Disease relevance of Ca5a

• A single 2.7-kb alpha1BAR mRNA was detected in aorta and vena cava during normoxia and hypoxia [1].
• Venous thrombosis was induced by ligature of the inferior vena cava in rats whose blood was made hypercoagulable by intravenous (IV) administration of tissue thromboplastin [2].
• Heart failure was induced by a fistula between the aorta and vena cava [3].
• We examined the water, sodium, and potassium composition of the thoracic aorta, abdominal aorta (plus iliac arteries), and veins (vena cava and portal vein) from rats with aortic coarctation [4].
• Endothelin-1 concentrations in blood collected from the suprahepatic vena cava were measured before and after ischemia/reperfusion by use of a sandwich enzyme immunoassay [5].

Psychiatry related information on Ca5a

• Feeding during 6 h of water deprivation was restored by slowly infusing the volume of water normally drunk into the stomach, jejunum, or cecum, but not in the vena cava or hepatic portal vein [6].

High impact information on Ca5a

• Further characterization of the vascular response revealed that HSP70 induction occurred in both the thoracic and abdominal aortas as well as in the vena cava [7].
• Microdialysis probes placed within the vena cava and brain cortex were used to directly compare steady-state, interstitial unbound diazepam levels in both Wistar and genetically analbuminemic rats [8].
• Indeed after an oral or intraduodenal dose of 5 mg/kg aspirin, generation of portal vein 6-keto-PGF1 alpha was inhibited to much the same extent as platelet TxB2, while inferior vena cava 6-keto-PGF1 alpha formation was spared [9].
• In contrast, AII infusion did not alter release of 6-keto-PGF1 alpha or PGE2 from inferior vena cava segments or from renal cortex slices [10].
• Heparinized catheters were placed into the portal vein, inferior vena cava, aorta, and left ventricle with exit from the neck [11].

Chemical compound and disease context of Ca5a

• One hundred fifty-two growing Fischer 344 rats were either transplanted with a sarcoma (TB) or injected with saline (NTB, day 0), had aseptic placement of superior vena cava catheter (day 14), and were infused with total parenteral nutrition solutions (days 18-28) [12].
• METHODS: Parenchymal liver disease was induced by carbon tetrachloride administration, portal hypertension by partial portal vein ligation, and portasystemic shunting by end to side anastomosis of the portal vein to the inferior vena cava [13].
• The ability of vessels (rings of arteries and vena cava) to synthesize prostacyclin (PGI2) "in vitro" was analyzed in the initial (6-day) and chronic (6-week) phase of two-kidney, two clip hypertension [14].
• Forty-five rats had feeding catheters placed into either the stomach (IG, n = 31) or the superior vena cava (IV, n = 14) and then received acetic acid (colitis) or saline (control) enemas [15].
• Conversion of D-tryptophan to the L-isomer in the rat was found by an examination of plasma from the posterior vena cava and the portal vein, following stomach intubation of 100 micromoles D-tryptophan/100 g of body weight [16].

Biological context of Ca5a

• Transient transfection experiments identify the minimal promoter region between -270 and -143 and sequence between -270 and -248 that are required for transcription of the alpha1BAR gene in aorta and vena cava SMC during normoxia and hypoxia [1].
• Elevation of venous pressure within the vascular bed by gradual occlusion of the inferior vena cava led to a significant vasoconstriction of the smaller vessels, suggesting that a significant myogenic component was present [17].
• Isolated SMC from these rabbit blood vessels as well as from the aorta and vena cava of the rat, when cultured on a collagen or laminin matrix, uniformly revealed an ETB-R-mediated increase in apoptosis upon exposure to mechanical deformation plus exogenous ET-1 (10 nmol/L) [18].
• Removal of the adrenal glands or cannulation of the vena cava prevented the accumulation of epinephrine and the rise in inhibitor-1 phosphorylation [19].
• Reporter gene transfection assays in rat aorta and vena cava SMCs showed that this 5'-flanking region, which lacks a TATA-box, possesses strong promoter activity [20].

Anatomical context of Ca5a

• A systematic survey of endothelial junctions in elastic (aorta) and muscular (mesenteric) arteries and in medium (renal and mesenteric) and large (cava inferior) size veins has been carried out in the rat using freeze-cleaved preparations [21].
• Consequently, we prepared acid extracts of the pulmonary artery and vena cava of female rats [22].
• We previously demonstrated that alpha1B-adrenergic receptor (AR) gene transcription, mRNA, and functionally coupled receptors increase during 3% O2 exposure in aorta, but not in vena cava smooth muscle cells (SMC) [1].
• The discharge characteristics of mechanoreceptors located in the left superior vena cava were determined in an in vitro preparation developed from the rat [23].
• In cirrhotic rats, blood pressures in the portal vein and the terminal portal venule were 173 and 100 mm H2O, respectively, while those in the terminal hepatic venule and the inferior vena cava were elevated only slightly above normal [24].

Associations of Ca5a with chemical compounds

• After 4 days of biliary drainage, rat livers were perfused in vitro in either forward (through the portal vein) or backward direction (through the vena cava) in single-pass arrangement with taurodeoxycholate (32 nmol.min-1.g liver-1) [25].
• Using the selective OT receptor ligand compound VI, we detected a high number of OT-binding sites in the rat vena cava and aorta [22].
• An inverted V-shape polyethylene cannula, either heparin bonded or silicon coated, was inserted into the portal vein and inferior vena cava to maintain venous return from the splanchnic and lower caval regions of the anhepatic rat [26].
• After 30 min of vena cava occlusion and 10 min of reperfusion a more marked increase in chemiluminescence (37 +/- 5 cps/cm2), hydrogen peroxide (0.30 +/- 0.01 mumol/L), lactate dehydrogenase (730 +/- 10 U/L) and aspartate aminotransferase (140 +/- 10 U/L) was observed [27].
• The role of the liver in the pancreatic hormonal response to endotoxin was investigated by infusing lipopolysaccharide slowly into the portal vein or systemic inferior vena cava [28].

Analytical, diagnostic and therapeutic context of Ca5a

• In contrast, if the liver was bypassed by performing a portacaval shunt or by injecting into the inferior vena cava, radioactivity was maximal in the lung (2,454.3% +/- 302.3 10 min after IVC injection) with activity in the liver of only 89.3% +/- 10 [29].
• Reverse-phase HPLC of aorta and vena cava extracts revealed a single peak corresponding to the amidated OT nonapeptide [22].
• In group 1, completion of portal vein (PV), suprahepatic vena cava (SVC), and descending vena cava anastomoses resulted in decreased NADH levels toward those after preparation of the vessels before ligation [30].
• Rapid (1 min) antegrade (by way of portal vein) or retrograde (through hepatic veins by way of vena cava) perfusions were performed in a nonrecirculating (once-through) mode in Ca+(+)-free medium [31].
• Blood samples for the measurement of tumor necrosis factor and endotoxin were collected by way of an indwelling catheter placed in the suprahepatic vena cava [32].

References