Sodium nitroprusside relaxes goat coronary artery through activation of calcium-dependent K⁺ channels

Abstract

In the present investigation we have examined the hypothesis that calcium-dependent K⁺ channels (K_Ca) are involved in the sodium nitroprusside (SNP)-induced vasodilatation of goat coronary artery. SNP (10^-9- 3×10^-6 <i>M</i>), added cumulatively, relaxed K⁺ (30 m<i>M</i>)-contracted coronary artery ring segments in a concentration-dependent manner with an EC₅₀ of 1.32 ×

10^-7<i> M </i>(95% CL, 0.93 -1.86×10^-7 <i>M; </i>n = 21). K_Ca blocker, tetraethyl ammonium (1m<i>M</i>) caused a rightward shift in the concentration-response curve of SNP with a corresponding increase in EC₅₀ (1.62×10^-6 <i>M; </i>95% CL, 0.44-6.02×10^-6 <i>M</i>, n = 4) of nitro vasodilator. Lowering of extra cellular Ca²⁺ in the physiological saline solution to 1/4 of normal selectively attenuated the vasorelaxant response of SNP, thereby causing an increase in its EC₅₀ (2.4 × 10^-6 <i>M; </i>95% CL, 1.23 - 4.68 ×10^-6<i> M, </i>n = 4). Exposure of the tissues to high K⁺ (80 m<i>M</i>) solution, a protocol adopted to reduce the K⁺ gradient across the cell membrane, markedly inhibited the coronary artery relaxations induced by SNP (EC₅₀, 2.54 × 10^-6 <i>M; </i>95% CL, 1.31 -4.91×10^-6 <i>M</i>,<i> </i>n = 4), when compared with tissues contracted with low K⁺ (30 mM) solution (EC₅₀ 7.9 × 10^-8; 95% CL, 4.4×10^-8-1.44 × 10^-7 <i>M</i>,<i> </i>n = 6). The results suggested that a major component of SNP-induced relaxation of goat coronary artery was mediated by K_Cachannels.