TY - JOUR
T1 - Activation of the iberiotoxin-sensitive BKCa channels by salvianolic acid B of the porcine coronary artery smooth muscle cells
AU - Lam, Francis Fu Yuen
AU - Seto, Sai Wang
AU - Kwan, Yiu Wa
AU - Yeung, John Hok Keung
AU - Chan, Paul
N1 - Funding Information:
We are grateful to Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong (PR of China), for financial supports. The authors are indebted to Mr. W.C. Lai (Manager of the Production Department, Ng Fung Slaughterhouse (H.K.) Co. Ltd.) and staff of the Sheung Shui Slaughterhouse (Hong Kong SAR, PR of China) for the excellent technical assistance in providing fresh pig's hearts for this study. Mr. S.W. Seto is a recipient of a post-graduate (Ph.D.) studentship of the Department of Pharmacology (The Chinese University of Hong Kong, Hong Kong SAR, PR of China). Excellent technical assistance provided by Ms. Alice LS Au is appreciated. Assistance provided by Ms. Penelope MY Or and Mr. Kam Ming Chan during the course of this study is acknowledged. This work was financially supported by the RGC Earmarked Grants of Hong Kong SAR, PR of China (Ref.: 4107/01M and Ref.: 4166/02M), and Direct Grant for Research (Faculty of Medicine, The Chinese University of Hong Kong; Ref.: 2401149).
PY - 2006/9/28
Y1 - 2006/9/28
N2 - In this study, we examined the effects of Salvia miltiorrhiza (Danshen) crude extract, some of its lipid-soluble components (tanshinone I, tanshinone IIA, cryptotanshinone, dihydroisotanshinone I) and the water-soluble compounds (danshensu and salvianolic acid B) on the K+ channels such as the iberiotoxin-sensitive Ca2+-activated K+ (BKCa) channels and the glibenclamide-sensitive ATP-dependent K+ (IKATP) channels of the porcine left anterior descending coronary artery smooth muscle cells. Cumulative application of salvianolic acid B (30-300 μM) caused a l-NNA (100 μM)-insensitive, potentiation of the outward BKCa current amplitude with no apparent effect on the IKATP channels opening. Salvianolic acid B (300 μM) caused an ODQ (10 μM, a guanylate cyclase inhibitor)-sensitive enhancement of the outward BKCa current amplitude. In contrast, none of the other isolated chemical constituents of S. miltiorrhiza modified the openings of the two types of K+ channels studied. In conclusion, our results suggest that salvianolic acid B, a major hydrophilic constituent found in Radix S. miltiorrhiza, activated the opening of the BKCa channels of the porcine coronary artery smooth muscle cells through the activation of guanylate cyclase without the involvement of the nitric oxide synthase activation.
AB - In this study, we examined the effects of Salvia miltiorrhiza (Danshen) crude extract, some of its lipid-soluble components (tanshinone I, tanshinone IIA, cryptotanshinone, dihydroisotanshinone I) and the water-soluble compounds (danshensu and salvianolic acid B) on the K+ channels such as the iberiotoxin-sensitive Ca2+-activated K+ (BKCa) channels and the glibenclamide-sensitive ATP-dependent K+ (IKATP) channels of the porcine left anterior descending coronary artery smooth muscle cells. Cumulative application of salvianolic acid B (30-300 μM) caused a l-NNA (100 μM)-insensitive, potentiation of the outward BKCa current amplitude with no apparent effect on the IKATP channels opening. Salvianolic acid B (300 μM) caused an ODQ (10 μM, a guanylate cyclase inhibitor)-sensitive enhancement of the outward BKCa current amplitude. In contrast, none of the other isolated chemical constituents of S. miltiorrhiza modified the openings of the two types of K+ channels studied. In conclusion, our results suggest that salvianolic acid B, a major hydrophilic constituent found in Radix S. miltiorrhiza, activated the opening of the BKCa channels of the porcine coronary artery smooth muscle cells through the activation of guanylate cyclase without the involvement of the nitric oxide synthase activation.
KW - (Salvia miltiorrhiza (Danshen))
KW - BK channels
KW - Porcine coronary artery
KW - Salvianolic acid B
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U2 - 10.1016/j.ejphar.2006.07.038
DO - 10.1016/j.ejphar.2006.07.038
M3 - Article
C2 - 16928370
AN - SCOPUS:33748291559
SN - 0014-2999
VL - 546
SP - 28
EP - 35
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 1-3
ER -