title: Altered Ca-dependent fluxes of 42K in rat aorta during aldosterone-salt hypertension.
abstract: It was the objective of this paper to integrate recent findings concerning Ca-dependent 42K effluxes from rat aorta with observations of elevated basal 42K efflux and supersensitivity to norepinephrine (NE) stimulation of 42K effluxes during aldosterone-salt induced hypertension (Aldo). The results of several protocols show a close correlation (0.94) between changes in 42K efflux and contraction, which led to the hypothesis that [Ca]cell is a controller of both contraction and K-channels during NE stimulation. Aldo was associated with a 2-fold increase in basal 42K efflux and a 10-fold increase in NE sensitivity. The basal 42K efflux and tension in Aldo were reduced to near control (C) levels by diltiazem (DZ) while the Ca-antagonist had no significant effect on basal values in C. The IC50 for DZ (2 X 10(-7) M) was similar for 42K and contractile effects, and was in the range reported to block potential dependent Ca-channels in other tissues. DZ (10(-5) M) also shifted the ED50 for NE in Aldo (4 X 10(-9) M) to the C range (20-30 X 10(-9) M). It is hypothesized that Aldo hypertension is associated with elevated activity of potential dependent channels which lead to elevated [Ca]cell. It is further suggested that elevated [Ca]cell increases the activity of Ca-dependent K-channels, contractile state and sensitivity to NE.
mesh_terms: D000450:Aldosterone; D000818:Animals; D001011:Aorta / Q000378:metabolism*; D002118:Calcium / Q000502:physiology*; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D007473:Ion Channels / Q000378:metabolism*; D051381:Rats; D012965:Sodium Chloride
chemical_list: D007473:Ion Channels; D012965:Sodium Chloride; D000450:Aldosterone; D002118:Calcium