Short‐term or long‐term treatments with a phosphodiesterase‐4 (PDE4) inhibitor result in opposing agonist‐induced Ca²⁺ responses in endothelial cells

Abstract

Our data suggest that sustained inhibition of PDE4 by rolipram induced an increase in PDE4 activity, possibly as a compensatory mechanism to accelerate cAMP degradation and that PDE4A and PDE4B were implicated in the regulation of [Ca(2+)](i). Thus, isozyme-specific PDE4 inhibitors might be useful as therapeutic agents in diseases where [Ca(2+)](i) handling is altered, such as atherosclerosis, hypertension and tolerance to beta-adrenoceptor agonists.