Abstract
To determine whether atrial natriuretic peptide (ANP) has an inotropic effet, the contractility of spontaneously beating cultured chick embryo ventricular cells was studied in response to rat-ANP (1–23) superfused at concentrations ranging from 10 −10 M to 2.5 × 10 −7 M. r-ANP reversibly decreased contractility with a threshold concentration of 10 −8 M; at the highest concentration, r-ANP decreased contractility to a moderate extent (−30 ± 4 %) r-ANP increased dose-dependently intracellular cGMP levels. Stimulation of contractility with [Ca2+], the calcium-channel agonist BAY K 8644 or isoproterenol attenuated to various degrees the inhibitory effect of r-ANP. By contrast, the inhibitory effect of r-ANP on contractility was unchanged or even enhanced after stimulation of contractility by angiotensin II. There was no difference in r-ANP-induced increase in cGMP whether cells were pre-incubated with angiotensin II or not. These results indicate that r-ANP was able to decrease contractility of cultured cardiac myocytes and suggest a preferential antagonism of the inotropic effect of angiontensin II.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
