The effect of Ba2+ on the nitrergic mechanism in the isolated frog lung preparation

PubMedID: 95952881. The present study was undertaken to investigate effects of Ba2+ on the isolated frog lung strips depolarized by 20 mM K+ in Ca2+ free Ringer solution. 2. Ba2+ produced monophasic relaxant response, whereas Ca2+ induced biphasic response consisting of a transient relaxation and a marked contraction. Both kinds of relaxation were inhibited completely by L-NOARG. L arginine reversed the action of L-NOARG. 3. Ferrous sulfate, pyrogallol, hydroquinone, and vanadate reduced the Ba2+-induced relaxation in a concentration dependent manner. 4. These findings suggest that Ba+-induced relaxation may fully be mediated by the nitrergic mechanism and the effect of Ba2+ on the nitric oxide synthase may be more selective than Ca2+

The Role of Na+ Channels in Twitch Generation during Exposure of the Frog Rectus Abdominis to Ca-Free Ringer Solution with Na2EDTA

PubMedID: 9227789The aim of the study was to investigate whether Na+ channels play a role in the twitch component of the response of the isolated frog rectus abdominis to Ca2+-free Ringer solution with 0.2mM Na2EDTA by using tetrodotoxin and some other well known drugs that exhibit a blocking action on Na+ channels. In the presence of 5 × 10-7M tetrodotoxin, the twitch component, measured isotonically, disappeared. Although 10-7 M d-tubocurarine was found to be ineffective, a complete blockage of twitch amplitude was observed at 5 × 10-6M concentration of the drug. The inhibitory action of d-tubocurarine on twitch response was not antagonized by 10-6 and 10-5 M carbachol. Propranolol (10-6 - 10-5M), lidocaine (2 × 10-6 - 10-5M), quinine (10-6 - 2 × 10-5M) and quinidine (10-6 - 2 × 10-5M) inhibited maximal twitch amplitude in a concentration dependent manner. These findings strongly suggest that activation of tetrodotoxin sensitive Na+ channel may play a primary role at twitch generation during exposure of the frog rectus abdominis to Ca2+-free Ringer solution with Na2 EDTA