Role of the Gastric Pacesetter Potential Defined by Electrical Pacing

1972 ◽  
Vol 50 (10) ◽  
pp. 1017-1019 ◽  
Author(s):  
Keith A. Kelly ◽  
Richard C. La Force
Keyword(s):  
Contractile Activity ◽  
Electrical Pacing ◽  
Electrical Stimuli ◽  
Gastric Contractions ◽  
Pacesetter Potential

This experiment substantiates the hypothesis that the gastric pacesetter potential sets the pace of gastric contractions. By pacing the gastric pacesetter potential with electrical stimuli during periods of spontaneous and pentagastrin-induced contractile activity, we also paced gastric contractions.

Adaptations in the Muscle Cell to Training: Role of the Na+-K+-Atpase

2000 ◽  
Vol 25 (3) ◽  
pp. 204-216 ◽  
Author(s):  
Howard J. Green
Keyword(s):  
Metabolic Flux ◽  
Contractile Activity ◽  
Integral Membrane Protein ◽  
Adaptive Responses ◽  
Muscle Strain ◽  
Muscle Contractility ◽  
Exercise Adaptation ◽  
Altered Regulation ◽  
Key Words Muscle

The plasticity of skeletal muscle is evident following the onset of regular contractile activity where extensive adaptations can be observed at all levels of organization. Among the properties subject to altered regulation is the Na+-K+-ATPase, an integral membrane protein distributed throughout the sarcolemma and t-tubule, which functions to maintain high Na+ and K+ transmembrane gradients. This protein is uniquely positioned to control muscle excitation and contraction processes, metabolic flux rates, and contractility. Pronounced and rapid upregulation in the Na+-K+-ATPase content can be observed within the first days of exercise and well before the other major ATPase proteins involved in Ca2+ and actomyosin cycling. Moreover, the Na+-K+-ATPase is subject to complex messenger regulation, involved both in the accommodation and the adaptive responses to contractile activity. This emphasizes that adaptive responses can be mediated soon after the onset of training and may have profound affects on muscle contractility and other cellular adaptations. Key Words: muscle, strain, exercise, adaptation, accommodation

PDGF-BB decreases systolic blood pressure through an increase in macrovascular compliance in rats

1997 ◽  
Vol 273 (4) ◽  
pp. H1719-H1726 ◽  
Author(s):  
Masahiro Ikeda ◽  
Chizuru Morita ◽  
Makoto Mizuno ◽  
Toshio Sada ◽  
Hiroyuki Koike ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diastolic Pressure ◽  
Contractile Activity ◽  
Isolated Heart ◽  
Systolic Pressure ◽  
Hypotensive Effect ◽  
Platelet Derived Growth Factor ◽  
High Concentration ◽  
Vasodilating Activity

The cardiovascular roles of platelet-derived growth factor (PDGF) were examined in anesthetized rats by monitoring blood pressure and in isolated blood vessels and heart preparations. Intravenous injection of PDGF-BB lowered blood pressure. The decrease in systolic pressure was greater than that in diastolic pressure, so the pulse pressure decreased. PDGF-AA and -AB, other isoforms of PDGF, did not have any effect on blood pressure. Pretreatment of rats with Nω-nitro-l-arginine methyl ester (l-NAME), an inhibitor of nitric oxide (NO) synthase, shortened duration of the hypotensive effect of PDGF-BB. The administration ofl-arginine withl-NAME partially prevented the effect of l-NAME. PDGF-BB relaxed aortic rings precontracted with phenylephrine with a 50% effective concentration of 3 ng/ml. In contrast, in isolated mesenteric vascular preparations, the vasodilating activity of PDGF-BB was observed only at a high concentration (>12.5 ng/ml). In isolated heart preparations, PDGF-BB had no effect on the beat rate or contractile activity. These results suggest a new role of PDGF-BB that may contribute to the regulation in circulation through the increase in macrovascular compliance mediated by NO.

Pulmonary vein sleeve cell excitation–contraction-coupling becomes dysynchronized by spontaneous calcium transients

2015 ◽  
Vol 43 (3) ◽  
pp. 410-416 ◽  
Author(s):  
Katja Rietdorf ◽  
Said Masoud ◽  
Fraser McDonald ◽  
Michael J. Sanderson ◽  
Martin D. Bootman
Keyword(s):  
Spontaneous Activity ◽  
Pulmonary Vein ◽  
Action Potentials ◽  
Pulmonary Veins ◽  
Electrical Field Stimulation ◽  
Spontaneous Action ◽  
Major Treatment ◽  
Electrical Pacing ◽  
Electrical Stimuli ◽  
Spontaneous Action Potentials

