Changes in synaptic proteins of the complex PSD-95/NMDA receptor/nNOS and mitochondrial dysfunction after levocabastine treatment.

Nitric oxide generation is related to the activity of certain proteins located at synaptic sites. Previous findings show that NOS activity, nNOS protein expression, respiratory parameters and mitochondrial complex activities are altered in rat cerebral cortex by administration of levocabastine, an antagonist of histamine H1 and neurotensin NTS2 receptors. ATP provision by mitochondria may play an important role in the functional interaction between synaptic proteins NMDA receptor and PSD-95 with NO synthesis.

The low affinity neurotensin receptor antagonist levocabastine impairs brain nitric oxide synthesis and mitochondrial function by independent mechanisms.

Neurotensin is known to inhibit neuronal Na , K -ATPase, an effect that is rescued by nitric oxide (NO) synthase inhibition. However, whether the neurotensinergic and the nitrergic systems are independent pathways, or are mechanistically linked, remains unknown. Here, we addressed this issue and found that the administration of low affinity neurotensin receptor (NTS2) antagonist, levocabastine (50 μg/kg, i.

The Administration of Levocabastine, a NTS2 Receptor Antagonist, Modifies Na(+), K(+)-ATPase Properties.

Neurotensin behaves as a neuromodulator or as a neurotransmitter interacting with NTS1 and NTS2 receptors. Neurotensin in vitro inhibits synaptosomal membrane Na(+), K(+)-ATPase activity. This effect is prevented by administration of SR 48692 (antagonist for NTS1 receptor).

Depressed erythroid progenitor cell activity in aluminum-overloaded mice.

The aim of the present study was to evaluate the effect of aluminum (Al) on in vivo erythropoiesis in mice that had received short- and long-term Al overloading. At the end of each treatment period, clonal assays of late erythroid progenitor cells (CFU-E) stimulated in vitro with erythropoietin were carried out, hematological parameters determined, and histological aluminon staining performed on bone and liver. After 2 weeks of oral ingestion of either Al chloride or Al citrate (10 mumol per day), poor CFU-E growth was obtained but no differences in hematocrit (Ht) and hemoglobin (Hb) values were found when comparing the treated and control groups.

Erythropoietin modified the cardiac action of ouabain in chronically anaemic-uraemic rats.

The results of the studies reported here demonstrate the cardiac non-haematopoietic effect of erythropoietin, providing a new physiological function of the hormone. We demonstrate that myocardium from rat with chronic renal failure (CRF) showed an abnormal response to ouabain associated with an inhibition of cardiac Na+/K+/ATPase activity and with a decrease in the high affinity 3H-ouabain binding sites. The extent to which both actions were improved with the recombinant human erythropoietin (rHuEpo) treatment suggests that the lack of the hormone is responsible for this phenomenon.