Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein secretion by the caput epididymidis has been examined in vitro using radioactive methionine as a precursor for protein synthesis. Newly synthesized and secreted proteins were separated by gel electrophoresis and visualized by fluorography. Local anesthetics such as procaine had the ability to reduce the secretion of some, but not all, proteins. Selective inhibition of secretion of the same proteins occurred when either dihydrocytochalasin B, monensin, ouabain, or dinitrophenol was added to the medium, or when the concentration of glucose was reduced below 1 mM. Calcium ionophore also selectively modified protein secretion, but the proteins affected were different from those influenced by local anesthetics. Other agents tested (eg, adrenergic and cholinergic agonists and antagonists, sodium pentobarbitone, antipsychotic drugs, cyclic AMP, colchicine) did not selectively modify protein secretion, even though overall protein synthesis and secretion was reduced in some instances. Procaine and dihydrocytochalasin B also reduced glucose utilization by epididymal tissue and it is suggested that these agents may reduce protein secretion by limiting the supply of energy for the exocytotic process. This conclusion is supported by the fact that dinitrophenol, an uncoupler of oxidative phosphorylation, caused a similar alteration in protein secretion. The possibility that a restricted energy supply modifies protein secretion primarily by creating a disturbed intracellular Na/K balance is suggested by the observation that the monovalent ionophore, monensin, and the Na/K ATPase inhibitor, ouabain, were both able to duplicate the effects of the local anesthetics.
 ...
PMID:Protein secretion by the rat epididymis can be selectively modified in vitro by local anesthetics, glucose deprivation, dinitrophenol, ouabain, and ionophores. 643 36

1. The actions of BaCl2 and 4-aminopyridine, blockers of K+ channels, on the mechanical activity of the epididymal half of the rat vas deferens were investigated. 2. Both BaCl2 and 4-aminopyridine dose-dependently evoked phasic contractions. High extracellular potassium (35-40 mM) caused a tonic contraction but abolished the BaCl2- and 4-aminopyridine-induced phasic activity and reduced the BaCl2-induced sustained component of contraction, but increased the 4-aminopyridine-induced tonic contraction. 3. Omission of calcium from the extracellular medium totally abolished the 4-aminopyridine-induced response but only reduced the mean amplitude of phasic contractions induced by BaCl. 4. Procaine (10 mM), an inhibitor of internal calcium release, completely abolished the phasic activity and reduced the sustained contraction induced by BaCl2. The remaining tone was abolished by nifedipine (1 microM). 5. Tetraethylammonium (1 mM) suppressed the amplitude of the BaCl2-induced phasic contractions, and induced a biphasic increase in tonic tension. 6. The BaCl2-induced responses were resistant to prazosin (1 microM), yohimbine (3 microM), propranolol (3 microM) or atropine (3 microM); in contrast, the 4-aminopyridine-induced activity was effectively inhibited by prazosin (1 microM) attenuated by yohimbine (1 microM) and atropine (1 microM) but not by propranolol (3 microM). The 4-aminopyridine-induced response was abolished by pretreatment of the vas deferens with 6-hydroxydopamine (0.5 mM). 7. The results indicate that the BaCl2-evoked activity in the vas deferens was mainly due to blockade of Ba(2+)-sensitive K+ channels on the smooth muscle plasma membrane. Subsequent calcium entry through the depolarized plasma membrane was needed to trigger generation of phasic contractions. 4-Aminopyridine-induced action, however, was largely mediated by neurotransmitters released from the depolarized nerve terminals as a result of blockade of K+ channels.
 ...
PMID:BaCl2- and 4-aminopyridine-evoked phasic contractions in the rat vas deferens. 854 86