Article date: March 1983
By: Yasushi Ohizumi in Volume 78, Issue 3, pages 461-467
In the guinea‐pig vas deferens, grayanotoxin I (G‐I), a diterpenic toxin isolated from certain ericaceous plants caused rhythmic contractions which were dose‐dependent (5 × 10−5m — 10−3m); these followed an initial transient contraction.
The G‐I (3 × 10−4m)‐induced contraction was markedly inhibited or abolished by reserpine (2 mg/kg on 2 days), phentolamine (2 × 10−7m and 10−6m) or tetrodotoxin (TTX, 5 × 10−7m), but remained almost unaffected by atropine (10−6m) or mecamylamine (3 × 10−5m). This contraction was also abolished after storage at 4°C for 7 days or incubation in Na‐deficient or Ca‐free medium.
After treatment with G‐I (3 × 10−5m), which did not alter the tension of the preparation, transmural stimulation (10–50 Hz, 0.5 ms, supramaximal voltage, for 3 s) induced a slower contraction (second contraction) following the first rapid contraction caused by stimulation.
The second contraction was inhibited or abolished by reserpine (2 mg/kg on 2 days), phentolamine (2 × 10−7m and 10−6m) and TTX (2 × 10−8m), but was not affected by atropine (10−6m) and mecamylamine (3 × 10−5m).
G‐I (3 × 10−5m) shifted the dose‐response curves for noradrenaline (NA), acetylcholine and high‐K contractions to the left in a parallel manner and slightly increased the maximal response to these agonists.
G‐I (3 × 10−4m) caused a release of endogenous NA from the vas deferens which was approximately 120 times that of control preparations. This response was inhibited or abolished by TTX (5 × 10−7m) or incubation in Ca‐free medium.
These results suggest that the G‐I‐induced contraction of the vas deferens and the G‐I‐induced second contraction on electrical stimulation are the result of an indirect action mediated through the release of NA from the adrenergic nerve endings.
In the guinea‐pig vas deferens, grayanotoxin I (G‐I), a diterpenic toxin isolated from certain ericaceous plants caused rhythmic contractions which were dose‐dependent (5 × 10−5m — 10−3m); these followed an initial transient contraction.
The G‐I (3 × 10−4m)‐induced contraction was markedly inhibited or abolished by reserpine (2 mg/kg on 2 days), phentolamine (2 × 10−7m and 10−6m) or tetrodotoxin (TTX, 5 × 10−7m), but remained almost unaffected by atropine (10−6m) or mecamylamine (3 × 10−5m). This contraction was also abolished after storage at 4°C for 7 days or incubation in Na‐deficient or Ca‐free medium.
After treatment with G‐I (3 × 10−5m), which did not alter the tension of the preparation, transmural stimulation (10–50 Hz, 0.5 ms, supramaximal voltage, for 3 s) induced a slower contraction (second contraction) following the first rapid contraction caused by stimulation.
The second contraction was inhibited or abolished by reserpine (2 mg/kg on 2 days), phentolamine (2 × 10−7m and 10−6m) and TTX (2 × 10−8m), but was not affected by atropine (10−6m) and mecamylamine (3 × 10−5m).
G‐I (3 × 10−5m) shifted the dose‐response curves for noradrenaline (NA), acetylcholine and high‐K contractions to the left in a parallel manner and slightly increased the maximal response to these agonists.
G‐I (3 × 10−4m) caused a release of endogenous NA from the vas deferens which was approximately 120 times that of control preparations. This response was inhibited or abolished by TTX (5 × 10−7m) or incubation in Ca‐free medium.
These results suggest that the G‐I‐induced contraction of the vas deferens and the G‐I‐induced second contraction on electrical stimulation are the result of an indirect action mediated through the release of NA from the adrenergic nerve endings.
DOI: 10.1111/j.1476-5381.1983.tb08806.x
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