Role of the enteric nervous system in the control of migrating spike complexes in the feline small intestine

1993 ◽  
Vol 265 (4) ◽  
pp. G628-G637
Author(s):  
W. C. De Vos
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Enteric Nervous System ◽  
Muscarinic Receptors ◽  
Neural Control ◽  
Muscle Cells ◽  
High Concentration ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist

The effects of agonists and antagonists of nicotinic, muscarinic (M1 and M2), and adrenergic receptors on migrating spike complexes (MSC) in ileum of fasting cats are reported. Hexamethonium decreased MSC frequency and blocked propagation. Atropine at low concentrations increased MSC frequency and increased velocity of propagation; atropine at high concentration blocked propagation. Pirenzepine (Pz; M1 antagonist) increased MSC frequency and propagation velocity. McNeil A-343 (M1 agonist), by a Pz-sensitive phentolamine-insensitive mechanism, and 4-diethylamine-methylpiperidine (4-DAMP; M2 antagonist) blocked propagation of an ongoing MSC but had no significant effect on frequency or velocity. Bethanechol (M2-receptor agonist) increased phasic spiking by a 4-DAMP-sensitive mechanism and blocked MSC propagation by a Pz-sensitive mechanism. Phenylephrine (alpha 1-adrenoceptor agonist) or oxymetazoline (alpha 2-adrenoceptor agonist) blocked MSC propagation but had no effect on MSC frequency or velocity. Phentolamine (nonselective alpha 1-adrenoceptor antagonist), prazosin (alpha 1-adrenoceptor antagonist), or yohimbine (alpha 2-adrenoceptor antagonist) alone had no effect on MSC activity. The conclusion is that the enteric nervous system controls and regulates the MSC by the following proposed mechanisms. 1) M1-muscarinic receptors, located either on postganglionic inhibitory neurons or presynaptically at a nicotinic synapse and/or neuromuscular junction, are involved in the tonic inhibitory control of MSC initiation and propagation. 2) Nicotinic and M2 muscarinic receptors, located on excitatory postganglionic motoneurons and smooth muscle cells, respectively, are important in the initiation and/or propagation of MSC. 3) alpha 1-Adrenoceptors on the smooth muscle cells and alpha 2-adrenoceptors located presynaptically at the nicotinic ganglionic synapses are not tonically active but inhibit MSC activity (4). Smooth muscle beta-adrenoceptors do not play a significant role in neural control of MSC activity.

scholarly journals Bioengineered intestinal muscularis complexes with long-term spontaneous and periodic contractions

2017 ◽  
Author(s):  
Qianqian Wang ◽  
Ke Wang ◽  
R. Sergio Solorzano-Vargas ◽  
Po-Yu Lin ◽  
Christopher M. Walthers ◽  
...  
Keyword(s):  
Stem Cells ◽  
Nervous System ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Enteric Nervous System ◽  
Interstitial Cells Of Cajal ◽  
Muscle Cells ◽  
Gut Motility ◽  
Spontaneous Contractions ◽  
Cells Of Cajal

