Hypertension: beta testing

Abstract

A new study demonstrates that angiotensin-induced hypertension results in a marked decrease in expression of the beta subunit of the BK channel, suggesting a role for this critical subunit in the regulation of vascular tone.

Figure 1

The β subunit tunes the coupling of BK channels to RyR Ca²⁺ release. Gating of ryanodine receptors (RyR) in the sarcoplasmic reticulum (SR) results in brief, localized increases in Ca²⁺, termed Ca²⁺ sparks (red stars). These Ca²⁺ sparks activate a few BK channels in the sarcolemma (SL), resulting in spontaneous transient outward currents, or STOCs (currents shown above), which hyperpolarize and relax the myocyte, leading to vasodilation. The β subunit of the BK channel plays a critical role in regulating the sensitivity of the BK channel complex to Ca²⁺ ions, and Amberg et al. (7) now establish a link between hypertension, produced by a chronic infusion of angiotensin (AngII), and this channel subunit. Equivalent Ca²⁺ sparks produce smaller and less frequent STOCs in hypertensive mice, and this appears to result from a decrease in expression of the β1 subunit following angiotensin infusion. The results focus attention on transcriptional regulation of the β subunit and how this may be affected by activation of AT1 receptors.