Title of article :
Role of Calcium Current and Sarcoplasmic Reticulum Calcium Released in Control of Myocardial Contraction in Rat and Rabbit Myocytes
Author/Authors :
S. Y. Wang، نويسنده , , L. Winka، نويسنده , , G. A. Langer، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1993
Pages :
9
From page :
1339
To page :
1347
Abstract :
The relative importance of calcium current and sarcoplasmic reticulum in supplying contraction-related calcium was investigated in isolated rat and rabbit cardiac ventricular myocytes using patch-clamp and video techniques. Calcium current and contractile response were manipulated via variation of [Ca2+]o between 0.25 and 8.0 mM. Sarcolemmal calcium influx was derived from integration of the calcium current. An increase in [Ca2+]o from 0.25 to 8 mM augmented the amplitude of contractile shortening from 7 to 375% of control (amplitude at 1.0 mM) in rat but only from 36.5 to 177.6% in rabbit. Upon variation in [Ca2+]o from 0.5 to 8.0 mM calcium current increased from 67 to 175% of control in rat and from 65 to 150% in rabbit. Sarcolemmal calcium influx in rat was, however, only about half of that in rabbit for the entire range of [Ca2+]o and saturated at [Ca2+]o over 2.0 mM in both species. Application of 1 μM ryanodine increased calcium current and slowed its inactivation time course in the rat, but in the rabbit a slight decrease in current was observed and the inactivation time course was not obviously affected. The sarcoplasmic reticulum calcium release: transsarcolemmal calcium flux ratio is at least four-fold greater in the rat than in the rabbit. The results from this study further explain the well-known marked differences in contractile control in the two species.
Keywords :
Sarcolemmal calcium influx , Sarcoplasmic reticulum calcium , rabbit , contraction , calcium current , rat , Cardiac ventricular myocytes
Journal title :
Journal of Molecular and Cellular Cardiology
Serial Year :
1993
Journal title :
Journal of Molecular and Cellular Cardiology
Record number :
525054
Link To Document :
بازگشت