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Mechanism of muscarinic receptor-mediated influx and release of Ca2+ in ileal smooth muscle
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MUSCARINIC RECEPTORS IN ISOLATED CANINE GASTRIC PARIETAL CELLS INVOLVED IN CYCLIC AMP FOg~TION AND INOSITOL PIIOSPHOLIPID BREAKDOWN. KUNIHIKO YOKOTANI~ AND TADATAKA YAMAHAz~, ± Department of Pharmacology, Kochl M e d i ~ and ~Departmcnt of I n t e r n a l Medicine, U n i v e r s i t y of Michigan, MI 48109. U.S.A.
We m e a s u r e d c~IP and lnosltol phosphates (IP 1, IP 2, IP 3) in Isolated canine parietal cells. Carbachol inhibited cAMP f o r m a t i o n induced by a submaximal concentration of forskolln ( 1 0 u M ) . On t h e o t h e r hand, carbaehol stimulated IP formation. NaF a l s o s t i m u l a t e d IP formation. Atropine and 4-DAMP (M3 blocker) attenuated both carbachol-medlated i n h i b i t o r y and s t l m u l a t o r y responses. Pirenzeplne, a M blocker, more markedly attenuated carbachol-lnduced I n h i b i t o r y e f f e c t s on c&MPI formation than carbachol-induced s t l m u l a t o r y e f f e c t s on IP formation. Pretreatment with p e r t u s s l s toxin (PT) (100 ng/ml, f o r 2 h r s ) a b o l i s h e d the i n h i b i t o r y e f f e c t of carbachol on cAMP formation but had no e f f e c t on carbachol-lnduced IP formation. From these r e s u l t s , i t was suggested t h a t MI receptors in canine parietal cells mediate the inhibition o f cAMP f o r m a t i o n v PT-sensltive G-proteins and M3 r e c e p t o r s mediate the stimulation of lnosltol phosphollpld breakdown via PT-lnsensitive G proteins.
STIMULATION BY ACETYLCHOLINE AND I N H I B I T I O N BY NOREPINEPHRINE OF TRANSGLUTAMINASE ACTIVITY IN THE SUPERIOR CERVICAL GANGLION OF RATS. MASATO ANDO, YUHZO NAKASHIMA*, AND YDTAKA NAGATA Department o__ffPhysiology. Fu~ita Health University School of Medicine, Toyoake, Aichi 470-11 Japan. Rapid changes in activity of calcium-dependent transglutaminase (TG), an enzyme catalyzing the covalent binding to glutamine residures on peptide chain to cause tissue degradation, in the superior cervical sympathetic ganglion (SCG) rich in synapses excised from rats were observed following application of either cholinergic or adrenergie agonist during aerobic incubation. Addition of aeetylcholine (ACh, ImM) caused an abrupt increase of TG activity in depolarized SCG within a few minutes, which continued for 30 min, and then subsided. The AChinduced depolarization-coupled increase of ganglionic TG activity was more markedly prevented by further addition of nicotinic antagonist, hexamethonium, than by a muscarinic blocker. In contrast, hyperpolarizing adrenergie agonists such as norepinephrine (NE, 50 pM) and isoproterenol (0.2 mM) inhibited TG activity in SCG, but the effect was nearly abolished by either a 6-adrenergie blocker, propranolol or an a2-antagonist, yohimbine. These results suggest that rapid stimulation and inhibition of ganglionic TG activity induced by eholinergle and adrenergic neurotransmitters is attributed to receptor-mediated depolarization and hyperpolarization processes during synaptic activity of nerve impulses.
MECHANISM OF MUSCARINIC RECEPTOR-MEDIATED INFLUX AND RELEASE OF Ca = - IN I L E A L SMOOTH MUSCLE. X I A O - B I N G WANG, TAKESHI OSUGI AND S H U J I UCHIDA, D e p a r t m e n t of Pharmacology I , Osaka U n i v e r s i t y School of Medicine, 2-2 Yamada-Oka, S u l t a , Osaka 565, Japan. In the l o n g i t u d i n a l smooth muscle of guinea p l g ileum, muscarlnic s t i m u l a t i o n elevated the I n t r a c e i i u l a r Ca2. c o n c e n t r a t i o n ( [ C a 2 " ] I ) . Dose-response a n a l y s l s showed a d i f f e r e n c e in the p o t e n c i e s of carbachol (CCh) to I n c r e a s e [Ca=*]x in the presence and absence o f e x t r a c e l l u l a r Ca2~, i n d i c a t i n g t h a t a low c o n c e n t r a t i o n of CCh(
MUSCARINIC RECEPTORS IN ISOLATED CANINE GASTRIC PARIETAL CELLS INVOLVED IN CYCLIC AMP FOg~TION AND INOSITOL PIIOSPHOLIPID BREAKDOWN. KUNIHIKO YOKOTANI~ AND TADATAKA YAMAHAz~, ± Department of Pharmacology, Kochl M e d i ~ and ~Departmcnt of I n t e r n a l Medicine, U n i v e r s i t y of Michigan, MI 48109. U.S.A.
