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Influence of 17- alpha-estradiol on catecholamine secretion from the perfused rat adrenal gland.

Park YH, Cho GS, Cho ET, Park YK, Lee MJ, Chung JY, Hong SP, Lee JJ, Jang Y, Yoo HJ, Choi CH, Lim DY - Korean J. Intern. Med. (1996)

Bottom Line: McN-A-343 (100 uM for 2 min) and Bay-K-8644 (10 uM for 4 min), while it did not affect the CA secretory effect of high K+ (56 mM).However, pre-treatment with 17-alpha-estradiol in the presence of meclopramide (dopaminergic antagonist) did not affect the secretory effect of CA evoked by ACh.These results suggest that 17-alpha-estradiol causes the marked inhibition of CA secretion evoked by cholinergic receptor stimulation, but not that by excess K+, indicating strongly that this effect may be mediated by inhibiting the influx of extracellular calcium into the rat adrenomedullary chromaffin cells through the activation of inhibitory estrogen receptors, and it also plays a modulatory role in regulating CA secretion.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine and Pharmacology, Chosun University, Kwang Ju, Korea.

ABSTRACT

Objectives: It has been known that adrenal corticosteroids influence the expression of adrenomedullary catecholamine-synthetizing enzymes and also suppress the emission of axonal-like processes in cultured chromaffin cells. In the present study, it was attempted to investigate the effect of 17-alpha-estradiol on catecholamine (CA) secretion evoked by acetylcholine (ACh). DMPP. McN-A-343, excess K+ and Bay-K-8644 from the isolated perfused rat adrenal gland.

Methods: Mature male Sprague-Dawley rats were anesthetized with ether. The adrenal gland was isolated by the method of WaKade. A cannula used for perfusion of the adrenal gland was inserted into the distal end of the renal vein. The adrenal gland, along with ligated blood vessels and the cannula, was carefully removed from the animal and placed on a platform of a leucite chamber.

Results: The perfusion of 17-alpha-estradiol (1-100 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM). DMPP (100 uM for 2 min). McN-A-343 (100 uM for 2 min) and Bay-K-8644 (10 uM for 4 min), while it did not affect the CA secretory effect of high K+ (56 mM). Also, in the presence of 17-beta-estradiol. CA secretion of ACh. DMPP and McN-A-343, without any effect on excess K(+)-evoked CA sectretion was depressed. However, in adrenal glands pre-loaded with 17-alpha-estradiol (10 uM) plus tamoxifen (2 uM), which is known to be a selective antagonist of estrogen receptors (for 20 min). CA secretory responses evoked by ACh. DMPP and McN-A-343 were condiderably recovered as compared to that of 17-alpha-estradiol only, but excess K(+)-induced CA secretion was not affected. However, pre-treatment with 17-alpha-estradiol in the presence of meclopramide (dopaminergic antagonist) did not affect the secretory effect of CA evoked by ACh. DMPP, McN-A-343 and high potassium.

Conclusions: These results suggest that 17-alpha-estradiol causes the marked inhibition of CA secretion evoked by cholinergic receptor stimulation, but not that by excess K+, indicating strongly that this effect may be mediated by inhibiting the influx of extracellular calcium into the rat adrenomedullary chromaffin cells through the activation of inhibitory estrogen receptors, and it also plays a modulatory role in regulating CA secretion.

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Influence of 1 uM 17-α-estradiol on nicotinic and muscarinic stimulated CA secretory responses. DMPP (100 uM) and McN-A-343 (100 uM) were perfused into an adrenal vein for 2 min before and after preloading with 1 uM 17-α-estradiol for 20 min, respectively. DMPP-induced perfusates was collected twice successively for each 4 minutes but McN-A-343-induced perfusate only for 4 minutes. Other legends are the same as in Fig. 2.
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f3-kjim-11-1-25-4: Influence of 1 uM 17-α-estradiol on nicotinic and muscarinic stimulated CA secretory responses. DMPP (100 uM) and McN-A-343 (100 uM) were perfused into an adrenal vein for 2 min before and after preloading with 1 uM 17-α-estradiol for 20 min, respectively. DMPP-induced perfusates was collected twice successively for each 4 minutes but McN-A-343-induced perfusate only for 4 minutes. Other legends are the same as in Fig. 2.

Mentions: When perfused through the rat adrenal gland, DMPP (100 uM for 2 min), which is a selective nicotinic receptor agonist in autonomic sympathetic ganglia, evoked a sharp and rapid increase in CA secretion. As shown in Fig. 3, DMPP-stimulated CA secretion before pre-loading with 1 uM 17-α-estradiol was 781.9±77.2 ng (0–4 min) and 147.9±32.8 ng (4–8 min), while after pre-treatment with 1 uM 17-α-estradiol for 20 min they were greatly reduced to 425.6±45.4 ng (0–4 min, p<0.01) and 30.0±8.7 ng (4–8 min, p<0.01), respectively from 8 rat adrenal glands. As illustrated in Fig. 3. McN-A-343 (100 uM), which is a selective muscarinic Mi-agonist18), perfused into and adrenal gland for 2 min caused an increased CA secretion to 113.3±24.5 ng for 4 min from 9 experiments. However, McN-A-343-stimulated CA secretion in the presence of 1 uM 17-α-estradiol was markedly inhibited to 28.3±4.6 ng (p<0.01) for 4 min, which is 25% of the corresponding control secretion.


Influence of 17- alpha-estradiol on catecholamine secretion from the perfused rat adrenal gland.

