Horseradish Peroxidase Permeability across Rat Nasal Mucosa in Selective Stimulation of Substance P Innervation with Capsaicin

1995 ◽  
Vol 104 (11) ◽  
pp. 895-898 ◽  
Author(s):  
Namju Kim ◽  
Soonkwan Hong ◽  
Seayuong Jeon ◽  
Euigee Hwang ◽  
Yang-Gi Min
Keyword(s):  
Electron Microscopy ◽  
Substance P ◽  
Horseradish Peroxidase ◽  
Enzyme Immunoassay ◽  
Nasal Mucosa ◽  
Time Course ◽  
Physiological Role ◽  
Selective Stimulation ◽  
Stimulation Of

To investigate the physiological role of substance P innervation (SPI) in the nasal mucosa from inhaled irritant macromolecules, SPI in the rat nasal mucosa was selectively stimulated with capsaicin and the degree of horseradish peroxidase (HRP) permeability across the nasal epithelium was evaluated by enzyme immunoassay or by histochemical electron microscopy. The serum level of HRP was reduced significantly in capsaicin-administered rats compared to control rats along the time course with quantitative analysis of the enzyme immunoassay. Control rats showed heavy permeation of HRP across the epithelium, but capsaicin-administered rats showed weak permeation of HRP across the epithelium with histochemical electron microscopy. The epithelial lining and its tight junctions were left intact as judged by electron microscopy. In conclusion, selective stimulation of SPI of the rat nasal mucosa with capsaicin decreased the epithelial absorption permeability to HRP without compromising the epithelial integrity. These findings imply that the physiological role of capsaicin-sensitive SPI in the rat mucosa is to protect the airway from inhaled irritant macromolecules.

Peripheral muscarinic control of norepinephrine release in the cardiovascular system

1980 ◽  
Vol 239 (6) ◽  
pp. H713-H720 ◽  
Author(s):  
E. Muscholl
Keyword(s):  
Physiological Role ◽  
Sympathetic Nerves ◽  
Adrenergic Nerve ◽  
Sequence Of Events ◽  
Adrenergic Response ◽  
Adrenergic Nerve Terminals ◽  
Muscarinic Cholinergic ◽  
Related Compounds ◽  
Stimulation Of

Activation of muscarinic cholinergic receptors located at the terminal adrenergic nerve fiber inhibits the process of exocytotic norepinephrine (NE) release. This neuromodulatory effect of acetylcholine and related compounds has been discovered as a pharmacological phenomenon. Subsequently, evidence for a physiological role of the presynaptic muscarinic inhibition was obtained on organs known to be innervated by the autonomic ground plexus (Hillarp, Acta. Physiol. Scand. 46, Suppl. 157: 1-68, 1959) in which terminal adrenergic and cholinergic axons run side by side. Thus, in the heart electrical vagal stimulation inhibits the release of NE evoked by stimulation of sympathetic nerves, and this is reflected by a corresponding decrease in the postsynaptic adrenergic response. On the other hand, muscarinic antagonists such as atropine enhance the NE release evoked by field stimulation of tissues innervated by the autonomic ground plexus. The presynaptic muscarine receptor of adrenergic nerve terminals probably restricts the influx of calcium ions that triggers the release of NE. However, the sequence of events between recognition of the muscarinic compound by the receptor and the process of exocytosis still remains to be clarified.

scholarly journals cAMP induces a rapid and reversible modification of the chemotactic receptor in Dictyostelium discoideum.

1985 ◽  
Vol 100 (3) ◽  
pp. 715-720 ◽  
Author(s):  
C Klein ◽  
J Lubs-Haukeness ◽  
S Simons
Keyword(s):  
Dictyostelium Discoideum ◽  
Concentration Dependence ◽  
Time Course ◽  
Camp Synthesis ◽  
Sds Page ◽  
Reversible Modification ◽  
Camp Receptor ◽  
Camp Stimulation ◽  
Stimulation Of

