Regulation of Transient Outward K + Current in Human Atria Involves G Proteins

The role of G protein in regulating the transient outward K + current (I to) was examined by using isolated human atrial myocytes. When a nonhydrolyzable analogue of guanosine 5′-triphosphate (GTPγs) was introduced intracellularly, I to was irreversibly decreased and reached a new steady-state within 3 minutes. These results suggest that regulation of I to is similar to that of other K + current in the heart and involves guanine nucleotide-binding proteins. This has important implications with respect to autonomic control of action potential duration in the human heart.