RESUMO
1. We investigated Na(+)-Ca2+ exchange and the involvement of the sarcoplasmic reticulum in frequency-dependent slow response excitability enhancement in rabbit atrial trabeculae. 2. Slow responses were induced in a modified Tyrode solution containing high K+ and Ba2+ and conventional electrophysiological techniques were used for stimulating and recording membrane potentials. 3. Under these conditions, the frequency-dependence of slow response excitability can be demonstrated with excitability enhancement as stimulation frequency is increased (0.25 to 1.0 Hz). 4. The frequency-dependent excitability enhancement depends on external Na+, increasing in high-[Na+]o (173.8 mM) and decreasing in low-[Na+]o (103.8 mM) media. 5. Quinidine (10 microM) and ryanodine (10 microM) decrease frequency-dependent slow response excitability enhancement. 6. These results indicate that the Na(+)-Ca2+ exchange might have an important role in frequency-dependent excitability enhancement of slow responses. Moreover, we suggest that the control of internal Ca2+ by the sarcoplasmic reticulum might have an additional role in regulating the excitability enhancement process in depolarized atrial trabeculae.
Assuntos
Função Atrial , Espaço Extracelular/metabolismo , Sódio/metabolismo , Animais , Cálcio/metabolismo , Estimulação Elétrica , Eletrofisiologia , Potenciais da Membrana/efeitos dos fármacos , Potenciais da Membrana/fisiologia , Quinidina/farmacologia , Coelhos , Rianodina/farmacologia , Retículo Sarcoplasmático/metabolismoRESUMO
1. We investigated Na(+)-Ca2+ exchange and the involvement of the sarcoplasmic reticulum in frequency-dependent slow response excitability enhancement in rabbit atrial trabeculae. 2. Slow responses were induced in a modified Tyrode solution containing high K+ and Ba2+ and conventional electrophysiological techniques were used for stimulating and recording membrane potentials. 3. Under these conditions, the frequency-dependence of slow response excitability can be demonstrated with excitability enhancement as stimulation frequency is increased (0.25 to 1.0 Hz). 4. The frequency-dependent excitability enhancement depends on external Na+, increasing in high-[Na+]o (173.8 mM) and decreasing in low-[Na+]o (103.8 mM) media. 5. Quinidine (10 microM) and ryanodine (10 microM) decrease frequency-dependent slow response excitability enhancement. 6. These results indicate that the Na(+)-Ca2+ exchange might have an important role in frequency-dependent excitability enhancement of slow responses. Moreover, we suggest that the control of internal Ca2+ by the sarcoplasmic reticulum might have an additional role in regulating the excitability enhancement process in depolarized atrial trabeculae
Assuntos
Animais , Coelhos , Espaço Extracelular/metabolismo , Átrios do Coração/fisiologia , Sódio/metabolismo , Cálcio/metabolismo , Estimulação Elétrica , Eletrofisiologia , Potenciais da Membrana/efeitos dos fármacos , Potenciais da Membrana/fisiologia , Quinidina/farmacologia , Retículo Sarcoplasmático/metabolismo , Rianodina/farmacologiaRESUMO
Single K channels from skeletal muscle sarcoplasmic reticulum were incorporated into artificial membranes. Ryanodine applied to either side of the membrane did not affect the gating nor the conductance properties of those channels. These results suggest that the site of action of ryanodine is limited only to the calcium channels present in the membrane of sarcoplasmic reticulum (1).
Assuntos
Alcaloides/farmacologia , Canais Iônicos/efeitos dos fármacos , Potássio/fisiologia , Rianodina/farmacologia , Retículo Sarcoplasmático/efeitos dos fármacos , Animais , Cálcio/metabolismo , Condutividade Elétrica , Técnicas In Vitro , Cinética , Bicamadas Lipídicas , Músculos/ultraestruturaRESUMO
Slow responses were induced in isolated rabbit left atrial trabeculae in a medium containing 20 mM K+ and 1.8 microM epinephrine. Under these conditions, the Na+-dependent upstroke of the cardiac action potential is absent but it is possible to obtain tetrodotoxin-resistant Ca2+-action potentials (slow responses). Conventional electrophysiological techniques were employed for stimulating the preparation and measuring transmembrane potentials. Under these experimental conditions, slow responses exhibit frequency-dependent excitability changes. The excitability of epinephrine-induced slow responses increases with increasing stimulation frequency. This increase is manifested by a decrease in the latency of the slow response and also by a decrease in the stimuli requirements. In this respect, slow responses induced by epinephrine are similar to barium-induced slow responses. These observations provide further support for the hypothesis that the Ca2+-inflow during slow response electrogenesis promotes an increase in slow response excitability. These results are discussed in relation to the propagation of the slow response through the atrioventricular node under physiological conditions.