Stimulation, within 1 min after cAMP stimulation, of aggregation-competent Dictyostelium discoideum amebae was found to cause a rapid (within 1 min) modification of the cell's surface cAMP receptor. The modified receptor migrated on SDS PAGE as a 47,000-mol-wt protein, as opposed to a 45,000-mol-wt protein labeled on unstimulated cells. The length of time this modified receptor could be detected depended upon the strength of the cAMP stimulus: 3-4 min after treatment with 10(-7) M cAMP, cells no longer possessed the 47,000-mol-wt form of the cAMP receptor. Instead, the 45,000-mol-wt form was present. Stimulation of cells with 10(-5) M cAMP, however, resulted in the persistent (over 15 min) expression of the modified receptor. The time course, concentration dependence, and specificity of stimulus for this cAMP-induced shift in the cAMP receptor were found to parallel the cAMP-stimulated phosphorylation of a 47,000-mol-wt protein. In addition, both phenomena were shown to occur in the absence of endogenous cAMP synthesis. The possibility that the cAMP receptor is phosphorylated in response to cAMP stimulation, and the role of this event in cell desensitization, are discussed.

scholarly journals Two Quenchers Formed During Photodamage of Phostosystem II and The Role of One Quencher in Preemptive Photoprotection

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Alonso Zavafer ◽  
Ievgeniia Iermak ◽  
Mun Hon Cheah ◽  
Wah Soon Chow
Keyword(s):  
Chlorophyll Fluorescence ◽  
Photosystem Ii ◽  
Time Course ◽  
Physiological Role ◽  
Reaction Centre ◽  
Time Resolved ◽  
Fluorescence Quencher

AbstractThe quenching of chlorophyll fluorescence caused by photodamage of Photosystem II (qI) is a well recognized phenomenon, where the nature and physiological role of which are still debatable. Paradoxically, photodamage to the reaction centre of Photosystem II is supposed to be alleviated by excitation quenching mechanisms which manifest as fluorescence quenchers. Here we investigated the time course of PSII photodamage in vivo and in vitro and that of picosecond time-resolved chlorophyll fluorescence (quencher formation). Two long-lived fluorescence quenching processes during photodamage were observed and were formed at different speeds. The slow-developing quenching process exhibited a time course similar to that of the accumulation of photodamaged PSII, while the fast-developing process took place faster than the light-induced PSII damage. We attribute the slow process to the accumulation of photodamaged PSII and the fast process to an independent quenching mechanism that precedes PSII photodamage and that alleviates the inactivation of the PSII reaction centre.

scholarly journals Dominant regulation of interendothelial cell gap formation by calcium-inhibited type 6 adenylyl cyclase

2002 ◽  
Vol 157 (7) ◽  
pp. 1267-1278 ◽  
Author(s):  
Donna L. Cioffi ◽  
Timothy M. Moore ◽  
Jerry Schaack ◽  
Judy R. Creighton ◽  
Dermot M.F. Cooper ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Physiological Role ◽  
Cell Types ◽  
Cytosolic Calcium ◽  
Calcium Entry ◽  
Gap Formation ◽  
Calcium Stimulation ◽  
Store Operated Calcium Entry ◽  
Stimulation Of

Acute transitions in cytosolic calcium ([Ca2+]i) through store-operated calcium entry channels catalyze interendothelial cell gap formation that increases permeability. However, the rise in [Ca2+]i only disrupts barrier function in the absence of a rise in cAMP. Discovery that type 6 adenylyl cyclase (AC6; EC 4.6.6.1) is inhibited by calcium entry through store-operated calcium entry pathways provided a plausible explanation for how inflammatory [Ca2+]i mediators may decrease cAMP necessary for endothelial cell gap formation. [Ca2+]i mediators only modestly decrease global cAMP concentrations and thus, to date, the physiological role of AC6 is unresolved. Present studies used an adenoviral construct that expresses the calcium-stimulated AC8 to convert normal calcium inhibition into stimulation of cAMP, within physiologically relevant concentration ranges. Thrombin stimulated a dose-dependent [Ca2+]i rise in both pulmonary artery (PAECs) and microvascular (PMVEC) endothelial cells, and promoted intercellular gap formation in both cell types. In PAECs, gap formation was progressive over 2 h, whereas in PMVECs, gap formation was rapid (within 10 min) and gaps resealed within 2 h. Expression of AC8 resulted in a modest calcium stimulation of cAMP, which virtually abolished thrombin-induced gap formation in PMVECs. Findings provide the first direct evidence that calcium inhibition of AC6 is essential for endothelial gap formation.

