Neuronal locus and cellular signaling for stimulation of ileal giant migrating and phasic contractions

2003 ◽  
Vol 284 (5) ◽  
pp. G789-G797 ◽  
Author(s):  
Sushil K. Sarna
Keyword(s):  
Ruthenium Red ◽  
Signaling Cascades ◽  
Receptor Subtype ◽  
Calcitonin Gene ◽  
Intracellular Ca ◽  
The Common ◽  
Higher Doses ◽  
Pkc Activation ◽  
Stimulation Of

We investigated the neuronal locus, the role of PKC activation, and utilization of extracellular Ca2+ and intracellular Ca2+ release in smooth muscle cells for the generation of giant migrating contractions (GMCs) and rhythmic phasic contractions (RPCs) in intact normal and inflamed canine ileum. Calcitonin gene-related peptide (CGRP), administered close intra-arterially, stimulated GMCs at higher doses and RPCs at smaller doses. These effects were blocked by prior close intra-arterial infusions of CGRP8–37, atropine, hexamethonium, and TTX but not by tachykinin, serotonin, and histaminergic receptor subtype antagonists. Both types of contractions were blocked by verapamil in normal and inflamed ileums. Dantrolene and ruthenium red blocked only the RPCs in normal ileum but blocked both GMCs and RPCs in the inflamed ileum. PKC inhibition by chelerythrine blocked GMCs only in inflamed ileum but blocked RPCs in both normal and inflamed ileums. The inhibition of phospholipase C by neomycin blocked both RPCs and GMCs in normal and inflamed ileums. In conclusion, acetylcholine is the common neurotransmitter for the stimulation of both GMCs and RPCs, but the signaling cascades for their stimulation are partially divergent, and they differ also in the normal and inflamed states.

scholarly journals Hormesis in Plants: The Role of Oxidative Stress, Auxins and Photosynthesis in Corn Treated with Cd or Pb

2020 ◽  
Vol 21 (6) ◽  
pp. 2099 ◽  
Author(s):  
Eugeniusz Małkowski ◽  
Krzysztof Sitko ◽  
Michał Szopiński ◽  
Żaneta Gieroń ◽  
Marta Pogrzeba ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Shoot Growth ◽  
Photosynthetic Apparatus ◽  
Growth Stimulation ◽  
Photosynthetic Parameters ◽  
Toxic Substances ◽  
Wide Range ◽  
The Common ◽  
Stimulation Of

Hormesis, which describes the stimulatory effect of low doses of toxic substances on growth, is a well-known phenomenon in the plant and animal kingdoms. However, the mechanisms that are involved in this phenomenon are still poorly understood. We performed preliminary studies on corn coleoptile sections, which showed a positive correlation between the stimulation of growth by Cd or Pb and an increase in the auxin and H2O2 content in the coleoptile sections. Subsequently, we grew corn seedlings in hydroponic culture and tested a wide range of Cd or Pb concentrations in order to determine hormetic growth stimulation. In these seedlings the gas exchange and the chlorophyll a fluorescence, as well as the content of chlorophyll, flavonol, auxin and hydrogen peroxide, were measured. We found that during the hormetic stimulation of growth, the response of the photosynthetic apparatus to Cd and Pb differed significantly. While the application of Cd mostly caused a decrease in various photosynthetic parameters, the application of Pb stimulated some of them. Nevertheless, we discovered that the common features of the hormetic stimulation of shoot growth by heavy metals are an increase in the auxin and flavonol content and the maintenance of hydrogen peroxide at the same level as the control plants.

Role of cyclic ADP-ribose in the regulation of [Ca2+]i in porcine tracheal smooth muscle

1998 ◽  
Vol 274 (6) ◽  
pp. C1653-C1660 ◽  
Author(s):  
Y. S. Prakash ◽  
Mathur S. Kannan ◽  
Timothy F. Walseth ◽  
Gary C. Sieck
Keyword(s):  
Smooth Muscle ◽  
Second Messenger ◽  
Ruthenium Red ◽  
Tracheal Smooth Muscle ◽  
Cyclic Adp Ribose ◽  
Intracellular Ca ◽  
Subsequent Exposure ◽  
Trisphosphate Receptor ◽  
Dose Dependent Increase

