| First Author | Sachse G | Year | 2014 |
| Journal | J Physiol | Volume | 592 |
| Issue | 12 | Pages | 2563-74 |
| PubMed ID | 24687584 | Mgi Jnum | J:222761 |
| Mgi Id | MGI:5645466 | Doi | 10.1113/jphysiol.2014.272880 |
| Citation | Sachse G, et al. (2014) Smooth muscle BK channel activity influences blood pressure independent of vascular tone in mice. J Physiol 592(Pt 12):2563-74 |
| abstractText | The large conductance voltage- and Ca(2+)-activated K(+) (BK) channel is an important determinant of vascular tone and contributes to blood pressure regulation. Both activities depend on the ancillary BKbeta1 subunit. To determine the significance of smooth muscle BK channel activity for blood pressure regulation, we investigated the potential link between changes in arterial tone and altered blood pressure in BKbeta1 knockout (BKbeta1(-/-)) mice from three different genetically defined strains. While vascular tone was consistently increased in all BKbeta1(-/-) mice independent of genetic background, BKbeta1(-/-) strains exhibited increased (strain A), unaltered (strain B) or decreased (strain C) mean arterial blood pressures compared to their corresponding BKbeta1(+/+) controls. In agreement with previous data on aldosterone regulation by renal/adrenal BK channel function, BKbeta1(-/-) strain A mice have increased plasma aldosterone and increased blood pressure. Consistently, blockade of mineralocorticoid receptors by spironolactone treatment reversibly restored the elevated blood pressure to the BKbeta1(+/+) strain A level. In contrast, loss of BKbeta1 did not affect plasma aldosterone in strain C mice. Smooth muscle-restricted restoration of BKbeta1 expression increased blood pressure in BKbeta1(-/-) strain C mice, implying that impaired smooth muscle BK channel activity lowers blood pressure in these animals. We conclude that BK channel activity directly affects vascular tone but influences blood pressure independent of this effect via different pathways. |
