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), phentolarnine (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 X 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.
A secoisopimarane diterpenoid from Salvia cinnabarina inhibits rat urinary bladder contractility in vitro
ROMUSSI, GIOVANNI;BISIO, ANGELA;
2004-01-01
Abstract
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), phentolarnine (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 X 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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