Figure 7. Scheme integrating the blood pressure phenotypes of BKβ1^−/− strain A, B and C mice.

BKβ1^+/+ control mice displayed increasing mean arterial blood pressure and plasma aldosterone levels from strain A over strain B to strain C. Loss of BKβ1 expression resulted in different phenotypic outcomes depending on strain. In BKβ1^−/− strain A mice, plasma aldosterone concentration was increased relative to BKβ1^+/+ controls, associated with a hypertensive phenotype that was completely reversible by mineralocorticoid receptor block, indicating a predominantly renal effect. Conversely, BKβ1^−/− strain C mice showed a hypotensive phenotype that was alleviated in conjunction with rescue of vascular BK channel activity, indicating this effect originates in smooth muscle. Arrows do not imply direct effects.