Abstract
In Triton X-100-skinned trachealis muscle, neither papaverine nor AH 21-132 modified responses to Ca 2+. The (−)-enantiomer of AH 21-132 was more potent than the (+)-enantiomer both in relaxing intact trachealis muscle and in inhibiting tracheal cAMP phosphodiesterase (PDE). AH 21-132 (0.6 μM) potentiated forskolin in causing tracheal relaxation but did not potentiate isoprenaline, cromakalim or sodium nitrite. AH 21-132 (2 μm) potentiated all four agents in relaxing the trachea. AH 21-132 (1 μM) potentiated forskolin in increasing tissue cAMP content and, in higher concentration, itself increased tissue cAMP. Electrical effects of AH 21-132 included suppression of spontaneous slow waves and cellular hyperpolarisation. It is concluded that AH 21-132 lacks a direct depressant effect on the intracellular contractile machinery. The weight of evidence suggests that AH 21-132-induced relaxation results from inhibition of cAMP-PDE. However, in common with other PDE inhibitors, AH 21-132 increases tissue cAMP content only at concentration greater than that required to cause full relaxation.
Published Version
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