Table 1.

Inhibitory effect of K⁺ channel blockers on the vasodilatation of tanshinone IIA in isolated SHR aortic rings contracted with phenylephrine or KCL^a.

	Contraction force (%)
	Phenylephrine (10 nmol l−1)		KCl (40 mmol l−1)
	Vehicle	Tanshinone IIA (10 μmol l−1)	Vehicle	Tanshinone IIA (10 μmol l−1)
Basal	100##	24.9 ± 5.1**	100##	28.3 ± 4.8**
Glibenclamide (μmol l−1)
1	99.2 ± 4.9##	59.3 ± 7.1**	98.6 ± 5.8##	53.5 ± 4.9**
10	98.8 ± 6.1##	73.3 ± 5.9∗,#	98.2 ± 4.9##	78.6 ± 6.4∗,#
100	98.6 ± 5.6##	87.4 ± 6.7##	97.9 ± 6.3##	90.3 ± 5.6##
Apamin (0.1 μmol l−1)	99.2 ± 3.7##	27.6 ± 4.7**	98.4 ± 4.7##	29.5 ± 5.7**
Charybdotoxin (0.1 μmol l−1)	98.7 ± 4.1##	26.4 ± 5.1**	98.6 ± 5.3##	31.2 ± 4.9**
Barium chloride (10 μmol l−1)	99.1 ± 5.6##	28.2 ± 3.9**	97.8 ± 4.6##	30.5 ± 5.1**
4-Aminopyridine (1 mmol l−1)	98.6 ± 3.9##	27.9 ± 4.2**	98.5 ± 6.9##	32.5 ± 6.1**

^aThe preparation of isolated aortic rings from male SHR was described in Section 2. Data (mean ± SD) indicate the percentage dilations of the maximal contractions in eight experiments. Data from phenylephrine (10 nmol l⁻¹)- or KCl (40 mmol l⁻¹)-treated sample without K⁺ channel blockers treatment was served as basal level in each group. *P < .05 and *P < .01 versus basal level obtained from samples treated with the same volume of vehicle to dissolve testing K⁺ channel blockers in each group. ^# P < .05 and ^## P < .01 versus value from sample received tanshinone IIA treatment in the absence of K⁺ channel blockers in each group.