| First Author | Xu H | Year | 2011 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 300 |
| Issue | 2 | Pages | H476-85 |
| PubMed ID | 21131476 | Mgi Jnum | J:167217 |
| Mgi Id | MGI:4867573 | Doi | 10.1152/ajpheart.00975.2010 |
| Citation | Xu H, et al. (2011) Large-conductance Ca2+-activated K+ channel beta1-subunit knockout mice are not hypertensive. Am J Physiol Heart Circ Physiol 300(2):H476-85 |
| abstractText | Large-conductance Ca2+-activated K+ (BK) channels are composed of pore-forming alpha-subunits and accessory beta1-subunits that modulate Ca2+ sensitivity. BK channels regulate arterial myogenic tone and renal Na+ clearance/K+ reabsorption. Previous studies using indirect or short-term blood pressure measurements found that BK channel beta1-subunit knockout (BK beta1-KO) mice were hypertensive. We evaluated 24-h mean arterial pressure (MAP) and heart rate in BK beta1-KO mice using radiotelemetry. BK beta1-KO mice did not have a higher 24-h average MAP when compared with wild-type (WT) mice, although MAP was approximately 10 mmHg higher at night. The dose-dependent peak declines in MAP by nifedipine were only slightly larger in BK beta1-KO mice. In BK beta1-KO mice, giving 1% NaCl to mice to drink for 7 days caused a transient (5 days) elevation of MAP ( approximately 5 mmHg); MAP returned to pre-saline levels by day 6. BK beta1-KO mesenteric arteries in vitro demonstrated diminished contractile responses to paxilline, increased reactivity to Bay K 8644 and norepinephrine (NE), and maintained relaxation to isoproterenol. Paxilline and Bay K 8644 did not constrict WT or BK beta1-KO mesenteric veins (MV). BK beta1-subunits are not expressed in MV. The results indicate that BK beta1-KO mice are not hypertensive on normal or high-salt intake. BK channel deficiency increases arterial reactivity to NE and L-type Ca2+ channel function in vitro, but the L-type Ca2+ channel modulation of MAP is not altered in BK beta1-KO mice. BK and L-type Ca(2+) channels do not modulate murine venous tone. It appears that selective loss of BK channel function in arteries only is not sufficient to cause sustained hypertension. |
