Disease relevance of RTA

• We have now examined the toxicity of EGF-RTA and EGF-DTA on cultured hepatocytes [1].
• We conclude that oral administration of tubular antigen can modulate the intensity of interstitial nephritis produced by immunization, but that the regulatory mechanism is not dependent (at all doses of fed antigen) on suppressed DTH reactivity to RTA or suppressed antigen-specific IgG [2].
• TNA-alpha (10(6) U/ml, iv) did not produce acute phase hypotension but initially raised arterial blood pressure and heart rate (HR), did not increase RNI production by PMN, and inhibited RNI production by A23187 stimulated RTA ex vivo [3].
• Anti-CD4 mAbs (MRC Ox35) given for 2 weeks after RTA/IFA completely prevented the induction of resistance to HN, all rats developing proteinuria as well as high titers of autoantibody and Ig and C deposits in glomeruli [4].

High impact information on RTA

• A disulfide-linked conjugate between asialofetuin (ASF) and the toxic A chain (RTA) of ricin is as potent a toxin for cultured rat hepatocytes as our previously described conjugate between ASF and fragment A of diphtheria toxin (DTA) [1].
• An RTA conjugate of epidermal growth factor (EGF) was a potent toxin for 3T3 cells [1].
• Rats receiving chronic intraventricular infusions of RTA showed significantly more low affinity NGF receptor immunoreactive (p75NGFR-IR) neurons on the lesioned side than did control animals 2 weeks following unilateral fimbria-fornix lesion [5].
• An antibody against the extracellular domain of TrkA (RTA) was used as ligand to stimulate internalization and phosphorylation of TrkA [6].
• Indeed, when saralasin was infused together with either PGE 2 or PGI2 the previously noted effects on delta P, QA, RTA and Kf were largely abolished [7].

Chemical compound and disease context of RTA

• The hypotension was associated with elevation of biologically active TNF-alpha in plasma, increased production of RNI (NO2- and NO3- anion) in rat neutrophils (PMN) and suppression of RNI production by A23187 (1 microM) stimulated thoracic aorta (RTA) ex vivo [3].

Biological context of RTA

• RESULTS: Histology revealed minimal peritubular and interstitial inflammation in the RTA/CFA group one week after immunization while extensive interstitial inflammation with few preserved superficial nephron was observed three weeks after RTA/CFA immunization [8].
• Renal histology, inulin clearance, DTH responses to RTA, and IgG antibody responses to RTA were monitored as endpoints of the study [2].
• We examined the effect of chronic administration of ETOH on Escherichia coli-mediated suppression of relaxation and nitric oxide (NO) production by the rat thoracic aorta (RTA) and gene expression for constitutive NO synthase (cNOS) by the adrenal gland [9].

Anatomical context of RTA

• To test the molecular nature of the NGF receptor responsible for the ability of NGF to rescue septal cholinergic neurons following axotomy, we infused polyclonal antibodies that act as specific agonists of trkA (RTA) into the lateral ventricle of fimbria-fornix lesioned animals [5].
• The goal of this study was to determine the relative importance of myosin light-chain kinase (MLCK) and PKC in basal and stimulated LC(20) phosphorylation in rat tail arterial smooth-muscle strips (RTA) [10].
• 1. The mechanisms of the sustained vasodilator actions of corticotrophin-releasing factor (CRF) and sauvagine (SVG) were studied using rings of endothelium de-nuded rat thoracic aorta (RTA) and the isolated perfused rat superior mesenteric arterial vasculature (SMA) [11].
• Intact WGA-SS-RTA, but not hybrid that was pretreated with dithiothreitol to uncouple RTA from the WGA carrier, reliably killed vagal motor neurons [12].
• This study has investigated the receptors mediating endothelin-induced contraction of isolated ring preparations of rat thoracic aorta (RTA) and rabbit carotid artery (RCA), pulmonary artery (RPA), and jugular vein (RJV) [13].

Associations of RTA with chemical compounds

• These increases in delta P and RTA and decreases in QA and Kf are typical of changes induced by angiotensin II (AII) [7].
• Thus, saralasin transformed the renal action of PGE2 and PGI2 from vasoconstrictor (low QA, high RTA) to vasodilator (high QA and low RTA) [7].
• Micropuncture studies on day 7 in the RTA/CFA group revealed a significant reduction in single nephron GFR due to a profound reduction in nephron plasma flow and in the ultrafiltration coefficient [8].
• To assess the role of increased nitric oxide production secondary to iNOS induction on the glomerular hemodynamic changes observed in the early stages of the disease, the iNOS blocker (l-N(6)-iminoethyl lysine, L-NIL) was administered IV (1 mg/h) in RTA/CFA rats and CFA rats [8].
• A23187- and ACh-induced relaxation was attenuated in RTA obtained from septic rats, whereas the relaxation to nitroglycerin was slightly enhanced [9].

Other interactions of RTA

• However, TNF-alpha mediates in part LPS-induced inhibition of RNI production by RTA [3].
• Identical results were obtained when a specific agonist of the NGF receptor TrkA, the bivalent anti-rat TrkA IgG (RTA), was infused into the cortex in place of NGF [14].

Analytical, diagnostic and therapeutic context of RTA

• Indirect peroxidase immunohistochemistry demonstrated transport of RTA to vagal sensory neurons and WGA to both vagal sensory and motor neurons [12].

References