To gain further insight into the excitation-contraction coupling mecha
nisms in hypertrophy, we studied rested-state contractions, rest decay
curves, and rest potentiation under different experimental conditions
using papillary muscles of spontaneously hypertensive rats (SHR) and
age-matched normotensive Wistar and Wistar-Kyoto (WKY) rats. Under con
stant stimulation at 1.1 Hz, contractility and relaxation were not sig
nificantly different in hypertensive when compared with normotensive a
nimals. Rested-state contraction (the first beat after a rest interval
of 15 minutes) increased to 159.2 +/- 23% and 123.5 +/- 7.5% of prere
st values in Wistar and WKY rats, respectively, whereas in SHR it did
not differ from prerest values (92.8 +/- 9.8%). Ryanodine, used to pre
ferentially inhibit sarcoplasmic reticulum function, eliminated the di
fferences in rested-state contractions observed between hypertensive a
nd normotensive rats. Maximal rest potentiation (the first beat after
a rest interval of 1 minute) was also significantly higher in Wistar a
nd WKY rats than in SHR. These differences persisted at low extracellu
lar Na+, when Ca2+ efflux via the Na+-Ca2+ exchanger was inhibited. Re
st decay curves (the decay in contractility from maximal rest potentia
tion to rested-state contraction) showed a similar pattern in the thre
e rat strains. The results suggest that the altered inotropic response
s of the SHR arise from an alteration in calcium handling by the sarco
plasmic reticulum. Experiments on saponin-skinned trabeculae indicated
that fractional calcium release induced by caffeine was significantly
reduced in the SHR. We conclude that the altered inotropic response o
bserved in SHR may reflect a diminished release of calcium from the sa
rcoplasmic reticulum.