Opposing effects of PKCα and PKCε on basolateral membrane dynamics in intestinal epithelia

2002 ◽  
Vol 283 (5) ◽  
pp. C1548-C1556 ◽  
Author(s):  
Jaekyung Cecilia Song ◽  
Patangi K. Rangachari ◽  
Jeffrey B. Matthews
Keyword(s):  
Time Course ◽  
Basolateral Membrane ◽  
Membrane Dynamics ◽  
T84 Cells ◽  
Intestinal Epithelia ◽  
Early Activation ◽  
Pkc Isoforms ◽  
Opposing Effects ◽  
Stimulation Of

PKC is a critical effector of plasma membrane dynamics, yet the mechanism and isoform-specific role of PKC are poorly understood. We recently showed that the phorbol ester PMA (100 nM) induces prompt activation of the novel isoform PKCε followed by late activation of the conventional isoform PKCα in T84 intestinal epithelia. PMA also elicited biphasic effects on endocytosis, characterized by an initial stimulatory phase followed by an inhibitory phase. Activation of PKCε was shown to be responsible for stimulation of basolateral endocytosis, but the role of PKCα was not defined. Here, we used detailed time-course analysis as well as selective activators and inhibitors of PKC isoforms to infer the action of PKCα on basolateral endocytosis. Inhibition of PKCα by the selective conventional PKC inhibitor Gö-6976 (5 μM) completely blocked the late inhibitory phase and markedly prolonged the stimulatory phase of endocytosis measured by FITC-dextran uptake. The PKCε-selective agonist carbachol (100 μM) induced prolonged stimulation of endocytosis devoid of an inhibitory phase. Actin disassembly caused by PMA was completely blocked by Gö-6850 but not by Gö-6976, implicating PKCε as the key isoform responsible for actin disruption. The Ca2+ agonist thapsigargin (5 μM) induced early activation of PKCα when added simultaneously with PMA. This early activation of PKCα blocked the ability of PMA to remodel basolateral F-actin and abolished the stimulatory phase of basolateral endocytosis. Activation of PKCα stabilizes F-actin and thereby opposes the effect of PKCε on membrane remodeling in T84 cells.

scholarly journals Regulation of nitric oxide synthase isoforms and role of nitric oxide during prostaglandin F2alpha-induced luteolysis in rabbits

Reproduction ◽  
2003 ◽  
pp. 807-816 ◽  
Author(s):  
C Boiti ◽  
G Guelfi ◽  
D Zampini ◽  
G Brecchia ◽  
A Gobbetti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Time Course ◽  
Plasma Concentrations ◽  
Physiological Role ◽  
Total Activity ◽  
Corpora Lutea ◽  
Prostaglandin F ◽  
Oxide Synthase

Total activity of nitric oxide synthase (NOS) and the gene expression of both endothelial NOS (eNOS) and inducible NOS (iNOS) isoforms in corpora lutea of pseudopregnant rabbits were examined during prostaglandin F(2alpha) (PGF(2alpha))-induced luteolysis. Corpora lutea were collected at 0, 6, 12, 24 and 48 h after an injection of PGF(2alpha) at day 9 of pseudopregnancy. At 12 h after PGF(2alpha) administration, luteal mRNA encoding eNOS decreased (P0.05) by 40% and remained low throughout the subsequent 36 h, whereas eNOS protein increased (P0.05) two- to threefold. By contrast, expression of mRNA encoding iNOS was poor and remained fairly constant, but transcription increased eightfold (P0.01) within 6 h after PGF(2alpha) treatment and then decreased to values similar to those of controls. Total NOS activity increased twofold (P0.01) at 6 h after treatment and remained high thereafter, whereas progesterone concentrations in explanted corpora lutea decreased (P0.01) from 302.4+/-42.3 pg x mg(-1) at day 9 to 58.6+/-8.3 at 48 h later, and peripheral plasma concentrations of progesterone declined too. Long-term administration of Nomega-nitro-L-arginine methyl ester (0.6 g l(-1) per os) from day 2 of pseudopregnancy onward partially blocked the luteolytic action of PGF(2alpha) administered at day 9 of pseudopregnancy. In nitric oxide (NO)-deficient rabbits, progesterone concentrations remained higher (P0.01) than in controls at 24-48 h after PGF(2alpha) administration (4.5 to 3.2 ng x ml(-1), respectively). These data are the first to characterize NOS activity. The time course of expression of eNOS and iNOS in rabbit corpora lutea during PGF(2alpha)-induced luteolysis gives additional support to a physiological role of NO in the regulation of regression of corpora lutea in rabbits.

