Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effects, and the mechanism of the effects, of isoproterenol on diaphragmatic contractility and fatigue in septic peritonitis in vitro. Ninety-six rats were divided into two groups of 48. One group (CLP group) was treated with cecal ligation and perforation (CLP) and the other (sham group) was treated with laparotomy. The left hemidiaphragm was removed at 16 h after the operation. We assessed the diaphragmatic contractility by twitch characteristics and force-frequency curves in vitro. Diaphragm fatigue was induced by rhythmically stimulating strips to contract at 60/ min (20 Hz, 0.33-s trains, 1 train/s) over a 4-min period. Force-frequency curves were determined before and after fatigue. Isoproterenol (10(-9), 10(-8), and 10(-7) M), a beta-adrenoceptor agonist, was cumulatively administered to the organ bath. Isoproterenol significantly increased diaphragmatic contractility. There were no significant changes in diaphragmatic contractility in the sham group. Isoproterenol (10(-7) M) significantly accelerated diaphragmatic recovery of fatigue and increased cAMP levels both in the sham group and the CLP group. Propranolol (10(-7) M), a general beta-adrenoceptor blocker, completely abolished the positive inotropic effect of isoproterenol (10(-7) M) and increased cAMP levels in the CLP group. Dibutyryl cAMP (10(-3) M), a derivative of cyclic AMP, mimicked the effects of isoproterenol in the CLP group. These results suggest that isoproterenol increases diaphragmatic contractility and accelerates diaphragmatic recovery of fatigue in septic peritonitis by activating the adenylate cyclase system.
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PMID:Effects of isoproterenol on diaphragmatic contractility in septic peritonitis. 1067 83

Effects of isoproterenol on contraction and membrane potential of gastric smooth muscle were studied in stroke prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar Kyoto rats (WKY). Circular muscle preparation from the gastric fundus developed tonic contraction by re administration of Ca2+ to a nominally Ca2+-free solution. The contraction was inhibited by nifedipine or nicardipine. Isoproterenol induced relaxation when it was applied to the Ca2+-induced contraction. The amplitude of isoproterenol induced relaxation was concentration-dependent. Propranolol 10(-6) M abolished the relaxation induced by isoproterenol 10(-7) M. In the preparation from SHRSP, the amplitude of isoproterenol induced relaxation was smaller than that from WKY between 3 x 10(-9) and 10(-7) M. Forskolin, an adenylate cyclase activator, induced concentration-dependent relaxation. There was no difference in the relaxation induced by forskolin between preparations from WKY and SHRSP. Dibutilyl cyclic AMP, a membrane permeable analogue of cyclic AMP, also induced similar relaxation in preparations from WKY and SHRSP. Resting membrane potential of smooth muscle cell was not different between preparations from WKY and SHRSP. Isoproterenol hyperpolarized the membrane concentration-dependently. Isoproterenol-induced hyperpolarization in the preparation from SHRSP was smaller than that from WKY between 10(-8) and 10(-6) M. When the membrane was depolarized by Tyrode's solution containing 40 mM K+, isoproterenol-induced hyperpolarization was almost abolished. In this condition, the isoproterenol-induced relaxation was inhibited partly, however, there was no difference in the amplitude of relaxation between preparations from WKY and SHRSP. Therefore, isoproterenol-induced hyperpolarization contributed at least partly to the relaxation. Forskolin hyperpolarized the membrane by the same amplitude in the preparations from WKY and SHRSP. These results indicate that a decrease in hyperpolarization may contribute to the decreased relaxation by isoproterenol in the preparation from SHRSP.
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PMID:Altered beta-adrenoceptor-mediated responses in the gastric smooth muscle of hypertensive rats. 1083 Apr 73

Candida albicans (C. albicans) is known as an opportunistic pathogen that changes from a yeast form to a hyphae form in response to various outside environmental signals. The addition of propranolol inhibited hyphae formation of C. albicans. Propranolol inhibited the expression of agglutinin like sequence 3 (ALS3) and ALS8mRNA, which are regulated by the cAMP-EFG1 pathway in C. albicans. Propranolol did not affect the expression of CST20, HST7 or CPH1mRNA, which are components of the mitogen-activated protein (MAP) kinase cascade in C. albicans. The expression of CYR1mRNA, which encodes adenylate cyclase of C. albicans, was not affected by propranolol. These findings indicated that the interruption of hyphae formation by propranolol is caused by inhibition of the cAMP-EFG1 pathway, but not effects on the MAP kinase cascade.
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PMID:Effect of propranolol on hyphae formation signal in Candida albicans. 1912 94


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