A Secoisopimarane Diterpenoid from Salvia cinnabarina Inhibits Rat Urinary Bladder Contractility in vitro
Raffaele Capasso1,2
, Angelo A. Izzo1
, Giovanni Romussi3
, Francesco Capasso1
, Nunziatina De Tommasi2
, Angela Bisio3
, Nicola Mascolo1
1Department of Experimental Pharmacology, University of Naples ”Federico II”, Naples, Italy
2Department of Pharmaceutical Sciences, University of Salerno, Fisciano (SA), Italy
3Department of Chemistry and Pharmaceutical Technology and Alimentary, University of Genoa, Genoa, Italy
This work was supported by Cofinanziamento Murst, Enrico and Enrica Sovena Foundation (Rome, Italy), Regione Campania. SR140333, SR48968 and S141716A were a kind gift from SANOFI (Montpellier, France)
We have evaluated the effect of 3,4-secoisopimar-4(18),7,15-triene-3-oic acid (compound 1), isolated from the aerial parts of Salvia cinnabarina, on the contractile response elicited by electrical field stimulation (EFS) in the rat isolated urinary bladder. Compound 1 (10 - 7 - 10 - 4 M) produced a concentration-dependent inhibition of the EFS contractile response without modifying the contractions produced by exogenous acetylcholine (10 - 6 M). A number of antagonists/inhibitors including a combination of atropine (10 - 6 M), phentolamine (10 - 6 M), propranolol (10 - 6 M) and hexamethonium (10 - 4 M), the NK1 receptor antagonist SR140333 (10 - 7 M) plus the NK2 receptor antagonist SR48968 (10 - 6 M), naloxone (10 - 6 M), verapamil (10 - 7 M), capsazepine (10 - 5 M) and the CB1 receptor antagonist SR141716A (10 - 6 M) did not modify the inhibitory effect of compound 1. However, the nitric oxide (NO) synthase inhibitor L-NAME (3 × 10 - 4 M), significantly reduced the inhibitory effect of compound 1. It is concluded that compound 1 inhibits rat bladder contractility with a mechanism involving, at least in part, NO production.
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