Previous reports have shown a stimulatory effect of vasopressin (VP) on Na-K-ATPase and rBSC-1 expression and activity. Whether these VP-dependent mechanisms are operating in vivo in physiological conditions as well as in chronic renal failure (CRF) has been less well studied. We measured ATPase expression and activity and rBSC-1 expression in the outer medulla of controls and moderate CRF rats both before and under in vivo inhibition of VP by OPC-31260, a selective V 2-receptor antagonist. OPC-31260 decreased Na-K-ATPase activity from 11.2 Ϯ 1.5 to 3.7 Ϯ 0.8 in controls (P Ͻ 0.05) and from 19.0 Ϯ 0.8 to 2.9 Ϯ 0.5 mol P i ⅐ mg protein Ϫ1 ⅐ h Ϫ1 in moderate CRF rats (P Ͻ 0.05). CRF was associated with a significant increase in Na-K-ATPase activity (P Ͻ 0.05). Similarly, CRF was also associated with a significant increase in Na-K-ATPase expression to 164.4 Ϯ 21.5% compared with controls (P Ͻ 0.05), and OPC-31260 decreased Na-K-ATPase expression in both controls and CRF rats to 57.6 Ϯ 9.5 and 105.3 Ϯ 10.9%, respectively (P Ͻ 0.05). On the other hand, OPC-31260 decreased rBSC-I expression in both controls and CRF rats to 60.8 Ϯ 6.5 and 30.0 Ϯ 6.9%, respectively (P Ͻ 0.05), and was not influenced by CRF (95.7 Ϯ 5.2%). We conclude that 1) endogenous VP modulated Na-K-ATPase and rBSC-1 in both controls and CRF; and 2) CRF was associated with increased activity and expression of the Na-K-ATPase in the outer medulla, in contrast to the unaltered expression of the rBSC-1. The data suggest that endogenous VP could participate in the regulation of electrolyte transport at the level of the outer medulla.vasopressin; rbsc-1; sodium-potassium-adenosine 5Ј-triphosphatase; chronic renal failure THERE IS STRONG EVIDENCE that vasopressin (VP) stimulates Na-K-ATPase and Na ϩ -K ϩ -Cl Ϫ cotransporter in the kidney outer medulla and, more precisely, in the medullary thick ascending limb of Henle (mTAL) (15). However, the experimental designs so far have been mostly related to the administration of exogenous VP, to either intact animals or in vitro preparations. The question of whether the level of endogenous VP activity plays a homeostatic role at the kidney outer medulla has not yet been examined. The introduction of powerful VP inhibitors has made it possible to design experiments looking at that question. OPC-31260 is a nonpeptide V 2 -receptor inhibitor developed by Yamamura et al. (21), and its actions are limited to states where VP activity is present. This approach was recently used by Ohara et al. (18), who were able to show a VP-mediated upregulation of the aquaporin-2 water channel in pregnant rats by using OPC-31260.In addition, previous experiments from our laboratory and those of others have suggested that in chronic renal failure the remaining nephrons suffer diverse adaptive mechanisms. Thus Bertuccio et al. (1, 2) showed an increase in intracellular cAMP levels in microdissected mTAL segments in chronic renal failure (CRF) rats, which were unresponsive to VP in vitro, opposed to baseline lower levels and a dose-respon...
We investigated the effect of ovariectomy(oVx) on renal and systemic hemodynamic, electrolyte excretion and total and dephosphorylated Na(+),K(+)-ATPase α1 subunit (t-d-NKA) in normotensive Wistar rats under a normal sodium (NS, 0.24%) or high sodium (HS, 1%) intake versus intact female (IF). On NS intake, t-d-NKA was higher in oVx rats and overexpressed in the thick ascending limbs (P < .01 vs. IF) and renal plasma flow was increased. On HS intake, oVx rats maintained a greater dephosphorylated NKA, excreted less sodium, and developed arterial hypertension (134 ± 4 vs. IF 112 ± 5 mm Hg, P < .05). Sodium load caused salt-sensitive hypertension in oVx Wistar rats.
In this work, we explored the relevance of a 35 kDa glycoprotein (Gm) of the outer membrane from E. histolytica in the diagnosis of the amoebic liver abscess (ALA) through ELISA and immunoblotting. We were interested in defining the relevance of this antigen in the immune response in patients with amoebic liver abscess and in exploring whether the mouse monoclonal antibody against this 35 kDa glycoprotein recognises the same epitope. We found that 87% of ALA patients had raised antibody levels to Gm antigen, whereas none of the healthy control subjects presented this same increase. We also found 90% sensitivity, 100% specificity, 100% positive predictive value, 90% negative predictive value, and 90% prevalence value for this Gm antigen. Nonetheless, we did not find any statistically significant differences in the levels of immunoglobulins against Gm, although IgG showed a tendency to increase, probably because we are dealing with a secondary immune response. Using electroimmunotransfer blot assay, we found that sera from ALA patients recognise the 35 kDa Gm protein in the same way as it is recognised by the mouse monoclonal antibody, suggesting that is a relevant molecule for the diagnosis of amebiasis, and eventually could lead to its use as protection against the disease.
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