Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antinociception induced by beta-endorphin given supraspinally has been demonstrated previously to be mediated by the release of Met-enkephalin acting on delta2-opioid receptors in the spinal cord. The present study was designed to determine the role of nitric oxide in the spinal cord on beta-endorphin-induced release of Met-enkephalin and antinociception. The experiments were performed in pentobarbital-anesthetized rats. The release of Met-enkephalin was performed using a spinal cord perfusion technique and the Met-enkephalin released in the spinal perfusates was measured by radioimmunoassay. Antinociception was assessed by the tail-flick test. beta-Endorphin (2 microg) given intraventricularly induced the release of Met-enkephalin from the spinal cord. The release of Met-enkephalin was dose-dependently attenuated by N(omega)-nitro-L-arginine (0.1 nM-1 microM) added into spinal perfusates and the attenuation was reversed by intrathecally applied L-arginine. The stereoisomer N(omega)-nitro-D-arginine given intrathecally, however, did not inhibit the release of Met-enkephalin induced by intraventricularly administered beta-endorphin. beta-Endorphin (4 microg) given intraventricularly produced antinociception in rats pretreated intrathecally with saline. The antinociception induced by beta-endorphin was blocked by intrathecally administered N(omega)-nitro-L-arginine (5 microg) and the blockade of antinociception was reversed by intrathecal injection of L-arginine (50 microg). N(omega)-Nitro-D-arginine (5 microg) given intrathecally did not block the intraventricularly administered beta-endorphin-induced antinociception. N(omega)-Nitro-L-arginine (10 microg) given intraventricularly did not affect intraventricularly administered beta-endorphin-induced Met-enkephalin release nor did it affect intraventricular beta-endorphin-induced antinociception, indicating that the effect of N(omega)-nitro-L-arginine is not at supraspinal sites. Intrathecal pretreatment with N(omega)-nitro-L-arginine did not affect intrathecally administered [D-Ala2]deltorphin II-induced antinociception. Our results indicate that N(omega)-nitro-L-arginine given intrathecally attenuates intraventricular beta-endorphin-administered inhibition of the tail-flick response by presynaptically inhibiting the release of Met-enkephalin.
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PMID:Inhibition of spinal nitric oxide synthase by N(omega)-nitro-L-arginine blocks the release of Met-enkephalin and antinociception induced by supraspinally administered beta-endorphin in the rat. 914 2

It is well known that hypertension is closely associated to the development of vascular diseases and that the inhibition of nitric oxide biosynthesis by administration of Nomega-Nitro-L-arginine methyl ester hydrochloride(L-NAME) leads to arterial hypertension. In the vascular system, extracellular purines mediate several effects;thus, ADP is the most important platelet agonist and recruiting ag ent, while adenosine, an end product of nucleotide metabolism, is a vasodilator and inhibitor of platelet activation and recruitment. Members of several families of enzymes, known as ectonucleotidases, including E-NTPDases (ecto-nucleoside triphosphate diphosphohydrolase), E-NPP (ecto-nucleotide pyrophosphatase/phosphodiesterase) and 5'-nucleotidase are able to hydrolyze extracellular nucleotides until their respective nucleosides. We investigated the ectonucleotidase activities of serum and platelets from rats made hypertensive by oral administration of L-NAME (30 mg/kg/day for 14 days or 30 mg/kg/day for 14 days plus 7 days of L-NAME washout, in the drinking water) in comparison to normotensive control rats. L-NAME promoted a significant rise in systolic blood pressure from 112 +/- 9.8 to 158 +/- 23 mmHg. The left ventricle weight index (LVWI) was increased in rats treated with L-NAME for 14 days when compared to control animals. In serum samples, ATP, ADP and AMP hydrolysis were reduced by about 27%, 36% and 27%, respectively. In platelets, the decrease in ATP, ADP and AMP hydrolysis was approximately 27%, 24% and 32%, respectively. All parameters recovered after 7 days of L-NAME washout. HPLC demonstrated a reduction in ADP, AMP and hypoxanthine levels by about 64%, 69% and 87%,respectively. In this study, we showed that ectonucleotidase activities are decreased in serum and platelets from L-NAME-treated rats, which should represent an additional risk for the development of hypertension. The modulation of ectonucleotidase activities may represent an approach to antihypertensive therapy via inhibition of spontaneous platelet activation and recruitment, as well as thrombus formation.
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PMID:Ectonucleotidase activities are altered in serum and platelets of L-NAME-treated rats. 1855 95