کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10847864 1070485 2005 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Progesterone inhibits gallbladder motility through multiple signaling pathways
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Progesterone inhibits gallbladder motility through multiple signaling pathways
چکیده انگلیسی
Progesterone (P) has an inhibitory effect on the contractility of gastrointestinal smooth muscle, including the gallbladder. Since P levels are elevated during pregnancy, a biliary stasis may develop during pregnancy that is characterized by an increase in the fasting and residual volumes and by a decrease in emptying capacity. This study investigates the effect of P and two metabolites on contraction in guinea pig gallbladder strips. P induced a concentration-dependent relaxation in guinea pig gallbladder strips precontracted with cholecystokinin octapeptide (CCK). Pretreatment of gallbladder strips with P (50 μM) also reduced the amount of CCK-induced tension. Nifedipine (1 μM) produced a similar effect. Pretreatment of the strips with PKA inhibitor 14-22 amide myristolated (180 nM) or the PKG inhibitor KT5823 (1.2 μM) either separately or in combination significantly reduced the amount of P-induced relaxation. Rp-cAMPs (0.1 mM) or H-89 (10 μM) separately or in combination significantly reduced the P-effect; however, the combination of agents produced the largest reduction. Genistein (1 μM), an inhibitor of protein tyrosine kinases, significantly (p < 0.01) reduced the amount of P-induced relaxation. The use of strontium in the Kreb's solution as a substitute for Ca2+ significantly (p < 0.01) reduced the amount of CCK-induced tension. Pretreatment of the strips with 2-APB (26 μM), an inhibitor of IP3, induced Ca2+ release, produced a significant (p < 0.01) reduction in P-induced relaxation. We conclude that P inhibits gallbladder motility rapidly by nongenomic actions of the hormone. Several pathways that include tyrosine kinase and PKA/cAMP activity may mediate this effect.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Steroids - Volume 70, Issue 9, August 2005, Pages 673-679
نویسندگان
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