RESTED-STATE CONTRACTIONS AND REST POTENTIATION IN SPONTANEOUSLY HYPERTENSIVE RATS

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.