Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.2 (guanylate cyclase)
 8,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been reported that prostaglandin E2 (PGE2) had anti-inflammatory and analgesic effects, although it was well known that PGE2 combined with bradykinin (BK) showed proinflammatory and algesic effects. On the other hand, it has recently been known that BK showed an indirect activating effect on cathepsin B, a lysosomal enzyme, which may be mediated through calcium ion-dependent steps, followed by production of enkephalins (EK), endogenous anti-inflammatory and analgesic peptides, in the rat incisor pulp. The purpose of the present study is to examine whether PGE2 could have an effect on activation or release of cathepsin B in the pulp tissue, or not. Intact whole pulps of the rat incisors were incubated with N alpha-benzoyl-arginine-beta-naphthylamide (BANA), a substrate for cathepsin B, in the presence or absence of BK and PGE2 in Hanks solution (pH 7.4), in order to determine the BANA-degrading activity and EK producing activity. Both hydrocortisone and lidocaine which were stabilizers for lysosomal membrane markedly inhibited the BANA-degrading activities in the presence of BK, and in contrast, retinol, a labilizer for lysosomal membrane, significantly enhanced the BK-induced BANA-degrading activity. PGE2, like hydrocortisone and lidocaine, inhibited the BANA-degrading activity, in a dose-dependent manner, regardless of the presence or absence of BK, as well as resulted in a decrease of EK production in the pulp. Furthermore, both arginine, a cleavage product of BK by carboxypeptidase B, and arachidonic acid, which were endogenous activators for soluble guanylate cyclase, enhanced the BANA-degrading activity in the pulp homogenate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Stabilizing effect of prostaglandin E2 on lysosomal membrane of the rat dental pulp]. 213 3

The effects of somatostatin (ST) on the regulation of the glomerular filtration rate have not been extensively studied. The present experiments were designed to analyze this possible relationship. ST alone did not modify the planar cell surface area (PCSA) of cultured rat mesangial cells (CRMC), but it prevented and reversed the reduction in PCSA induced by 10 nM angiotensin II (Ang II) in a dose- and time-dependent manner. ST (1 microM) completely prevented and reversed the increase in the myosin light chain phosphorylation induced by 10 nM Ang II. Incubation with pertussis toxin (PT, 0.5 micrograms/ml) inhibited the effect of ST on the Ang II-dependent changes in PCSA, but this effect was not inhibited by the blockade of the vasodilatory prostaglandins (indomethacin, 10 microM) or nitric oxide (L-N-methyl-arginine, 0.2 mM) synthesis. 2',5'-dideoxyadenosine (DDA, 0.1 mM), an adenylate cyclase blocker, and methylene blue (MB, 30 microM), a soluble guanylate cyclase blocker, did not interfere with the ST inhibitory effect on the Ang II-dependent reduction in PCSA of rat mesangial cells. ST also blocked the reduction in PCSA induced by phorbol myristate acetate (PMA, 300 nM). ST was also able to prevent and revert the Ang II dependent reduction in glomerular cross-sectional area of isolated rat glomeruli, also in a dose- and time-dependent fashion. Finally, intravenous administration of ST (200 ng/kg body wt as a bolus plus a continuous injection of 25 ng/min/kg body wt) partially blocked the reduction in GFR (measured as CIn) and RPF (measured as CPAH) and the increase in filtration fraction induced by the intravenous administration of Ang II (1.7 micrograms/min/kg body wt) in anesthetized rats. In summary, these results suggest that ST could antagonize the renal actions of Ang II, increasing the GFR and RPF decreased by Ang II, and this effect could be dependent, at least partially, on a direct relaxing effect of ST on mesangial cells.
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PMID:Somatostatin antagonizes angiotensin II effects on mesangial cell contraction and glomerular filtration. 809 76