Role of tympanic neurectomy in otalgia

1990 ◽  
Vol 104 (2) ◽  
pp. 114-117 ◽  
Author(s):  
J. A. Cook ◽  
R. M. Irving
Keyword(s):  
Local Anaesthesia ◽  
Accurate Diagnosis ◽  
Diagnosis And Treatment ◽  
Glossopharyngeal Neuralgia ◽  
Specific Reference ◽  
Selective Stimulation ◽  
History Of ◽  
Stimulation Of

AbstractTympanic neurectomy was first described 44 years ago. Although its indications have subsequently increased, it has not become a popular procedure. This paper concentrates on its use in treating otalgia. The history of tympanic neurectomy, the anatomy of the tympanic plexus and the aetiology of otalgia with specific reference to the tympanic plexus are discussed and a case of bilateral otalgia due to glossopharyngeal neuralgia successfully treated by staged, bilateral tympanic neurectomy reported. It is suggested tympanotomy performed under local anaesthesia with selective stimulation of the intra-tympanic nerves may lead to accurate diagnosis and treatment of the various forms of neuralgic otalgia.

scholarly journals Overexpression of membrane metalloendopeptidase inhibits substance P stimulation of cholangiocarcinoma growth

2014 ◽  
Vol 306 (9) ◽  
pp. G759-G768 ◽  
Author(s):  
Fanyin Meng ◽  
Sharon DeMorrow ◽  
Julie Venter ◽  
Gabriel Frampton ◽  
Yuyan Han ◽  
...  
Keyword(s):  
Substance P ◽  
Functional Role ◽  
Xenograft Model ◽  
Subsequent Increase ◽  
Proliferation In Vitro ◽  
Proteolytic Product ◽  
Stimulation Of

Substance P (SP) promotes cholangiocyte growth during cholestasis by activating its receptor, NK1R. SP is a proteolytic product of tachykinin (Tac1) and is deactivated by membrane metalloendopeptidase (MME). This study aimed to evaluate the functional role of SP in the regulation of cholangiocarcinoma (CCA) growth. NK1R, Tac1, and MME expression and SP secretion were assessed in human CCA cells and nonmalignant cholangiocytes. The proliferative effects of SP (in the absence/presence of the NK1R inhibitor, L-733,060) and of L-733,060 were evaluated. In vivo, the effect of L-733,060 treatment or MME overexpression on tumor growth was evaluated by using a xenograft model of CCA in nu/nu nude mice. The expression of Tac1, MME, NK1R, PCNA, CK-19, and VEGF-A was analyzed in the resulting tumors. Human CCA cell lines had increased expression of Tac1 and NK1R, along with reduced levels of MME compared with nonmalignant cholangiocytes, resulting in a subsequent increase in SP secretion. SP treatment increased CCA cell proliferation in vitro, which was blocked by L-733,060. Treatment with L-733,060 alone inhibited CCA proliferation in vitro and in vivo. Xenograft tumors derived from MME-overexpressed human Mz-ChA-1 CCA cells had a slower growth rate than those derived from control cells. Expression of PCNA, CK-19, and VEGF-A decreased, whereas MME expression increased in the xenograft tumors treated with L-733,060 or MME-overexpressed xenograft tumors compared with controls. The study suggests that SP secreted by CCA promotes CCA growth via autocrine pathway. Blockade of SP secretion and NK1R signaling may be important for the management of CCA.

Potent stimulation of glycoprotein secretion in canine trachea by substance P

1984 ◽  
Vol 57 (5) ◽  
pp. 1323-1327 ◽  
Author(s):  
S. J. Coles ◽  
K. H. Neill ◽  
L. M. Reid
Keyword(s):  
Substance P ◽  
Time Course ◽  
Collecting Duct ◽  
Regulatory Peptides ◽  
Submucosal Gland ◽  
Airway Mucosa ◽  
Glycoprotein Secretion ◽  
Median Effective Concentration ◽  
Stimulation Of

