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Influence of arachidonic acid on catecholamine secretion in the perfused rat adrenal medulla.

Lim DY, Choi MK, Kang TJ, Lee JJ, Jang Y, Moon B, Chung CH, Hong SP - Korean J. Intern. Med. (1993)

Bottom Line: Arachidonic acid, in the presence of ouabain (100 uM), an inhibitor of Na+, K(+) -ATPase, also produced a marked inhibitory effect of CA secretion evoked by ACh, DMPP and muscarine but did not modify the secretory effect of excess K+.The perfusion of arachidonic acid along with indomethacin (30 uM), which is an inhibitor of cyclooxygenase, for 20 min attenuated markedly CA secretory effect evoked by ACh, DMPP and muscarine while it did not influence that by excess K+.Prostaglandin F2 alpha perfused in a retrograde direction for 20 min inhibited greatly the CA secretion evoked by DMPP but did not affect the effect evoked by excess K+.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Chosun University Medical College, Kwangju, Korea.

ABSTRACT
The present study was conducted to investigate the influence of arachidonic acid, which is known to be an important unsaturated fatty acid component of membrane phospholipids and to be liberated by phospholipase A2 action, on secretion of catecholamines (CA) from the isolated perfused rat adrenal glands and to clarify the mechanism of its action. Arachidonic acid (10 uM) perfused into an adrenal gland of the rat for 20 min caused a significant inhibition of CA secretion evoked by ACh (5.32 x 10(-3) M), DMPP (10(-4) M) and muscarine (10(-4) M) while it did not affect that induced by excess K+ (5.6 x 10(-2) M). Arachidonic acid, in the presence of ouabain (100 uM), an inhibitor of Na+, K(+) -ATPase, also produced a marked inhibitory effect of CA secretion evoked by ACh, DMPP and muscarine but did not modify the secretory effect of excess K+. The perfusion of arachidonic acid along with indomethacin (30 uM), which is an inhibitor of cyclooxygenase, for 20 min attenuated markedly CA secretory effect evoked by ACh, DMPP and muscarine while it did not influence that by excess K+. Prostaglandin F2 alpha perfused in a retrograde direction for 20 min inhibited greatly the CA secretion evoked by DMPP but did not affect the effect evoked by excess K+. All of arachidonic acid, ouabain, indomethacin and prostaglandin F2 alpha used in the present study did not affect the spontaneous basal release of CA in the perfused rat adrenal glands. Taken together, these experimental results suggest that arachidonic acid, as well as prostaglandin F2 alpha, cause the inhibitory action of CA secretion evoked by cholinergic receptor-mediated stimulation, but not by membrane depolarization, and also play a modulatory role in regulating CA secretion from the rat adrenal medulla.

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Effect of arachidonic acid plus indomethacin, on ACh-and excess K+-evoked CA release. Secretgogues were introduced before and after pre-loading with 10 uM arachidonic acid plus 30 uM indomethacin (INDO) for 20 min, respectively. Other legends and methods are as in Fig. 1.
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f7-kjim-8-2-103-8: Effect of arachidonic acid plus indomethacin, on ACh-and excess K+-evoked CA release. Secretgogues were introduced before and after pre-loading with 10 uM arachidonic acid plus 30 uM indomethacin (INDO) for 20 min, respectively. Other legends and methods are as in Fig. 1.

Mentions: Since it has been shown that indomethacin, an inhibitor of cyclooxygenase, fails to inhibit the stimulatory effect of CA secretion evoked by arachidonic acid in digitonin-permeabilized bovine adrenal medullary cells13) and, it as well as aspirin, has no effect on the release evoked by carbachol and high K+25), it was particularly intersting to test the effect of arachidonic acid plus indomethacin on CA secretion evoked by various secretagogues. As illustrated in Fig. 8, ACh (5.32×10−3 M)- and excess K+ (5.6×10−2 M)-evoked CA secretions before preloading with arachidonic acid plus indomethacin amounted to 420.0±73.4 ng and 337.0±27.5 ng for 4 min, respectively, However, following the pre-perfusion with arachidonic acid(10−5 M) along with indomethacin(3×10−5 M), ACh-induced CA release was significantly reduced to 247.8±24.9 (p<0.05)ng for 4 min from 6 rat adrenal glands, as compared with its control release, while excess K+-induced CA release was 289.3±46.3 ng for 4 min from 15 glands. There was no significant change in excess K+-evoked CA secretion, as compared to tis corresponding control response as shown in Fig. 7.