AbstractAlthough critical for studies of gut motility and intestinal regeneration, the in vitro culture of intestinal muscularis with peristaltic function remains a significant challenge. Periodic contractions of intestinal muscularis result from the coordinated activity of smooth muscle cells (SMC), the enteric nervous system (ENS), and interstitial cells of Cajal (ICC). Reproducing this activity requires the preservation of all these cells in one system. Here we report the first serum-free culture methodology that consistently maintains spontaneous and periodic contractions of murine and human intestinal muscularis cells for months. In this system, SMC expressed the mature marker myosin heavy chain, and multipolar/dipolar ICC, uniaxonal/multipolar neurons and glial cells were present. Furthermore, drugs affecting ENS, ICC or SMC altered the contractions. Combining this method with scaffolds, contracting cell sheets were formed with organized architecture. With the addition of intestinal epithelial cells, this platform enabled at least 9 types of cells from mucosa and muscularis to coexist and function. The method constitutes a powerful tool for mechanistic studies of gut motility disorders and the regeneration of full-thickness engineered intestine.In the small intestine, the mucosa processes partially digested food and absorbs nutrients while the muscularis actuates the peristaltic flow to transport luminal content aborally. Gut motility is central to its digestive and absorptive function. The intestinal muscularis contains various types of cells: of these, smooth muscle cells, the enteric nervous system (ENS)1,2, and the pacemaker interstitial cells of Cajal (ICC)3 are three important players involved in the development of gut motility. Recent studies on intestinal tissue engineering have highlighted the importance of regenerating the functional intestinal muscularis4–9. A variety of systems derived from different cell sources, including pluripotent stem cells (PSC)4–6, embryonic stem cells (ESC)7 and primary tissue8,9, have been established to accomplish this goal and different contractile activities were developed in these systems. Notably, spontaneous contractions have been generated in culture systems that contained both ICC and smooth muscle cells4,6,10–13. In addition, electrical-induced neurogenic contractions were also successfully produced4,5,8 when ENS was introduced into culture. In one of the most recent studies, both spontaneous contractions and electrical-induced neurogenic contractions were developed in a PSC-based culture system4.

The role of globins in cardiovascular physiology

2021 ◽  
Author(s):  
T.C. Steven Keller ◽  
Christophe Lechauve ◽  
Alexander S Keller ◽  
Steven Brooks ◽  
Mitchell J Weiss ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Specific Cell ◽  
In Cells

Globin proteins exist in every cell type of the vasculature, from erythrocytes to endothelial cells, vascular smooth muscle cells, and peripheral nerve cells. Many globin subtypes are also expressed in muscle tissues (including cardiac and skeletal muscle), in other organ-specific cell types, and in cells of the central nervous system. The ability of each of these globins to interact with molecular oxygen (O2) and nitric oxide (NO) is preserved across these contexts. Endothelial α-globin is an example of extra-erythrocytic globin expression. Other globins, including myoglobin, cytoglobin, and neuroglobin are observed in other vascular tissues. Myoglobin is observed primarily in skeletal muscle and smooth muscle cells surrounding the aorta or other large arteries. Cytoglobin is found in vascular smooth muscle but can also be expressed in non-vascular cell types, especially in oxidative stress conditions after ischemic insult. Neuroglobin was first observed in neuronal cells, and its expression appears to be restricted mainly to the central and peripheral nervous systems. Brain and central nervous system neurons expressing neuroglobin are positioned close to many arteries within the brain parenchyma and can control smooth muscle contraction and, thus, tissue perfusion and vascular reactivity. Overall, reactions between NO and globin heme-iron contribute to vascular homeostasis by regulating vasodilatory NO signals and scaveging reactive species in cells of the mammalian vascular system. Here, we discuss how globin proteins affect vascular physiology with a focus on NO biology, and offer perspectives for future study of these functions.

scholarly journals The antagonism of 6-shogaol in high-glucose-activated NLRP3 inflammasome and consequent calcification of human artery smooth muscle cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Te-Chuan Chen ◽  
Chia-Kung Yen ◽  
Ying-Chen Lu ◽  
Chung-Sheng Shi ◽  
Rong-Ze Hsieh ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Muscle Cells ◽  
Underlying Mechanism ◽  
Cardiovascular Complications ◽  
High Concentration ◽  
Human Artery ◽  
Caspase 1 ◽  
Potential Therapeutic Role

Abstract Background Vascular calcification is the major reason for high mortality of cardiovascular complications for diabetes. Interleukin (IL)-1β has been implicated in this pathogenesis, but its precise role and clinical evidence have not been clearly identified. Hence, this study was aimed to investigate whether high concentration of glucose (HG), which mimics the hyperglycemia environment, could initiate vascular calcification through NLRP3/IL-1β inflammasome and the underlying mechanism. Recently, 6-shogaol, a major ginger derivate, has been elucidated its pharmaceutic role for various diseases. Therefore, the aims of this study also determined 6-shogaol effect in vascular calcification of HG initiation. Result Human artery smooth muscle cells (HASMCs) were used in this study. Glucose concentrations at 5 and 25 mM were defined as normal and HG status, respectively. The results showed that HG could increase the NLRP3, cleaved caspase 1, and pro/mature IL-1β levels to induce the expressions of bone-related matrix proteins and subsequent HASMC calcification. This process was regulated by Akt activation and reactive oxygen species (ROS) production. Moreover, 6-shogaol could inhibit the Akt/ROS signaling and NLRP3/caspase 1/IL-1β inflammasome and hence attenuated HASMC calcification. Conclusions This study elucidates the detailed mechanism of HG-initiated HASMC calcification through NLRP3/caspase 1/IL-1β inflammasome and indicates a potential therapeutic role of 6-shogaol in vascular calcification complication of diabetes.

