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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone is a target tissue of androgens, but the mechanisms by which they act on bone are still unclear. This study examines the early (5-60 s) effects of 1 pM to 1 microM testosterone on cytosolic free Ca2+ concentration ([Ca2+]i) and inositol 1,4,5-trisphosphate (InsP3) and diacyglycerol (DAG) formation in confluent male rat osteoblasts. 10 pM to 10 nM testosterone increased [Ca2+]i within 5 s via Ca2+ influx as shown by the effects of EGTA and the Ca2+ channel blockers nifedipine and verapamil and via Ca2+ mobilization from the endoplasmic reticulum as shown by the effects of thapsigargin and neomycin. 10 pM to 10 nM testosterone increased InsP3 and DAG formation within 10 s. Testosterone immobilized on bovine serum albumin (testosterone (O-carboxymethyl)oxime/bovine serum albumin) and its derivative, (O-carboxymethyl)oxime, rapidly increased [Ca2+]i and InsP3 and DAG formation and were full agonists, although they were less potent than the free steroid. Cyproterone acetate, a nuclear antagonist, did not block the increase in [Ca2+]i and InsP3 and DAG formation induced by testosterone. Finally, neomycin and pertussis toxin totally abolished the effects of testosterone on InsP3 and DAG. These results suggest that male rat osteoblasts bear nongenomic unconventional cell-surface receptors for testosterone that belong to the class of the membrane receptors coupled to a phospholipase C via a pertussis toxin-sensitive G-protein.
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PMID:Androgens increase intracellular calcium concentration and inositol 1,4,5-trisphosphate and diacylglycerol formation via a pertussis toxin-sensitive G-protein. 812 34

Short-circuit current (I(sc)) technique was used to investigate the role of testosterone in the regulation of chloride secretion in cultured rat efferent duct epithelia. Among the steroids tested, only testosterone, and to a lesser extent, 5alpha-dihydrotestosterone (5alpha-DHT), reduced the basal and forskolin-induced I(sc) in cultured rat efferent duct epithelia when added to the apical bathing solution. Indomethacin, a 3alpha-hydroxysteroid dehydrogenase, did not affect the inhibitory effect of 5alpha-DHT. The effect of testosterone occurred within 10-20 s upon application and was dose dependent with apparent IC(50) value of 1 microM. The effect was abolished by removal of Cl(-) but not HCO from the normal Krebs-Henseleit solution, suggesting that testosterone mainly inhibited Cl(-) secretion. The efferent duct was found to be most sensitive to testosterone, while the caput and the cauda epididymidis were only mildly sensitive. Cyproterone acetate, a steroidal antiandrogen, or flutamide, a nonsteroidal antiandrogen, did not block the effect of testosterone on the forskolin-induced I(sc), nor did protein synthesis inhibitors, cycloheximide, or actinomycin D. However, pertussis toxin, a G(i) protein inhibitor, attenuated the inhibition of forskolin-induced I(sc) by testosterone. Testosterone caused a dose-dependent inhibition of forskolin-induced rise in cAMP in efferent duct cells. It is suggested that the rapid effect of testosterone was mediated through a membrane receptor that is negatively coupled to adenylate cyclase via G(i) protein. The role of nongenomic action of testosterone in the regulation of electrolyte and fluid transport in the efferent duct is discussed.
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PMID:Nongenomic effect of testosterone on chloride secretion in cultured rat efferent duct epithelia. 1128 29