The effects have been investigated of the regulatory peptides, substance P (SP) and bombesin, on the secretion of [14C]glucosamine-labeled trichloroacetic acid-phosphotungstic acid precipitable glycoproteins by canine tracheal explants. SP (10(10) to 10(-7) M) induced a dose-dependent increase in secretion of high-molecular-weight (greater than 2 X 10(6) radiolabeled glycoproteins predominantly from the submucosal glands. On a molar basis, SP [median effective concentration (EC50) = 8.2 X 10(-10) M] was about 1,000-fold more potent than methacholine (EC50 = 6.3 X 10(-7) M). Bombesin (10(-10) to 10(-4) M) had no effect on glycoprotein secretion. The time course of SP effect was characterized by an initial stimulation of glycoprotein secretion followed by a period of inhibition, suggesting that it rapidly exhausts a pool of glycoprotein, possibly that present within the duct lumen of the submucosal gland. Consistent with this are the findings that SP-induced secretion of glycoprotein was augmented by preincubation with methacholine while methacholine-induced secretion was diminished by preincubation with SP. Our findings show that SP is a potent stimulant of airway glycoprotein secretion in vitro and suggest that it acts by increasing the rate of clearance of mucus from the ducts of the submucosal gland, possibly by induced constriction of the secretory tubules and collecting duct. A role is discussed for SP in mucus hypersecretion induced by local axonal reflexes in the airway mucosa.

Cellular mechanisms mediating the stimulation of ovine endometrial secretion of prostaglandin F2α in response to oxytocin: role of phospholipase C and diacylglycerol

1994 ◽  
Vol 141 (3) ◽  
pp. 481-490 ◽  
Author(s):  
W J Silvia ◽  
J-S Lee ◽  
D S Trammell ◽  
S H Hayes ◽  
L L Lowberger ◽  
...  
Keyword(s):  
Time Course ◽  
Prostaglandin F2α ◽  
Endometrial Tissue ◽  
Indole Derivatives ◽  
Cellular Mechanisms ◽  
Response Curves ◽  
The Relationship ◽  
Stimulation Of

Abstract The first objective was to describe and evaluate the relationship between the ability of oxytocin to stimulate the activity of phospholipase (PL) C and its ability to stimulate the release of prostaglandin (PG) F2α in ovine endometrial tissue. Caruncular endometrial tissue was collected from ovariectomized ewes after completion of an 11-day steroid replacement protocol. In experiment 1, explants were incubated either in the presence (10−6 m) or absence of oxytocin for 0, 1, 3, 10, 30 or 100 min to examine the time-course for activation of PLC and release of PGF2α in response to oxytocin. An increase in the activity of PLC was detected at 3 min while an increase in the release of PGF2α was not detected until 10 min (P<0·05). In experiment 2, explants were incubated in the presence of various oxytocin analogues (10−6 m) to compare their abilities to activate PLC and release PGF2α. Oxytocin and three receptor angonists stimulated the activity of PLC and the release of PGF2α (P<0·05) while two oxytocin receptor antagonists had no effect on either response. In experiment 3, explants were incubated in the presence of oxytocin or arginine vasopressin at 10−9 to 10−6 m to establish dose–response curves for the activation of PLC and release of PGF2α. For both hormones, significant increases (P<0·05) in the release of PGF2α were observed at 10−8 m while increases in PLC activity were not detected until 10−7 m was used. In experiment 4, explants were pretreated with either U-73122 (an inhibitor of PLC activity) or U-73343 (an inactive analogue of U-73122). Explants were then treated with control medium, oxytocin or AlF4−. Both oxytocin and AlF4− stimulated the activity of PLC and the release of PGF2α (P<0·05). U-73122 blocked the ability of oxytocin to stimulate the release of PGF2α (P<0·05) but had no effect on its ability to stimulate the activity of PLC (P>0·1). Based on the results from these experiments, the role of PLC in mediating the stimulatory effect of oxytocin on the release of PGF2α remains unclear. The second objective was to evaluate the role of diacylglycerol (DAG) in mediating the stimulatory effect of oxytocin on endometrial secretion of PGF2α. In experiment 5, explants were incubated in vitro with varying doses of two DAG analogues. Both analogues stimulated the release of PGF2α at 10−6 m (P<0·05), the highest dose tested. Corresponding inactive control compounds had no stimulatory effect. In experiment 6, explants were incubated with two synthetic DAGs and two indole-derived analogues of DAG. The indole derivatives stimulated the release of PGF2α. The synthetic DAGs were less effective in stimulating the release of PGF2α at the doses tested. In experiment 7, explants were preincubated with R59022 or LiCl. R59022 enhanced both the basal and oxytocin-stimulated released of PGF2α (P=0·07). LiCl promoted an increase in the accumulation of inositol trisphosphate (P<0·05) but had no effect on the release of PGF2α (P>0·5). These data indicate that DAG stimulates release of PGF2α from ovine endometrial tissue and may mediate the stimulatory effect of oxytocin on release of PGF2α. Journal of Endocrinology (1994) 141, 481–490

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