The electrical basis for contraction and relaxation in canine fundal smooth muscle

182

121

SUMMARY1. Intracellular recordings were made from cells located in the longitudinal, inner and outer circular muscle layers of the dog, cat, rabbit, opossum and human small intestine.2. In whole-thickness preparations in all five species, longitudinal muscle cells generated slow waves and spikes. However, in isolated longitudinal muscle preparations, all cells tested were electrically silent.3. In whole-thickness and in isolated preparations, cells in the inner circular muscle layer generated spontaneous spikes superimposed on slow potentials. However, the occurrence of spikes and slow potentials was more regular in whole-thickness preparations.4. In whole-thickness preparations, cells in the outer circular muscle layer generated slow waves which were coupled with phasic contractions. However, in isolated outer circular muscle preparations, all cells tested were electrically silent and spontaneous phasic contractions were absent.5. In whole-thickness preparations, non-neural cells located on the serosal side of the outer circular muscle layer generated slow waves.6. The data suggest that spontaneous slow waves of the small intestine of the dog, cat, rabbit, opossum and human are generated in non-neural cells located between the longitudinal and outer circular muscle layer and by non-neural cells located between the outer and inner circular muscle layers.

Section: Introductionmentioning

confidence: 99%

Electrophysiology of smooth muscle of the small intestine of some mammals.

Hara¹,

Kubota²,

Szurszewski³

1986

182

121

“…Stimulation with ACh or pentagastrin at concentrations less than or equal toED50 levels increases the amplitude of phasic contractions, but does not elevate tone between contractions (for review, see Szurszewski, 1987). The activation of contractions in antral muscles appears to be mainly due to the influx of Ca21 through voltage-dependent Ca2+ channels because dihydropyridines essentially abolish spontaneous contractions and responses to most excitatory agonists (Morgan, Muir & Szurszewski, 1981;Hohnsbein & Golenhofen, 1985;Vogalis, Publicover, Hume & Sanders, 1991).…”

Section: Introductionmentioning

confidence: 99%

Ca2+ regulation of the contractile apparatus in canine gastric smooth muscle.

Ozaki

Gerthoffer

Hori

et al. 1993

SUMMARY1. The relationships between cytosolic Ca2" ([Ca2`],yt; expressed as a fluorescence ratio at 400 nm and 500 nm using Indo-1) and contractile force was examined in strips of circular smooth muscles of canine gastric antrum. Rhythmic increases in [Ca2+]Yt were observed and contractions were biphasic.2. In most muscles (70 %), the amplitude of the second phase of the Ca21 transient was less than or equal to the first phase of the Ca2+ transient, but the second phase of the contraction was much smaller than the first phase, suggesting a decrease in Ca2+ sensitivity during the second contractile phase. In 30 % of muscles, the amplitude of the second phase of the Ca2+ transient was 2-to 3-fold greater than the first phase. In these muscles, the second phase of contraction was 10-fold greater than the first phase of contraction.

“…The relationship between excitation and contraction in smooth muscle can be determined by using K+ depolarization as a chemical voltage clamp (Kuriyama,Osa & Tasaki, 1970;Morgan & Szurszewski, 1980;Morgan, Muir & Szurszewski, 1981; Morgan & Morgan, 1984). Voltage and tension relationships have been determined for fundal, corporal and antral muscle of the dog stomach (Morgan & Szurszewski, 1980;Morgan et al 1981).…”

Section: Introductionmentioning

confidence: 99%

Effect of potassium and acetylcholine on canine intestinal smooth muscle.

Hara¹,

Szurszewski²

1986

SUMMARY1. Mechanical and intracellular electrical activity were recorded simultaneously from small intestinal smooth muscle of the dog.2. Tonic and phasic contractions due to exogenous acetylcholine and elevated external K+ concentration were spike-dependent in longitudinal and inner circular muscle layers and spike-independent in the outer circular muscle layer.3. Voltage-tension curves were generated by graded depolarization of the membrane. In spike-dependent longitudinal and inner circular muscle layers the threshold voltage for initiation of spikes and contraction was approximately -53 mV. In spike-independent outer circular muscle layer the voltage threshold for contraction was approximately -42 mV.4. The resting membrane potential in longitudinal and inner circular muscle layers was close to the voltage threshold for initiation of spikes and contraction. In contrast, in the outer circular muscle it was approximately 20 mV more negative to the voltage threshold for contraction.5. In the outer circular muscle layer of whole-thickness preparations an increase in the amplitude of phasic contractions caused by acetylcholine was associated with an increase in the amplitude of the slow waves. Tone was related to the resting membrane potential.6. In preparations of isolated outer circular muscle acetylcholine caused depolarization of the membrane potential, slow waves and phasic contractions; comparable depolarization by increases in external K+ concentration did not induce slow waves or phasic contractions. 7. Comparison of the effect of acetylcholine on outer circular muscle with the voltage-tension curve for this muscle layer showed that the top of the slow wave was associated with just the contractile force predicted by the voltage-tension curve. This suggests that acetylcholine altered the force ofphasic contraction ofthe outer circular muscle through a voltage-dependent mechanism.8. In non-neural cells located on the serosal side of the outer circular muscle layer of the dog, cat and rabbit, changes in external K+ concentration depolarized the membrane and abolished slow waves. There was no response to acetylcholine.