Beta-blockade of epinephrine-induced cyclic AMP formation in heart, liver, fat and trachea.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Murad.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A protein-binding assay for guanosine 3':5'-monophosphate, which employs an enzyme preparation from lobster tail muscle, is described. The binding constant for cyclic GMP was 2-10 nM for four different enzyme preparations. The method can be set up in several days and permits the detection of as little as 0.5-1 pmol of cyclic GMP. In some instances, it is possible to assay the nucleotide in urine or deproteinized extracts of tissue without purification. For other samples, a simple method for separating and purifying cyclic AMP and cyclic GMP is described.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Thyrocalcitonin (TCT) increased the rate of accumulation of adenosine 3':5'-cyclic phosphate (cyclic AMP) when added to incubations containing washed particles from whole rat kidney, adenosine triphosphate (ATP), MgSO(4), and caffeine. The maximum stimulatory effect of TCT, 44 +/- 6.7 per cent, was always less than the 150 to 250 per cent increase produced by parathyroid hormone (PTH). The effect of both hormones together was no greater than that of PTH alone when each was present at a maximally effective concentration. Since neither TCT nor PTH altered the rate of degradation of cyclic AMP by the kidney preparation, it may be inferred that their effects on cyclic AMP accumulation are the result of increased formation of cyclic AMP. Adenyl cyclase activity in homogenates of renal cortex was stimulated to a greater extent by TCT and PTH than was that of medulla, whereas, as reported earlier, the effect of vasopressin was much larger with homogenates of medulla. The accumulation of cyclic AMP in incubations of rat kidney cortex slices was increased 20 to 60 per cent by TCT and 50 to 140 per cent by PTH. The accumulation of cyclic AMP in incubations of rat calvaria was increased about threefold with TCT and nine to tenfold with PTH, while reduced and alkylated TCT had less than 10 per cent of the activity of TCT. These observations are consistent with the view that the physiological effects of TCT and PTH in kidney and bone are secondary to the enhanced formation of cyclic AMP.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.