| First Author | Rindler TN | Year | 2011 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 301 |
| Issue | 4 | Pages | H1396-404 |
| PubMed ID | 21856916 | Mgi Jnum | J:177051 |
| Mgi Id | MGI:5293553 | Doi | 10.1152/ajpheart.00121.2011 |
| Citation | Rindler TN, et al. (2011) Knockout of the Na,K-ATPase {alpha}2-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension. Am J Physiol Heart Circ Physiol 301(4):H1396-404 |
| abstractText | The alpha(2)-isoform of Na,K-ATPase (alpha(2)) is thought to play a role in blood pressure regulation, but the specific cell type(s) involved have not been identified. Therefore, it is important to study the role of the alpha(2) in individual cell types in the cardiovascular system. The present study demonstrates the role of vascular smooth muscle alpha(2) in the regulation of cardiovascular hemodynamics. To accomplish this, we developed a mouse model utilizing the Cre/LoxP system to generate a cell type-specific knockout of the alpha(2) in vascular smooth muscle cells using the SM22alpha Cre. We achieved a 90% reduction in the alpha(2)-expression in heart and vascular smooth muscle in the knockout mice. Interestingly, tail-cuff blood pressure analysis reveals that basal systolic blood pressure is unaffected by the knockout of alpha(2) in the knockout mice. However, knockout mice do fail to develop ACTH-induced hypertension, as seen in wild-type mice, following 5 days of treatment with ACTH (Cortrosyn; wild type = 119.0 +/- 6.8 mmHg; knockout = 103.0 +/- 2.0 mmHg). These results demonstrate that alpha(2)-expression in heart and vascular smooth muscle is not essential for regulation of basal systolic blood pressure, but alpha(2) is critical for blood pressure regulation under chronic stress such as ACTH-induced hypertension. |
