Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of different neurotransmitters were tested in vitro on a hypothalamic tissue, collagenase-digested isolated anterior pituitary and Leydig cell suspension system by measuring the testosterone production of the Leydig cells. Neurotransmitters were used in concentrations of 0.25, 1.0, 2.5, 5.0, and 10.0 micrograms/ml incubation medium. Dopamine in doses of 1.0, 2.5, and 5.0 micrograms/ml increased the hypothalamic tissue-induced pituitary-testis activation, while it had no direct effect on pituitary and Leydig cells. Noradrenaline in the concentration range 2.5--10.0 micrograms/ml decreased the luteinizing-hormone-releasing-hormone (LHRH) sensitivity of the pituitary cells. 5.0 and 10.0 micrograms/ml 5-hydroxytryptamine decreased the testosterone production and the hCG sensitivity of the isolated Leydig cells. Carbamylcholine and pilocarpine had no action on the in vitro system at the different levels studied.
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PMID:Study of the effects of neurotransmitters on the hypothalamus-pituitary-testis function in in vitro cell suspension system. 4 66

We have recently demonstrated that dopamine (DA) inhibits Na,K-ATPase in single proximal tubule (PCT) segments dissected from previously collagenase perfused rat kidney. The aim of the present study was to ascertain whether this effect was directly mediated by DA or if DA was the precursor of an inhibitor. When PCT segments were incubated with L-DOPA, Na,K-ATPase was significantly lower than in vehicle incubated tubules. Inhibition of dopa decarboxylase abolished the effect of L-DOPA on Na,K-ATPase activity. The metabolites of DA, 3, 4-dihydroxphenyl acetic acid (DPAC) and homovanillic acid (HVA) both inhibited Na,K-ATPase activity in doses higher than 10(-6) M. Both HVA and DPAC 10(-4) M caused approximately 35% inhibition. Dopamine inhibited Na,K-ATPase activity even in a dose as low as 10(-7) M. Maximal inhibition (greater than 60%) was found with DA-5 M. Na,K-ATPase activity was significantly lower in tubules exposed to DA 10(-4) and 10(-5) M than in tubules exposed to DPAC or HVA 10(-4) and 10(-5) M. Dopamine produced in proximal tubule cells from L-DOPA, is an active inhibitor of the Na,K-pump in these cells. The DA metabolites DPAC and HVA are less potent Na,K-pump-inhibitors.
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PMID:Effect of L-DOPA, dopamine, dihydroxyphenyl acetic acid and homovanillic acid on Na,K-ATPase activity in rat proximal tubule segments. 282 Jan 98

Metoclopramide (MCP), a dopaminergic antagonist, increases the levels of plasma aldosterone in man and sheep. The present studies were designed to determine how MCP exerts this effect. In in vitro studies using collagenase-dispersed rabbit adrenal zona glomerulosa cells, MCP (10(-4) M) failed to increase aldosterone biosynthesis and had no effect on the dose-related increases induced by angiotensin II (AII) or ACTH. Dopamine (10(-5) M) had no effect on the AII- or ACTH-induced aldosterone responses of these cells. Aldosterone production of cells pretreated with dopamine and stimulated by AII or ACTH was unaltered by the addition of MCP. Bolus intraarterial injections of MCP increased plasma aldosterone significantly; however, this response was completely abolished by concomitant administration of L-dopa. Chronic im administration of MCP produced significant elevations of plasma aldosterone that were associated with increases in adrenal weight and in the adrenal weight to body weight ratio. Glomerulosa cells isolated from these adrenal glands had normal basal aldosterone production and exhibited enhanced sensitivity to AII but normal responses to ACTH. These results suggest that MCP is devoid of intrinsic steroidogenic activity and that it increases aldosterone production by antagonizing a tonic inhibitory dopaminergic mechanism that leads to enhanced aldosterone production. This enhanced aldosterone production is mediated in part by increased adrenocortical sensitivity to AII.
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PMID:In vitro and in vivo evidence for an indirect mechanism mediating enhanced aldosterone secretion by metoclopramide. 629 Jan 89

We have evaluated the inhibitory effect of dopamine on PRL secretion induced by blocking K+ channels. Tumor-derived GH4C1 cells and collagenase-dispersed normal anterior pituitary (AP) cells from young adult male rats were perifused with Krebs-Ringer Hepes medium. In both cell types blocking K+ channels with tetraethylammonium (TEA) induced PRL secretion but did not stimulate cyclic AMP generation. Blocking Na+ channels with 1 microM tetrodotoxin had no effect on basal or TEA-induced PRL secretion. Dopamine inhibited the TEA-induced rise in [Ca2+]i in GH4C1 cells expressing dopamine D2 short receptors. In normal AP cells, 1-100 nM dopamine blocked PRL secretion induced by 20 mM TEA in a log-linear concentration-dependent fashion, with a plateau at > 100 nM dopamine (IC50 30 nM). The D2 dopaminergic receptor agonist, quinpirole, at 100 nM completely blocked PRL secretion induced by 20 mM TEA. The D2 dopaminergic receptor antagonist, sulpiride, at 10 microM reversed the inhibitory effect of 10 microM dopamine on PRL secretion induced by 20 mM TEA. Pretreatment of cells with 100 ng/ml pertussis toxin (PTX) for 24 h prevented 100 nM dopamine inhibition of PRL secretion induced by 20 mM TEA. The data indicate that in both normal lactotroph cells and in tumor-derived cells expressing D2 receptors, PRL secretion stimulated by blocking K+ channels is inhibited by dopamine binding to D2 receptors on the plasma membrane. This inhibition involves interaction with PTX-sensitive Gi protein.
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PMID:Pituitary PRL secretion induced by tetraethylammonium is inhibited by dopamine through D2 receptors. 748 18