Abstract:
:(-)Bay K 8644 produced a concentration-dependent contraction of porcine coronary artery rings with the maximal contraction at 10(-6) M. Pretreatment of the rings with 10(-6) M nitrendipine inhibited (-)Bay K 8644-induced contraction, while pretreatment with 10(-8) M nitrendipine potentiated the contraction elicited by (-)Bay K 8644. (-)Bay K 8644 (10(-6) M) significantly stimulated Ca2+ influx. Although 10(-8) M nitrendipine never stimulated Ca2+ influx, Ca2+ influx induced by (-)Bay K 8644 was significantly potentiated by pretreatment with 10(-8) M nitrendipine. Pretreatment with 10(-6) M nitrendipine significantly decreased Ca2+ influx in tissues treated with (-)Bay K 8644. Our results suggest that the increased Ca2+ influx might be involved in the mechanisms by which (-)Bay K 8644-induced contraction was potentiated by pretreatment with nitrendipine.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Miwa K,Schwartz Adoi
10.1016/0006-291x(87)91068-0subject
Has Abstractpub_date
1987-10-14 00:00:00pages
1-8issue
1eissn
0006-291Xissn
1090-2104pii
0006-291X(87)91068-0journal_volume
148pub_type
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