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)

Na+-K+-ATPase was inhibited by 1 times 10-4M ethacrynic acid and mercuderamide, and by 1 times 10-3M hydrochlorothiazide and furosemide. A modification of Gilman's (1970) protein displacement assay has been used to measure c-AMP levels in toad bladder epithelial cells. Vasopressin (50 mU/ml) caused c-AMP levels to rise from 4.27 to 9.27 pmol/mg protein. Ethacrynic acid had no effect on cellular c-AMP levels after 10 min exposure to the drug, but at 90 min caused a reduction of both basal and vasopressin stimulated levels. Furosemide caused an apparent rise in c-AMP levels, dilution ratio measurements indicated interference by this drug in the assay procedure, mecuderamide also caused substantial interference with the c-AMP assay. Hydrochlorothiazide had no effect on basal or hormone stimulated levels of c-AMP. It was concluded that the inhibition of sodium transport produced by ethacrynic acid in toad bladder is probably due to inhibition of adenylate cyclase, an effect not shared by other dieuretics.
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PMID:The effect of diuretics on Na+-K+-ATPase and c-AMP levels in toad bladder epithelial cells. 16 90

Hydrochlorothiazide, tienilic acid, chlorthalidone and indapamide inhibit membrane adenylate cyclase of pigeon erythrocytes in vitro. This effect is related to the action of these substances on the interface between the membranous phospholipids and adenylate cyclase. Indapamide with its strong lipophic properties, has a more specific action on the intracellular regulation of adenylate cyclase. The relationship between the inhibition of adenylate cyclase and the antihypertensive effects of these drugs is discussed.
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PMID:[Mechanism of action of benzothiadiazides in arterial hypertension: the energetic theory]. 630 85