{'fraction_non_alphanumeric': 0.05681159420289855, 'fraction_numerical': 0.013333333333333334, 'mean_word_length': 5.345588235294118, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Inhibition of the endothelium-dependent relaxation by 18beta-glycyrrhetinic acid in the guinea-pig aorta.

The effect of 18beta-glycyrrhetinic acid (GA), an agent which interferes with gap junction conductivity, on endothelium-dependent relaxation produced by substance P was investigated in isolated aortic rings of the guinea-pig. In nor-adrenaline (NA)-contracted aortic rings, substance P (10(-7) M) induced an endothelium-dependent, transient relaxation. The relaxation was only slightly reduced by the co-application of nitroarginine and diclofenac. When GA (2x10(-5) M) was applied first, it slightly reduced substance P-induced relaxation, and a subsequent co-application of nitroarginine and diclofenac strongly reduced the relaxation. In aortic rings contracted with high-K solution ([K(+)](o) = 29.4 mM), substance P-induced relaxation was reduced by the simultaneous application of GA, nitroarginine and diclofenac, but not by GA alone. In endothelium-denuded aortic rings, GA reduced the threshold concentration of NA required to produce contractions and increased the amplitude of NA-induced contractions. GA increased the amplitude of contraction produced by small increases of [K(+)](o) (<30 mM) but reduced those produced by higher concentrations of [K(+)](o) (>54 mM). In NA-contracted aortic rings, Y-26763, a K(+)-channel opener, could relax muscles with reduced amplitude in the presence of GA. It is concluded that in guinea-pig aortic rings, GA inhibits mainly the EDHF-induced components of endothelium-dependent relaxation. GA also modulated contractions produced by NA or high-K solutions. The possible effects of inhibition of gap junctions by GA on endothelium-dependent relaxation were discussed.