The purpose of the present study was to determine whether cyclic ADP-ribose (cADPR) acts as a second messenger for Ca2+ release through ryanodine receptor (RyR) channels in tracheal smooth muscle (TSM). Freshly dissociated porcine TSM cells were permeabilized with β-escin, and real-time confocal microscopy was used to examine changes in intracellular Ca2+ concentration ([Ca2+]i). cADPR (10 nM–10 μM) induced a dose-dependent increase in [Ca2+]i, which was blocked by the cADPR receptor antagonist 8-amino-cADPR (20 μM) and by the RyR blockers ruthenium red (10 μM) and ryanodine (10 μM), but not by the inositol 1,4,5-trisphosphate receptor blocker heparin (0.5 mg/ml). During steady-state [Ca2+]ioscillations induced by acetylcholine (ACh), addition of 100 nM and 1 μM cADPR increased oscillation frequency and decreased peak-to-trough amplitude. ACh-induced [Ca2+]ioscillations were blocked by 8-amino-cADPR; however, 8-amino-cADPR did not block the [Ca2+]iresponse to a subsequent exposure to caffeine. These results indicate that cADPR acts as a second messenger for Ca2+ release through RyR channels in TSM cells and may be necessary for initiating ACh-induced [Ca2+]ioscillations.

Central nystagmus. III. Functional correlations of mesodiencephalic nystagmogenic center

1959 ◽  
Vol 197 (2) ◽  
pp. 454-460 ◽  
Author(s):  
F. Bergmann ◽  
J. Lachmann ◽  
M. Monnier ◽  
P. Krupp
Keyword(s):  
Electrical Stimulation ◽  
Eye Movements ◽  
Vestibular Nuclei ◽  
Rabbit Brain ◽  
Vestibular Nystagmus ◽  
Posterior Commissure ◽  
Common Substrate ◽  
The Common ◽  
Stimulation Of

Transverse cuts at various levels of the rabbit brain stem have different effects on vestibular nystagmus and on central nystagmus elicited by electrical stimulation of the mesodiencephalic nystagmogenic area. While transections rostral to the sensitive region enhance both, probably by elimination of inhibitory influences from cortex or retina, transections caudal to this region, but rostral to the colliculi, abolish central nystagmus only. Transections at the level of the inferior colliculus abolish vestibular nystagmus only, while intermediate cuts may eliminate either response. When central nystagmus alone survives, its character is changed in a specific way indicating the important role of the vestibular nuclei in normal central nystagmus. These observations lead to an approximate localization of the common substrate for conjugate eye movements involved both in central and vestibular nystagmus. Longitudinal cuts through the posterior commissure provoke a temporary disconjugated nystagmus not described hitherto.

scholarly journals Role of calcium and calmodulin in ciliary stimulation induced by acetylcholine

2001 ◽  
Vol 280 (1) ◽  
pp. C100-C109 ◽  
Author(s):  
Orna Zagoory ◽  
Alex Braiman ◽  
Larisa Gheber ◽  
Zvi Priel
Keyword(s):  
Phospholipase C ◽  
Muscarinic Receptors ◽  
Elevated Level ◽  
Beat Frequency ◽  
Ciliary Beat Frequency ◽  
Combined Effect ◽  
Molecular Events ◽  
Intracellular Ca ◽  
Stimulation Of

The goal of this work was to elucidate the molecular events underlying stimulation of ciliary beat frequency (CBF) induced by acetylcholine (ACh) in frog esophagus epithelium. ACh induces a profound increase in CBF and in intracellular Ca2+ concentration ([Ca2+]i) through M1 and M3 muscarinic receptors. The [Ca2+]i slowly decays to the basal level, while CBF stabilizes at an elevated level. These results suggest that ACh triggers Ca2+-correlated and -uncorrelated modes of ciliary stimulation. ACh response is abolished by the phospholipase C (PLC) inhibitor U-73122 and by depletion of intracellular Ca2+ stores but is unaffected by reduction of extracellular Ca2+ concentration and by blockers of Ca2+influx. Therefore, ACh activates PLC and mobilizes Ca2+solely from intracellular stores. The calmodulin inhibitors W-7 and calmidazolium attenuate the ACh-induced increase in [Ca2+]i but completely abolish the elevation in CBF. Therefore, elevation of [Ca2+]i is necessary for CBF enhancement but does not lead directly to it. The combined effect of Ca2+ elevation and of additional factors, presumably mobilized by Ca2+-calmodulin, results in a robust CBF enhancement.