We m e a s u r e d c~IP and lnosltol phosphates (IP 1, IP 2, IP 3) in Isolated canine parietal cells. Carbachol inhibited cAMP f o r m a t i o n induced by a submaximal concentration of forskolln ( 1 0 u M ) . On t h e o t h e r hand, carbaehol stimulated IP formation. NaF a l s o s t i m u l a t e d IP formation. Atropine and 4-DAMP (M3 blocker) attenuated both carbachol-medlated i n h i b i t o r y and s t l m u l a t o r y responses. Pirenzeplne, a M blocker, more markedly attenuated carbachol-lnduced I n h i b i t o r y e f f e c t s on c&MPI formation than carbachol-induced s t l m u l a t o r y e f f e c t s on IP formation. Pretreatment with p e r t u s s l s toxin (PT) (100 ng/ml, f o r 2 h r s ) a b o l i s h e d the i n h i b i t o r y e f f e c t of carbachol on cAMP formation but had no e f f e c t on carbachol-lnduced IP formation. From these r e s u l t s , i t was suggested t h a t MI receptors in canine parietal cells mediate the inhibition o f cAMP f o r m a t i o n v PT-sensltive G-proteins and M3 r e c e p t o r s mediate the stimulation of lnosltol phosphollpld breakdown via PT-lnsensitive G proteins.
STIMULATION BY ACETYLCHOLINE AND I N H I B I T I O N BY NOREPINEPHRINE OF TRANSGLUTAMINASE ACTIVITY IN THE SUPERIOR CERVICAL GANGLION OF RATS. MASATO ANDO, YUHZO NAKASHIMA*, AND YDTAKA NAGATA Department o__ffPhysiology. Fu~ita Health University School of Medicine, Toyoake, Aichi 470-11 Japan. Rapid changes in activity of calcium-dependent transglutaminase (TG), an enzyme catalyzing the covalent binding to glutamine residures on peptide chain to cause tissue degradation, in the superior cervical sympathetic ganglion (SCG) rich in synapses excised from rats were observed following application of either cholinergic or adrenergie agonist during aerobic incubation. Addition of aeetylcholine (ACh, ImM) caused an abrupt increase of TG activity in depolarized SCG within a few minutes, which continued for 30 min, and then subsided. The AChinduced depolarization-coupled increase of ganglionic TG activity was more markedly prevented by further addition of nicotinic antagonist, hexamethonium, than by a muscarinic blocker. In contrast, hyperpolarizing adrenergie agonists such as norepinephrine (NE, 50 pM) and isoproterenol (0.2 mM) inhibited TG activity in SCG, but the effect was nearly abolished by either a 6-adrenergie blocker, propranolol or an a2-antagonist, yohimbine. These results suggest that rapid stimulation and inhibition of ganglionic TG activity induced by eholinergle and adrenergic neurotransmitters is attributed to receptor-mediated depolarization and hyperpolarization processes during synaptic activity of nerve impulses.
MECHANISM OF MUSCARINIC RECEPTOR-MEDIATED INFLUX AND RELEASE OF Ca = - IN I L E A L SMOOTH MUSCLE. X I A O - B I N G WANG, TAKESHI OSUGI AND S H U J I UCHIDA, D e p a r t m e n t of Pharmacology I , Osaka U n i v e r s i t y School of Medicine, 2-2 Yamada-Oka, S u l t a , Osaka 565, Japan. In the l o n g i t u d i n a l smooth muscle of guinea p l g ileum, muscarlnic s t i m u l a t i o n elevated the I n t r a c e i i u l a r Ca2. c o n c e n t r a t i o n ( [ C a 2 " ] I ) . Dose-response a n a l y s l s showed a d i f f e r e n c e in the p o t e n c i e s of carbachol (CCh) to I n c r e a s e [Ca=*]x in the presence and absence o f e x t r a c e l l u l a r Ca2~, i n d i c a t i n g t h a t a low c o n c e n t r a t i o n of CCh(