Atrial fibrillation (AF) is the most common form of sustained cardiac arrhythmia. Substantial evidence indicates that cardiomyocytes located in the pulmonary veins [pulmonary vein sleeve cells (PVCs)] cause AF by generating ectopic electrical activity. Electrical ablation, isolating PVCs from their left atrial junctions, is a major treatment for AF. In small rodents, the sleeve of PVCs extends deep inside the lungs and is present in lung slices. Here we present data, using the lung slice preparation, characterizing how spontaneous Ca2+ transients in PVCs affect their capability to respond to electrical pacing. Immediately after a spontaneous Ca2+ transient the cell is in a refractory period and it cannot respond to electrical stimulation. Consequently, we observe that the higher the level of spontaneous activity in an individual PVC, the less likely it is that this PVC responds to electrical field stimulation. The spontaneous activity of neighbouring PVCs can be different from each other. Heterogeneity in the Ca2+ signalling of cells and in their responsiveness to electrical stimuli are known pro-arrhythmic events. The tendency of PVCs to show spontaneous Ca2+ transients and spontaneous action potentials (APs) underlies their potential to cause AF.

Role of stomach in regulation of activities of hypothalamic feeding centers

1961 ◽  
Vol 201 (4) ◽  
pp. 593-598 ◽  
Author(s):  
K. N. Sharma ◽  
B. K. Anand ◽  
S. Dua ◽  
Baldev Singh
Keyword(s):  
Blood Glucose ◽  
Electrical Activity ◽  
High Voltage ◽  
Glucose Utilization ◽  
Irregular Waves ◽  
Gastric Distention ◽  
Implanted Electrodes ◽  
Gastric Contractions ◽  
Balloon System

Gastric distention was produced through a water-filled-balloon system and the electrical activity of the hypothalamic "satiety" and "feeding" centers were recorded electroencephalographically through stereotaxically implanted electrodes. Gastric distention leads to production of high voltage irregular waves and occasional spikes, selectively in the region of the satiety centers. Gastric hunger contractions do not change the electrical activity of either feeding or satiety centers. Glucagon does not produce any direct effect on the hypothalamic centers or stomach contractions. Later, when glucagon raises blood glucose and arteriovenous Δ-glucose, activity of satiety centers increases and gastric contractions are inhibited. After lesions of satiety centers, rise in blood glucose with glucagon does not inhibit gastric contractions. Therefore, the inhibition of gastric hunger contractions is a result of activation of satiety centers by increased glucose utilization.

Exercise and glycogen depletion: effects on ability to activate muscle phosphorylase

1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy
Keyword(s):  
Muscle Contraction ◽  
Muscle Glycogen ◽  
Contractile Activity ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
Significant Difference ◽  
Muscle Phosphorylase ◽  
Glycogen Repletion ◽  
Stimulation Of

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.

scholarly journals Attenuation of Canonical Transient Receptor Potential-Like Channel 6 Expression Specifically Reduces the Diacylglycerol-Mediated Increase in Intracellular Calcium in Human Myometrial Cells

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 406-416 ◽  
Author(s):  
Daesuk Chung ◽  
Yoon-Sun Kim ◽  
Jennifer N. Phillips ◽  
Aida Ulloa ◽  
Chun-Ying Ku ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transient Receptor Potential ◽  
Contractile Activity ◽  
Receptor Potential ◽  
Myometrial Cells ◽  
Canonical Transient Receptor Potential ◽  
Voltage Dependent ◽  
Transient Receptor ◽  
Entry Mechanism

Abstract An increase in intracellular Ca2+ ([Ca2+]i) as a result of release of Ca2+ from intracellular stores or influx of extracellular Ca2+ contributes to the regulation of smooth muscle contractile activity. Human uterine smooth muscle cells exhibit receptor-, store-, and diacylglycerol (OAG)-mediated extracellular Ca2+-dependent increases in [Ca2+]i (SRCE) and express canonical transient receptor potential-like channels (TRPC) mRNAs (predominantly TRPC1, -4, and -6) that have been implicated in SRCE. To determine the role of TRPC6 in human myometrial SRCE, short hairpin RNA constructs were designed that effectively targeted a TRPC6 mRNA reporter for degradation. One sequence was used to produce an adenovirus construct (TC6sh1). TC6sh1 reduced TRPC6 mRNA but not TRPC1, -3, -4, -5, or -7 mRNAs in PHM1-41 myometrial cells. Compared with uninfected cells or cells infected with empty vector, the increase in [Ca2+]i in response to OAG was specifically inhibited by TC6sh1, whereas SRCE responses elicited by either oxytocin or thapsigargin were not changed. Similar findings were observed in primary pregnant human myometrial cells. When PHM1-41 cells were activated by OAG in the absence of extracellular Na+, the increase in [Ca2+]i was partially reduced. Furthermore, pretreatment with nifedipine, an L-type calcium channel blocker, also partially reduced the OAG-induced [Ca2+]i increase. Similar effects were observed in primary human myometrial cells. These findings suggest that OAG activates channels containing TRPC6 in myometrial cells and that these channels act via both enhanced Na+ entry coupled to activation of voltage-dependent Ca2+ entry channels and a nifedipine-independent Ca2+ entry mechanism to promote elevation of intracellular Ca2+.

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