Nociceptive inhibition of migrating myoelectric complex by nitric oxide and monoaminergic pathways in the rat

1998 ◽  
Vol 274 (3) ◽  
pp. G480-G486
Author(s):  
Per M. Hellström ◽  
Mikael Thollander ◽  
Elvar Theodorsson
Keyword(s):  
Nitric Oxide ◽  
Cycle Length ◽  
Intraperitoneal Administration ◽  
Neurokinin A ◽  
Migrating Myoelectric Complex ◽  
Calcitonin Gene ◽  
Dopaminergic Mechanisms ◽  
Intraperitoneal Instillation ◽  
Stimulation Of

This study investigated the role of nitric oxide (NO) and adrenergic and dopaminergic mechanisms in reflex inhibition of the migrating myoelectric complex (MMC) after intraperitoneal administration of acid in rats. Acid instilled immediately after an activity front inhibited the migrating complex and prolonged the cycle length from 13.0 ± 0.7 to 98.5 ± 17.2 min ( P < 0.001). Administration of Nω-nitro-l-arginine, reserpine, or guanetidine before acid decreased the prolonged cycle length to 18.1 ± 2.8 ( P < 0.001), 19.0 ± 2.0 ( P < 0.001), and 27.5 ± 9.3 min ( P < 0.001), respectively. Similarly, haloperidol given before acid shortened the prolonged cycle length to 46.7 ± 5.2 min ( P < 0.05). There was no effect of phentolamine in combination with propranolol or hexamethonium given alone. After intraperitoneal instillation of acid there was an increase in the plasma levels of somatostatin and a decrease of calcitonin gene-related peptide, but there was no change of neuropeptide Y, vasoactive intestinal peptide, substance P, neurokinin A, or neurotensin. The results indicate that NO and adrenergic, dopaminergic, and somatostatinergic mechanisms cooperate in inhibiting the MMC after nociceptive stimulation of the peritoneum.

Mechanisms of endothelial P2Y1- and P2Y2-mediated vasodilatation involve differential [Ca2+]i responses

2001 ◽  
Vol 281 (4) ◽  
pp. H1759-H1766 ◽  
Author(s):  
Sean P. Marrelli
Keyword(s):  
Nitric Oxide ◽  
Simultaneous Measurement ◽  
Cerebral Arteries ◽  
No Synthase ◽  
Fura 2 ◽  
Middle Cerebral Arteries ◽  
Intracellular Ca ◽  
The Difference ◽  
Stimulation Of

The present study was designed to evaluate the role of endothelial intracellular Ca2+ concentration ([Ca2+]i) in the difference between P2Y1- and P2Y2-mediated vasodilatations in cerebral arteries. Rat middle cerebral arteries were cannulated, pressurized, and luminally perfused. The endothelium was selectively loaded with fura 2, a fluorescent Ca2+indicator, for simultaneous measurement of endothelial [Ca2+]i and diameter. Luminal administration of 2-methylthioadenosine 5′-triphosphate (2-MeS-ATP), an endothelial P2Y1 agonist, resulted in purely nitric oxide (NO)-dependent dilation and [Ca2+]i increases up to ∼300 nM (resting [Ca2+]i = 145 nM). UTP, an endothelial P2Y2 agonist, resulted in dilations that were both endothelium-derived hyperpolarizing factor (EDHF)- and NO-dependent with [Ca2+]iincreases to >400 nM. In the presence of N G-nitro-l-arginine-indomethacin to inhibit NO synthase and cyclooxygenase, UTP resulted in an EDHF-dependent dilation alone. The [Ca2+]ithreshold for NO-dependent dilation was 220 vs. 340 nM for EDHF. In summary, the differences in the mechanism of vasodilatation resulting from stimulation of endothelial P2Y1 and P2Y2purinoceptors result in part from differential [Ca2+]i responses. Consistent with this finding, these studies also demonstrate a higher [Ca2+]i threshold for EDHF-dependent responses compared with NO.

scholarly journals Stimulation of astrocyte Na+/H+ exchange activity in response to in vitro ischemia depends in part on activation of ERK1/2

