Example sentences for: myocytes

How can you use “myocytes” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • First, PMA reduces the sensitivity of K ATP to ATP as reports using myocytes [ 17 18 19 20 ] . Second, PMA may reduce ATP production.

  • These transcription factors are known to be important for the expression of genes in myocytes.

  • Recently, it has been noted that the JNK and p38 pathways can be activated by G-protein coupled receptor agonists, notably angiotensin II, in vascular smooth muscle cells [ 19 20 ] . In cardiac myocytes, both the p38 and JNK pathways have been activated by endothelin-1 (ET-1) and the α 1 adrenergic receptor agonist phenylephrine [ 21 ] . The ability of the JNK and p38 pathways to be activated by the same agonists of G-protein coupled receptors which activate the ERK pathway led to the investigation of 5-HT as a possible activator of the JNK and p38 pathways.

  • In cardiac myocytes, PMA is known to activate K ATP through activation of PKC [ 18 19 20 ] . In insulin-secreting cell lines as well, PKC activation by PMA was shown to potentiate K ATP activity [ 11 12 ] . In the present study, however, the activation of K ATP activity by PMA is independent on activation of PKC for two reasons.

  • have demonstrated that spontaneously hypertensive rats(SHR) with symptoms of heart failure had significantly higher levels ofapoptotic myocytes than control myocytes [ 37 ] .When treated with an angiotensin-converting enzyme inhibitor, thenumber of apoptotic cells in the SHR with symptoms of heart failurewas dramatically reduced to control levels; controls were SHR withoutsymptoms of heart failure [ 37 ] . Kajstura et al.have also reported that angiotensin II increased the percentageof apoptotic cells in isolated adult rat ventricular myocytes, andthis effect was mediated by AT-1 receptors [ 38 ] .Although ventricular function was not assessed in these studies,the observations raise the possibility that, like our findings withcarvedilol, the beneficial effect of ACE-inhibitors or AT-1 receptorblockers in heart failure may in part be attributed to an inhibitionof myocyte apoptosis with a resultant improvement in in vivo cardiacfunction, a concept that needs further study.


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