Altered L-type Ca2+ channel currents in vascular smooth muscle cells from experimental diabetic rats

2000 ◽  
Vol 278 (3) ◽  
pp. H714-H722 ◽  
Author(s):  
Rui Wang ◽  
Yuejin Wu ◽  
Guanghua Tang ◽  
Lingyun Wu ◽  
Salma Toma Hanna
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Complications ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Diabetic Rats ◽  
High Concentration ◽  
Voltage Dependent

Vascular complications of diabetes are associated with abnormal Ca2+ handling by vascular smooth muscle cells (SMCs) in which the alteration in L-type voltage-dependent Ca2+ channel (VDCC) currents may play an important role. In the present study, the characteristics of L-type VDCC currents in tail artery SMCs from streptozotocin-induced diabetic rats were examined. The densities, but not the voltage dependence, of L-type VDCC currents were reduced as diabetes progressed from 1 wk to 3 mo. The inhibitory effect of dibutyryl-cAMP on L-type VDCC currents was greater in diabetic SMCs than in age-matched control cells ( P < 0.01). Both the stimulatory effect of BAY K 8644 and the inhibitory effect of nifedipine on L-type VDCC currents were significantly enhanced in diabetic cells. The diabetes-related abnormalities in L-type VDCC currents were mimicked by culturing SMCs with a high concentration of glucose. Our results suggest that the properties of L-type VDCC in diabetic vascular SMCs were significantly altered, partially related to the increased L-type VDCC sensitivity to cAMP and hyperglycemia.

Penetration-induced hyperpolarization as evidence for Ca2+ activation of K+ conductance in isolated smooth muscle cells

1980 ◽  
Vol 239 (5) ◽  
pp. C182-C189 ◽  
Author(s):  
J. V. Walsh ◽  
J. J. Singer
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Smooth Muscle Cells ◽  
State Level ◽  
Input Resistance ◽  
Muscle Cells ◽  
Enzymatic Digestion ◽  
Resting Potential ◽  
High Concentration ◽  
State Potential

Single smooth muscle cells, freshly isolated by enzymatic digestion of the stomach muscularis of the toad Bufo marinus were studied under direct microscopic observation using standard electrophysiological techniques. Following penetration with a microelectrode, a hyperpolarization lasting many seconds occurred before the membrane depolarized to a steady-state level. The following lines of evidence indicate that the penetration-induced hyperpolarization results from an increase in K+ conductance caused by Ca2+ that enters the cell at the time of penetration: 1) The cell contracted at the time of penetration indicating that [Ca2+]i was elevated even though no action potential had occurred; the cell subsequently relaxed. 2) The input resistance was much lower during the hyperpolarization than during the steady-state resting potential. In the steady state all cells displayed outward-going rectification. 3) At constant [Ca2+]0, the amplitude of the hyperpolarization varied with log[K+]0 (1.3-56 mM) to a much greater degree than did the steady-state potential. Tetraethylammonium chloride (TEA) (18.2 mM) reduced the hyperpolarization. 4) At constant [K+]0, the amplitude of the hyperpolarization increased as the [Ca2+]0 was raised (1.8-52.1 mM). 5) With [Ca2+]0 low (less than or equal to 0.16 mM), the hyperpolarization was almost completely abolished in the presence of a high concentration of Ba2+ (80 mM) or Mn2+ (79.2 mM); this was not the case with Sr2+.

Sign in / Sign up

Export Citation Format

Share Document