density-to-low density lipoprotein ratio (HDL/LDL). However, the lipid profile in NTX rats on the high-calcium diet did not differ from sham-operated controls. The endothelium-mediated relaxations induced by acetylcholine were impaired in NTX rats, whereas the response was normalized by a high-calcium diet. No differences in vasorelaxations by the endothelium-independent vasodilator nitroprusside were detected. In conclusion, improved vasorelaxation after a high-calcium diet could be due to reduced plasma total cholesterol and ameliorated HDL/LDL ratio, although decreased plasma phosphate and parathyroid hormone may also play a significant role in the vascular effects of increased calcium intake.

Animals↗
PubMed1980

Indices of sympathetic activity in the sinoaortic-denervated hypertensive rat.

Blood pressure and circulating levels of norepinephrine (NE), epinephrine (Epi), and dopamine-beta-hydroxylase (DBH) were measured sequentially in sinoaortic-denervated (SAD) Wistar rats and in sham-operated (SO) rats. Systolic tail pressure, plasma NE and E, and plasma DBH all increased significantly within 2 days in SAD rats. In separate studies of rats with indwelling arterial catheters, arterial pressure and plasma NE and DBH were increased in SAD rats in home cages; restraint caused similar increases of pressure and catecholamines in both groups. Systolic pressure remained increased up to 4 mo and plasma DBH for 10 wk in SAD rats; plasma NE and E, however, declined by 3 wk and thereafter remained close to values of SO rats. Additionally, DBH was increased in heart, mesenteric blood vessels and adrenal glands of SAD rats up to 6 wk; tissue monoamine oxidase activity was also increased up to 4 mo. These findings suggest that activation of the sympathetic nervous system initiates and probably sustains hypertension in SAD rats up to 6 wk after operation; thereafter some other mechanism(s) sustains the hypertension.

Animals↗