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At least 307 records · Page 17Linked to original sources
PubMed1987

Antiarrhythmic-like actions of the smooth muscle spasmolytic agent, cinnamedrine, on action potentials of mammalian ventricular tissue.

Cinnamedrine is an active ingredient in preparations used to relieve dysmenorrhea. It has been reported to have local anesthetic properties in nerve. This property prompted us to evaluate the effects of cinnamedrine on the cardiac action potential. Cinnamedrine (10-35 microM) significantly reduced the overshoot and maximum rate of rise, and also prolonged the duration of action potentials recorded from rat and guinea pig ventricular tissues. The action of cinnamedrine to depress upstroke velocity in guinea pig papillary muscle was dependent on the rate of stimulation. In addition, the refractory period of rat ventricular muscle was prolonged markedly. Finally, cinnamedrine (10 microM) significantly reduced, or totally abolished, epinephrine-induced automatic activity in both dog and rat myocardium in vitro. Prolongation of action potential duration and refractory period, and depression of upstroke velocity are characteristics which cinnamedrine shares with antiarrhythmic drugs.

Action Potentials↗
PubMed1995

Calcium-and G-protein-related spasmolytic effects of nonsteroidal anti-inflammatory drugs on rat uterus contractions in vitro.

The effects of the nonsteroidal anti-inflammatory drugs (NSAIDs) acetylsalicylic acid, metamizole, phenylbutazone, indometacin, piroxicam, naproxen, tolmetin, diclofenac, and mefenamic acid on methacholine (10 mumol/l), prostaglandin F2 alpha (1 mumol/l), and KCl (60 mmol/l) induced contractions of isolated rat uterus were assayed. All of these cause a concentration-dependent inhibition of methacholine and prostaglandin F2 alpha-induced contractions with the exception of acetylsalicylic acid, metamizole, and naproxen. All except acetylsalicylic acid and metamizole relaxed in a concentration-dependent manner the tonic contractions induced by KCl. CaCl2 (0.1-10 mmol/l) totally counteracted the relaxant effects of naproxen and tolmetin, but not those of the other NSAIDs. Bay K8644 did not revert the effect of the NSAIDs. Pertussis toxin (50 micrograms/l) did not modify the effect of indometacin, mefenamic acid, and tolmetin, but partially antagonized the effects of diclofenac and naproxen and increased the effect of phenylbutazone and piroxicam. These results suggest that some of the NSAIDs assayed induce smooth muscle relaxation by mechanisms independent of prostaglandin synthesis inhibition, but related to the inhibition of extracellular calcium influx through mechanisms related or unrelated to pertussis toxin sensible G proteins.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