Table 6.

Effects of PLMS68E and PLMS68A mutants on PLM KO myocytes

	KO-GFP		KO-PLM		KO-S68E		KO-S68A
	Means ± SE	n	Means ± SE	n	Means ± SE	n	Means ± SE	n
Maximal contraction amplitude, %resting cell length
1.8 mM [Ca2+]o	4.91±0.33	16	5.16±0.40	4	5.02±0.27	15	4.92±0.28	13
5.0 mM [Ca2+]o	8.99±0.22	26	7.35±0.33*	13	7.19±0.21*	28	8.73±0.41	19
[Ca2+]i transient amplitude, %increase in fluorescence
1.8 mM [Ca2+]o	18.2±0.6	33	18.6±1.0	13	17.9±1.2	16	17.8±1.3	17
5.0 mM [Ca2+]o	37.1±0.9	54	27.1±1.0*	23	26.4±1.3*	22	36.2±1.0	12
t1/2 of [Ca2+]i decline, ms
1.8 mM [Ca2+]o	191±12		186±9		188±10		195±17
5.0 mM [Ca2+]o	149±5		163±9		174±6		159±14
SR Ca2+ content, fmol/fF
5.0 mM [Ca2+]o	12.1±0.2	4	5.4±1.6*	5	6.0±0.9*	8	11.3±0.9	6

Values are means ± SE; n, no. of cells. Contractility, [Ca²⁺]_i transients, t_1/2 of [Ca²⁺]_i decline, and sarcoplasmic reticulum (SR) Ca²⁺ contents were measured after adenovirus infection and 48 h of culture. For comparison, SR Ca²⁺ content measured at 5 mM [Ca²⁺]_o was 14.3 ± 0.6 fmol/fF (n = 9) in freshly isolated PLM KO myocytes (22). KO-S68E and KO-S68A, PLM KO myocytes infected with adenovirus expressing PLMS68E and PLMS68A mutants, respectively.

^*P < 0.025 compared with KO-GFP myocytes.