Influence of arachidonic acid on catecholamine secretion in the perfused rat adrenal medulla.

Lim DY, Choi MK, Kang TJ, Lee JJ, Jang Y, Moon B, Chung CH, Hong SP - Korean J. Intern. Med. (1993)

Effect of arachidonic acid plus indomethacin, on ACh-and excess K+-evoked CA release. Secretgogues were introduced before and after pre-loading with 10 uM arachidonic acid plus 30 uM indomethacin (INDO) for 20 min, respectively. Other legends and methods are as in Fig. 1.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4532085&req=5

f7-kjim-8-2-103-8: Effect of arachidonic acid plus indomethacin, on ACh-and excess K+-evoked CA release. Secretgogues were introduced before and after pre-loading with 10 uM arachidonic acid plus 30 uM indomethacin (INDO) for 20 min, respectively. Other legends and methods are as in Fig. 1.
Mentions: Since it has been shown that indomethacin, an inhibitor of cyclooxygenase, fails to inhibit the stimulatory effect of CA secretion evoked by arachidonic acid in digitonin-permeabilized bovine adrenal medullary cells13) and, it as well as aspirin, has no effect on the release evoked by carbachol and high K+25), it was particularly intersting to test the effect of arachidonic acid plus indomethacin on CA secretion evoked by various secretagogues. As illustrated in Fig. 8, ACh (5.32×10−3 M)- and excess K+ (5.6×10−2 M)-evoked CA secretions before preloading with arachidonic acid plus indomethacin amounted to 420.0±73.4 ng and 337.0±27.5 ng for 4 min, respectively, However, following the pre-perfusion with arachidonic acid(10−5 M) along with indomethacin(3×10−5 M), ACh-induced CA release was significantly reduced to 247.8±24.9 (p<0.05)ng for 4 min from 6 rat adrenal glands, as compared with its control release, while excess K+-induced CA release was 289.3±46.3 ng for 4 min from 15 glands. There was no significant change in excess K+-evoked CA secretion, as compared to tis corresponding control response as shown in Fig. 7.

Bottom Line: Arachidonic acid, in the presence of ouabain (100 uM), an inhibitor of Na+, K(+) -ATPase, also produced a marked inhibitory effect of CA secretion evoked by ACh, DMPP and muscarine but did not modify the secretory effect of excess K+.The perfusion of arachidonic acid along with indomethacin (30 uM), which is an inhibitor of cyclooxygenase, for 20 min attenuated markedly CA secretory effect evoked by ACh, DMPP and muscarine while it did not influence that by excess K+.Prostaglandin F2 alpha perfused in a retrograde direction for 20 min inhibited greatly the CA secretion evoked by DMPP but did not affect the effect evoked by excess K+.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Chosun University Medical College, Kwangju, Korea.

ABSTRACT
The present study was conducted to investigate the influence of arachidonic acid, which is known to be an important unsaturated fatty acid component of membrane phospholipids and to be liberated by phospholipase A2 action, on secretion of catecholamines (CA) from the isolated perfused rat adrenal glands and to clarify the mechanism of its action. Arachidonic acid (10 uM) perfused into an adrenal gland of the rat for 20 min caused a significant inhibition of CA secretion evoked by ACh (5.32 x 10(-3) M), DMPP (10(-4) M) and muscarine (10(-4) M) while it did not affect that induced by excess K+ (5.6 x 10(-2) M). Arachidonic acid, in the presence of ouabain (100 uM), an inhibitor of Na+, K(+) -ATPase, also produced a marked inhibitory effect of CA secretion evoked by ACh, DMPP and muscarine but did not modify the secretory effect of excess K+. The perfusion of arachidonic acid along with indomethacin (30 uM), which is an inhibitor of cyclooxygenase, for 20 min attenuated markedly CA secretory effect evoked by ACh, DMPP and muscarine while it did not influence that by excess K+. Prostaglandin F2 alpha perfused in a retrograde direction for 20 min inhibited greatly the CA secretion evoked by DMPP but did not affect the effect evoked by excess K+. All of arachidonic acid, ouabain, indomethacin and prostaglandin F2 alpha used in the present study did not affect the spontaneous basal release of CA in the perfused rat adrenal glands. Taken together, these experimental results suggest that arachidonic acid, as well as prostaglandin F2 alpha, cause the inhibitory action of CA secretion evoked by cholinergic receptor-mediated stimulation, but not by membrane depolarization, and also play a modulatory role in regulating CA secretion from the rat adrenal medulla.

Show MeSH
Related in: MedlinePlus