Calcineurin and PDE5 activities underlie the decay in transient ANP-induced cGMP signals in MA-10 cells.

<p>(A,B) Exposure to ANP triggered transient cGMP responses in the absence and presence of 500 µM IBMX. (C) Pretreatment with both 50 µM CIP and 500 µM IBMX substantially increased the peak response and reduced the extent of the decay in the response. (D) 14 and 40 nM sildenafil as well as 200 µM IBMX significantly inhibited cGMP PDE activity (assayed at 0.1 µM ³HcGMP) in total cell lysates from vehicle or ANP (10 nM, 20 min) treated MA-10 cells, indicating that PDE5 is primarily responsible for cGMP hydrolysis in these cells. (E) 10 nM ANP triggered an increase in peak cGMP PDE activity under these experimental conditions. (F) Treatment with both IBMX and ANP did not induce significant increases in extracellular cGMP, even after 100 min. * P<0.05.