2005 ◽  
Vol 289 (4) ◽  
pp. C934-C945 ◽  
Author(s):  
Douglas B. Kintner ◽  
Andy Look ◽  
Gary E. Shull ◽  
Dandan Sun
Keyword(s):  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
In Vitro Ischemia ◽  
Reverse Mode ◽  
Intracellular Ca ◽  
Nhe1 Activity ◽  
Underlying Mechanisms ◽  
Stimulation Of

We recently reported that Na+/H+ exchanger isoform 1 (NHE1) activity in astrocytes is stimulated and leads to intracellular Na+ loading after oxygen and glucose deprivation (OGD). However, the underlying mechanisms for this stimulation of NHE1 activity and its impact on astrocyte function are unknown. In the present study, we investigated the role of the ERK1/2 pathway in NHE1 activation. NHE1 activity was elevated by ∼75% in NHE1+/+ astrocytes after 2-h OGD and 1-h reoxygenation (REOX). The OGD/REOX-mediated stimulation of NHE1 was partially blocked by 30 μM PD-98059. Increased expression of phosphorylated ERK1/2 was detected in NHE1+/+ astrocytes after OGD/REOX. Moreover, stimulation of NHE1 activity disrupted not only Na+ but also Ca2+ homeostasis via reverse-mode operation of Na+/Ca2+ exchange. OGD/REOX led to a 103% increase in intracellular Ca2+ concentration ([Ca2+]i) in NHE1+/+ astrocytes in the presence of thapsigargin. Inhibition of NHE1 activity with the NHE1 inhibitor HOE-642 decreased OGD/REOX-induced elevation of [Ca2+]i by 73%. To further investigate changes of Ca2+ signaling, bradykinin-mediated Ca2+ release was evaluated. Bradykinin-mediated intracellular Ca2+ transient in NHE1+/+ astrocytes was increased by ∼84% after OGD/REOX. However, in NHE1−/− astrocytes or NHE1+/+ astrocytes treated with HOE-642, the bradykinin-induced Ca2+ release was increased by only ∼34%. Inhibition of the reverse mode of Na+/Ca2+ exchange abolished OGD/REOX-mediated Ca2+ rise. Together, our data suggest that ERK1/2 is involved in activation of NHE1 in astrocytes after in vitro ischemia. NHE1-mediated Na+ accumulation subsequently alters Ca2+ homeostasis via Na+/Ca2+ exchange.

Signaling mechanisms of elevated neutrophil O 2 − generation after burn injury

1998 ◽  
Vol 274 (2) ◽  
pp. R476-R485 ◽  
Author(s):  
Farideh Sabeh ◽  
Philip Hockberger ◽  
Mohammed M. Sayeed
Keyword(s):  
Burn Injury ◽  
Total Body Surface Area ◽  
Skin Thickness ◽  
Text Generation ◽  
Intracellular Ca ◽  
Effect Of Treatment ◽  
Peak Release ◽  
Total Body ◽  
Pkc Activation

A full skin thickness burn injury was produced in anesthetized rats by exposing 25% of total body surface area to 98°C water for 10 s. Sham (exposed to 37°C water) and burn rats were killed 1, 3, 7, or 10 days later. The role of Ca2+signaling and Ca2+-related protein kinase C (PKC) activation in neutrophil[Formula: see text] generation was ascertained by evaluating the effect of treatment of the rats with the Ca2+entry blocker, diltiazem. There was an overt enhancement of[Formula: see text] generation by polymorphonuclear leukocytes from burn rats on days 1, 3, and 7 postburn, with the peak release occurring on day 3 postburn.[Formula: see text] generation comparable to the sham was noted on day 10 after the burn.[Formula: see text] releases on days 1, 3, and 7 postburn were accompanied by marked elevation of [Formula: see text] and PKC responses. Like the [Formula: see text] release, intracellular Ca2+concentration ([Ca2+]i) response on day 10 after burn was suppressed to levels found in the sham group. The treatment of burn rats with diltiazem prevented the upregulation of both [Ca2+]iand PKC responses as well as [Formula: see text]generation in neutrophils in rats on days 1, 3, and 7 after the burn. Because previous studies have shown that increases in [Ca2+]iprecede [Formula: see text] generation and degranulation, our results suggest that neutrophil[Formula: see text] release enhancement in the early stages after burn injury (e.g., days 1- 7postburn) results from an overactivation of the[Formula: see text] and PKC signaling pathways. The heightened [Formula: see text] generation during the early burn injury phase might play a role in tissue damage in one or more of host organs.

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