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 stimulatory effect of metoclopramide upon aldosterone secretion is independent of the known aldosterone-regulating mechanisms (renin, potassium, adrenocorticotropic hormone), is unrelated to its effect on prolactin and is absent when metoclopramide is directly added to isolated adrenal zona glomerulosa cells. To examine the possibility of a "humoral" mediation of aldosterone stimulation by metoclopramide, we evaluated the effect of serum of 10 normal subjects injected with metoclopramide (10 mg i.v.) on aldosterone production by collagenase-dispersed calf adrenal zona glomerulosa cells. Whereas no effect was observed with serum collected before the injection, serum collected from 5 to 30 min after the injection stimulated aldosterone production. The effect was seen 2.5 min after the injection, was significant at 5 min (P 0.05), 10, 15, 20 and 30 min (P 0.01). The effect disappeared 40 min after the injection, when plasma aldosterone in subjects was still elevated (P 0.01). The biological half-life of the factor (t1/2) is about 12.5 min. A significant correlation was found between the maximal aldosterone response to metoclopramide in vivo and the maximal effect of serum in vitro (r2=0.69;P 0.01). We suggest that metoclopramide stimulates aldosterone production in vivo by the increase in serum of a factor which, in turn, stimulates aldosterone and whose physiological significance remains to be evaluated.
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PMID:Evidence for a role of a serum factor stimulated by metoclopramide in regulating aldosterone secretion. 670 35

After postnatal day 1 (d1), the hypothalamo-pituitary-adrenal axis of neonatal rats becomes less responsive to certain stimuli for up to 2 weeks. The present study was designed to quantify the development of adrenocortical cell responsiveness to its normal secretagogue, adrenocorticotropic hormone (ACTH), and to better localize intracellular sites of adrenal cell hyporesponsivity. Maximum steroidogenic responses of collagenase-dispersed adrenocortical cells (using two isolation methods) to ACTH varied significantly in the order adult > d1 > d10. The response pattern to dibutyryl cAMP ((Bu)2cAMP) was identical to that observed for ACTH (adult > d1 > d10), suggesting that neonatal adrenal responsiveness is limited by a site distal to cAMP formation. Sensitivity (EC50) of adult cells to ACTH was approximately 3-fold greater than in neonatal cells, but there was no age-dependent shift in sensitivity to (Bu)2cAMP. 20 alpha-Hydroxycholesterol (20 alpha-OHCHOL), a membrane permeable analog of cholesterol, also failed to normalize the d10 adrenal response to ACTH. This result indicates that one site of refractoriness is apparently distal to cholesterol transport, and strongly suggests possible differential cytochrome P450 enzyme expression or activity in neonatal rat adrenal cells. Finally, although stimulated secretion was lower in neonatal cells, basal corticosterone secretion was significantly greater in neonatal adrenals, suggesting that constitutive activity of neonatal adrenal cells is high compared to that of adult cells.
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PMID:Steroidogenesis in isolated adrenocortical cells during development in rats. 838 18

Unsaturated long chain fatty acids modulate hormone secretion from a variety of endocrine glands, including the adrenal cortex. Oleic acid and linoleic acid have been shown to stimulate production of glucocorticoids in the absence of adrenocorticotropic hormone, but at a high concentration appeared to inhibit the action of this hormone. In the present study, the concentration dependence of the inhibitory actions of these two fatty acids was tested in collagenase-dispersed rat adrenal fasciculata cells, and the effects of both lipids on cAMP production were also determined. Adrenocorticotropic hormone stimulated steroid production from isolated cells approximately ten-fold above unstimulated cells. Oleic and linoleic acid significantly inhibited the response to this hormone by 44% and 54%, respectively. The half-maximally effective inhibitory concentration of both lipids was between 75-100 microM. A maximal concentration of adrenocorticotropic hormone increased cAMP secretion 138-fold above unstimulated cells. Oleic and linoleic acids inhibited the increase in cAMP secretion by 47% and 33%, respectively. It is concluded that pathophysiological concentrations of unsaturated fatty acids inhibit the action of adrenocorticotropic hormone on the adrenal gland, and that the mechanism of action of the lipids may be partly via inhibition of cAMP production.
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PMID:Fatty acids inhibit adrenocorticotropin-induced adrenal steroidogenesis. 954 89

In the present study, adrenocorticotropic hormone (ACTH) release and intracellular calcium ([Ca(2+)](i)) increase induced by arginine vasopressin (AVP) were characterized in collagenase-dispersed and 3-day cultured rat anterior pituitary cells. AVP and the selective vasopressin V(1b) receptor agonist, [1-deamino-4-cyclohexylalanine]AVP (d[Cha(4)]AVP) induced ACTH release with nanomolar potencies in both cell preparations, and produced a maximal stimulation that was about 1.5 fold greater in the 3-day cultured cells, indicating that the vasopressin V(1b) receptor-ACTH release pathway is enhanced over time in culture. In dispersed cells, AVP, oxytocin and d[Cha(4)]AVP induced [Ca(2+)](i) increases with nanomolar potencies. The selective vasopressin V(1a) receptors antagonist, SR49059 (100 nM), together with the selective oxytocin receptors antagonist (d(CH(2))(5)(1)Tyr(Me)(2),Thr(4),Orn(8),Tyr-NH(2)(9)-vasotocin (100 nM), inhibited the maximal AVP response by ~70%, without affecting the response to d[Cha(4)]AVP, suggesting that the V(1b) receptor was only partially responsible for the AVP-induced [Ca(2+)](i) increase. In contrast, in 3-day cultures, AVP induced an increase in [Ca(2+)](i), while oxytocin and d[Cha(4)]AVP did not. The response to AVP was completely antagonized by SR49059, whereas the vasopressin V(1b) receptor antagonists, SSR149415 and (d(CH(2))(5)(1)Tyr(Me)(2),Thr(4),Orn(8),Tyr-NH(2)(9))-vasotocin had no effect, indicating that the [Ca(2+)](i) increase was mediated exclusively by vasopressin V(1a) receptors. In conclusion, the enhancement of vasopressin V(1b) receptor-mediated ACTH release and the lack of a detectable vasopressin V(1b) receptor coupling to [Ca(2+)](i) increase in cultured cells suggests the activation of a different/additional signaling pathway in the molecular mechanism of ACTH release.
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PMID:Distinct receptor subtypes mediate arginine vasopressin-dependent ACTH release and intracellular calcium mobilization in rat pituitary cells. 2228 55


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