Abstract:
OBJECTIVE:To study the cellular mechanism of the effect of Ang II on ICa,L in single guinea-pig ventricular cells by using losartan and 1-(5-lsoquinolinylsulfonyl)-2-Methyl-Piperazine (H-7) as the Ang II type 1 receptor (AT1) inhibitor and protein kinase C inhibitor, respectively. METHODS:Patch clamp techniques were used to study the cellular mechanism of the effect of Ang II on ICa,L in single guinea-pig ventricular cells. RESULTS:In the whole cell patch clamp recording model, Ang II stimulated ICa,L in a concentration dependent manner; the maximal effect was obtained at 100 nmol/L (n = 9). At 30 nmol/L, Ang II stimulated peak ICa,L from 11.3 +/- 0.6 pA/pF to 15.3 +/- 0.6 pA/pF (at + 10 mV, n = 9, P < 0.05). 100 nmol/L Losartan, a specific AT1 receptor inhibitor, had no effect on ICa,L (n = 9), but the effect of Ang II on ICa,L was inhibited by 100 nmol/L Losartan. Ang II on ICa,L was also inhibited by 20 mumol/L H-7, a specific protein kinase C inhibitor, whereas H-7 alone has no effect on ICa,L (n = 9). CONCLUSION:Ang II stimulates ICa,L in guinea-pig ventricular cells by binding to AT1 through a transduction pathway involving protein kinase C.
journal_name
Chin Med J (Engl)journal_title
Chinese medical journalauthors
Yang X,Hui J,Jiang Wkeywords:
subject
Has Abstractpub_date
2001-06-01 00:00:00pages
577-82issue
6eissn
0366-6999issn
2542-5641journal_volume
114pub_type
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