Abstract
Although both neurokinin A (NKA) and norepinephrine (NE) induced similar maximal contractions in the epididymal and the prostatic site of vas deferens, NKA affected sensitivity more potently than did NE in both sites. The NKA-induced contractions were more strongly inhibited by nicardipine, a dihydropyridine Ca 2+ entry blocker, or by elimination of extracellular Ca 2+ (Ca 2+ o) in both sites. However, ryanodine, which interferes with the release of intracellular C 2+ (Ca 2+ i), abolished the contractions caused by NKA in the prostatic site whereas it had no effect in the epididymal site. These results suggest that NKA-induced contraction utilizes both Ca 2+ i and Ca 2+ o in the prostatic site but mobilizes only Ca 2+ o in the epididymal site. Ca 2+ i concentration ([Ca 2+] i)was measured directly with a Ca 2+ -sensitive fluorescent dye, fura-2. In the epididymal site NKA induced contractions with smaller increase in [Ca 2+] i compared to that necessary for NE-induccd contractions. These results suggest that NKA utilizes Ca 2+ more efficiently than does NE and plays a role as a neuromodulator in rat vas deferens.
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