title: Effects of mechanical stretch on the membrane potential of guinea pig ventricular muscles.
abstract: We studied the effect of stretch on the membrane potentials and ultrastructure of isolated ventricular papillary muscles of guinea pigs. The muscles were stimulated at 0.5 Hz and stretched stepwise from slack length (90% of Lmax) to 100% (mild stretch), 110-120% (moderate stretch), and 130-140% of Lmax (severe stretch), under microscopic control. In control Tyrode solution (K+ = 5.4 mM, Ca2+ = 1.8 mM, Mg2+ = 0.5 mM), the mild to moderate stretch significantly depolarized the resting potential (RP) by about 6 mV as compared to that in slack length, whereas the severe stretch hyperpolarized the membrane by about 5 mV. The latter finding was new and was focused on in later experiments. Both the hyperpolarization and depolarization became more marked when [K+]o was decreased to 1.35-2.7 mM, and became less with elevated [K+]o to 10.8-21.6 mM, thereby suggesting the participation of altered K+ conductance (gK) with these changes in the RP. Perfusion with low [Ca2+]o (0.45 mM) enhanced the depolarization but eliminated the hyperpolarization; high [Ca2+]o (7.2 mM) inhibited the depolarization without effect on the hyperpolarization. D-600 (1 microM), caffeine (10 mM), and ryanodine (1 microM), all of which may produce decreases in [Ca2+]i, abolished the hyperpolarization with inconsistent effects on the depolarization. Moderate to severe stretches decreased the maximum rate of rise of action potential (Vmax), by shifting the Vmax-RP relationship toward hyperpolarizing direction. The shift could be reversed partially after increasing [Mg2+]o to 8.0 mM. Electron microscopic examination revealed that the sarcoplasmic reticulum (SR) remained intact with mild to moderate stretches with significant lengthening of sarcomere length, while with a severe stretch, the SR showed a structural disarrangement with a non-uniform lengthening of sarcomere length. Our observations suggest that stretch-induced hyperpolarization is probably mediated by the increase in gK, presumably secondary to the increase in [Ca2+]i. Ca2+ may be released from the SR upon mechanical stretch of the organelle.
authors.affiliation: Department of Physiology, Faculty of Medicine, Medical College of Oita, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Nakagawa
authors.forename: M
authors.initials: M
authors.lastname: Arita
authors.forename: T
authors.initials: T
authors.lastname: Shimada
authors.forename: J
authors.initials: J
authors.lastname: Shirabe
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D002110:Caffeine / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D005711:Gallopamil / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D009119:Muscle Contraction / Q000187:drug effects; D009132:Muscles / Q000502:physiology* / Q000648:ultrastructure; D010210:Papillary Muscles / Q000502:physiology; D012433:Ryanodine / Q000494:pharmacology; D013997:Time Factors
chemical_list: D012433:Ryanodine; D005711:Gallopamil; D002110:Caffeine; D001262:Atenolol; D001285:Atropine