Park YH, Cho GS, Cho ET, Park YK, Lee MJ, Chung JY, Hong SP, Lee JJ, Jang Y, Yoo HJ, Choi CH, Lim DY - Korean J. Intern. Med. (1996)

Influence of 1 uM 17-α-estradiol on nicotinic and muscarinic stimulated CA secretory responses. DMPP (100 uM) and McN-A-343 (100 uM) were perfused into an adrenal vein for 2 min before and after preloading with 1 uM 17-α-estradiol for 20 min, respectively. DMPP-induced perfusates was collected twice successively for each 4 minutes but McN-A-343-induced perfusate only for 4 minutes. Other legends are the same as in Fig. 2.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4531998&req=5

f3-kjim-11-1-25-4: Influence of 1 uM 17-α-estradiol on nicotinic and muscarinic stimulated CA secretory responses. DMPP (100 uM) and McN-A-343 (100 uM) were perfused into an adrenal vein for 2 min before and after preloading with 1 uM 17-α-estradiol for 20 min, respectively. DMPP-induced perfusates was collected twice successively for each 4 minutes but McN-A-343-induced perfusate only for 4 minutes. Other legends are the same as in Fig. 2.
Mentions: When perfused through the rat adrenal gland, DMPP (100 uM for 2 min), which is a selective nicotinic receptor agonist in autonomic sympathetic ganglia, evoked a sharp and rapid increase in CA secretion. As shown in Fig. 3, DMPP-stimulated CA secretion before pre-loading with 1 uM 17-α-estradiol was 781.9±77.2 ng (0–4 min) and 147.9±32.8 ng (4–8 min), while after pre-treatment with 1 uM 17-α-estradiol for 20 min they were greatly reduced to 425.6±45.4 ng (0–4 min, p<0.01) and 30.0±8.7 ng (4–8 min, p<0.01), respectively from 8 rat adrenal glands. As illustrated in Fig. 3. McN-A-343 (100 uM), which is a selective muscarinic Mi-agonist18), perfused into and adrenal gland for 2 min caused an increased CA secretion to 113.3±24.5 ng for 4 min from 9 experiments. However, McN-A-343-stimulated CA secretion in the presence of 1 uM 17-α-estradiol was markedly inhibited to 28.3±4.6 ng (p<0.01) for 4 min, which is 25% of the corresponding control secretion.

Bottom Line: McN-A-343 (100 uM for 2 min) and Bay-K-8644 (10 uM for 4 min), while it did not affect the CA secretory effect of high K+ (56 mM).However, pre-treatment with 17-alpha-estradiol in the presence of meclopramide (dopaminergic antagonist) did not affect the secretory effect of CA evoked by ACh.These results suggest that 17-alpha-estradiol causes the marked inhibition of CA secretion evoked by cholinergic receptor stimulation, but not that by excess K+, indicating strongly that this effect may be mediated by inhibiting the influx of extracellular calcium into the rat adrenomedullary chromaffin cells through the activation of inhibitory estrogen receptors, and it also plays a modulatory role in regulating CA secretion.

View Article: PubMed Central - PubMed

Affiliation: Department of Internal Medicine and Pharmacology, Chosun University, Kwang Ju, Korea.

ABSTRACT

Objectives: It has been known that adrenal corticosteroids influence the expression of adrenomedullary catecholamine-synthetizing enzymes and also suppress the emission of axonal-like processes in cultured chromaffin cells. In the present study, it was attempted to investigate the effect of 17-alpha-estradiol on catecholamine (CA) secretion evoked by acetylcholine (ACh). DMPP. McN-A-343, excess K+ and Bay-K-8644 from the isolated perfused rat adrenal gland.

Methods: Mature male Sprague-Dawley rats were anesthetized with ether. The adrenal gland was isolated by the method of WaKade. A cannula used for perfusion of the adrenal gland was inserted into the distal end of the renal vein. The adrenal gland, along with ligated blood vessels and the cannula, was carefully removed from the animal and placed on a platform of a leucite chamber.

Results: The perfusion of 17-alpha-estradiol (1-100 uM) into an adrenal vein for 20 min produced relatively dose-dependent inhibition in CA secretion evoked by ACh (5.32 mM). DMPP (100 uM for 2 min). McN-A-343 (100 uM for 2 min) and Bay-K-8644 (10 uM for 4 min), while it did not affect the CA secretory effect of high K+ (56 mM). Also, in the presence of 17-beta-estradiol. CA secretion of ACh. DMPP and McN-A-343, without any effect on excess K(+)-evoked CA sectretion was depressed. However, in adrenal glands pre-loaded with 17-alpha-estradiol (10 uM) plus tamoxifen (2 uM), which is known to be a selective antagonist of estrogen receptors (for 20 min). CA secretory responses evoked by ACh. DMPP and McN-A-343 were condiderably recovered as compared to that of 17-alpha-estradiol only, but excess K(+)-induced CA secretion was not affected. However, pre-treatment with 17-alpha-estradiol in the presence of meclopramide (dopaminergic antagonist) did not affect the secretory effect of CA evoked by ACh. DMPP, McN-A-343 and high potassium.

Conclusions: These results suggest that 17-alpha-estradiol causes the marked inhibition of CA secretion evoked by cholinergic receptor stimulation, but not that by excess K+, indicating strongly that this effect may be mediated by inhibiting the influx of extracellular calcium into the rat adrenomedullary chromaffin cells through the activation of inhibitory estrogen receptors, and it also plays a modulatory role in regulating CA secretion.

Show MeSH
Related in: MedlinePlus