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Effects of propionate and ammonium on contractions produced by Na+ removal (0-Na+ contraction, replaced with N-methyl-D-glucamine) were studied and compared with those produced by 60 mM K+ in muscle strips isolated from human internal mammary artery (IMA) and saphenous vein (SV), clinically used as bypass vessels. Contractions induced by 60 mM K+ (60-K+ contractions) were similar in both vessels. 0-Na+ contraction was significantly larger in the vein than in the artery. Neither 60-K+ nor 0-Na+ contractions were significantly affected by NG-nitro-L-arginine (30 microM) or phenoxybenzamine (1 microM). Ouabain (2 microM) slowly potentiated 0-Na+ contractions and the 3rd contraction produced 60 min after ouabain application was 291 +/- 36% in the artery and 184 +/- 41% of the control (n = 10) in the vein. Propionate (20 mM) potentiated 60-K+ contraction more strongly in the vein than in the artery, but potentiation of 0-Na+ contraction was greater in the artery than in the vein. On the other hand, ammonium (20 mM) inhibited 60-K+ contractions more strongly in the artery than the vein, whereas inhibition of 0-Na+ contraction was stronger in the vein. 0-Na+ contraction is likely to be produced by an Na(+)-Ca2+ exchange mechanism, and the effects of propionate and ammonium are considered to be mediated by intracellular acidification and alkalinization, respectively. It is speculated that an Na(+)-H+ exchange may also be involved in 0-Na+ contraction and that SV has slightly lower pHi than IMA.

Effects of Propionate and Ammonium on Contractions Produced by Sodium Removal in Human Internal Mammary Artery and Saphenous Vein.