| Title | Characterization of an extensive transverse tubular network in sheep atrial myocytes and its depletion in heart failure. | | Author(s) | Dibb KM, Clarke JD, Horn MA, Richards MA, Graham HK, Eisner DA, Trafford AW | | Institution | Unit of Cardiac Physiology, University of Manchester, Core Technology Facility, 46 Grafton St, Manchester M13 9NT, United Kingdom. katharine.dibb@man.ac.uk | | Source | Circ Heart Fail 2009 Sep; 2(5):482-9. | | Abstract | BACKGROUND: In ventricular myocytes, the majority of structures that couple excitation to the systolic rise of Ca(2+) are located at the transverse tubular (t-tubule) membrane. In the failing ventricle, disorganization of t-tubules disrupts excitation contraction coupling. The t-tubule membrane is virtually absent in the atria of small mammals resulting in spatiotemporally distinct profiles of intracellular Ca(2+) release on stimulation in atrial and ventricular cells. The aims of this study were to determine (i) whether atrial myocytes from a large mammal (sheep) possess t-tubules, (ii) whether these are functionally important, and (iii) whether they are disrupted in heart failure.
METHODS AND RESULTS: Sheep left atrial myocytes were stained with di-4-ANEPPS. Nearly all control cells had an extensive t-tubule network resulting in each voxel in the cell being nearer to a membrane (sarcolemma or t-tubule) than would otherwise be the case. T-tubules decrease the distance of 50% of voxels from a membrane from 3.35 + or - 0.15 to 0.88 + or- 0.04 microm. During depolarization, intracellular Ca(2+) rises simultaneously at the cell periphery and center. In heart failure induced by rapid ventricular pacing, there was an almost complete loss of atrial t-tubules. The distance of 50% of voxels from a membrane increased to 2.04 + or - 0.08 microm, and there was a loss of early Ca(2+) release from the cell center.
CONCLUSIONS: Sheep atrial myocytes possess a substantial t-tubule network that synchronizes the systolic Ca(2+) transient. In heart failure, this network is markedly disrupted. This may play an important role in changes of atrial function in heart failure. | | Language | eng | | Pub Type(s) | Journal Article
Research Support, Non-U.S. Gov't
| | PubMed ID | 19808379 |
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