Up-Regulation of the Voltage-Gated K2.1 K Channel in the Renal Arterial Myocytes of Dahl Salt-Sensitive Hypertensive Rats.

Salt-sensitive hypertension induces renal injury via decreased blood flow in the renal artery (RA), and ion channel dysfunction in RA myocytes (RAMs) may be involved in the higher renal vascular resistance. We examined the effects of several voltage-gated K (K) channel blockers on the resting tension in endothelium-denuded RA strips and delayed-rectifier K currents in RAMs of Dahl salt-sensitive hypertensive rats (Dahl-S) fed with low- (Dahl-LS) and high-salt diets (Dahl-HS). The tetraethylammonium (TEA)-induced contraction in RA strips were significantly larger in Dahl-HS than Dahl-LS. Correspondingly, TEA-sensitive K currents were significantly larger in the RAMs of Dahl-HS than Dahl-LS. Among the TEA-sensitive K channel subtypes, the expression levels of K2.1 transcript and protein were significantly higher in the RA of Dahl-HS than Dahl-LS, while those of K1.5, K7.1, and K7.4 transcripts was comparable in two groups. K2.1 currents detected as the guangxitoxin-1E-sensitive component were larger in the RAMs of Dahl-HS than Dahl-LS. These suggest that the up-regulation of the K2.1 channel in RAMs may be involved in the compensatory mechanisms against decreased renal blood flow in salt-sensitive hypertension.