scholarly journals Apelin-13 inhibits gastric motility through vagal cholinergic pathway in rats

2018 ◽  
Vol 314 (2) ◽  
pp. G201-G210 ◽  
Author(s):  
Mehmet Bülbül ◽  
Osman Sinen ◽  
Melahat Gök ◽  
R. Alberto Travagli
Keyword(s):  
Methyl Ester ◽  
Receptor Antagonist ◽  
Gastric Motility ◽  
Dorsal Vagal Complex ◽  
Central Administration ◽  
Sprague Dawley ◽  
Male Adult ◽  
Motor Functions ◽  
Gastric Tone ◽  
Cholinergic Pathway

The expression of apelin and its receptors (APJ) in central autonomic networks suggests that apelin may regulate gastrointestinal motor functions. In rodents, central administration of apelin-13 has been shown to inhibit gastric emptying; however, the mechanisms involved remain to be determined. Using male adult Sprague-Dawley rats, the aims of the present study were 1) to determine the expression of APJ receptor in the dorsal vagal complex (DVC), 2) to assess the effects of central application of apelin-13 into the DVC on gastric tone and motility, and 3) to investigate the neuronal pathways responsible for apelin-induced alterations. APJ receptor immunoreactivity was detected in gastric-projecting and choline acetyltransferase-positive neurons of the DVC. Microinjection of apelin-13 into the DVC significantly decreased gastric tone and motility in both corpus and antrum. The apelin-induced reduction in gastric tone and motility was prevented by surgical vagotomy or fourth ventricular application of the APJ receptor antagonist, [Ala13]apelin-13 (F13A). Systemic administration of the muscarinic receptor antagonist atropine, but not the nitric oxide synthase inhibitor nitro-l-arginine methyl ester (l-NAME), abolished the apelin-induced inhibitory responses. The present results indicate a central modulatory role of apelin in the vagal neurocircuitry that controls gastric motor functions via withdrawal of the tonically active cholinergic pathway. NEW & NOTEWORTHY This is the first study investigating the effects induced by brain stem application of apelin-13 while monitoring gastric tone and motility in rats. We have found that gastric-projecting neurons of the dorsal vagal complex express apelin receptors (APJ), which mediate the inhibitory actions of apelin-13. The inhibitory effects of apelin were abolished by systemic preadministration of atropine, but not nitro-l-arginine methyl ester (l-NAME). Apelin seems to modulate gastric motility via withdrawal of the tonically active vagal cholinergic pathway.

Anticonvulsant and procognitive properties of the non-imidazole histamine H3 receptor antagonist DL77 in male adult rats

2016 ◽  
Vol 106 ◽  
pp. 46-55 ◽  
Author(s):  
Bassem Sadek ◽  
Ali Saad ◽  
Dhanasekaran Subramanian ◽  
Mohamed Shafiullah ◽  
Dorota Łażewska ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Adult Rats ◽  
Male Adult ◽  
Histamine H3 Receptor ◽  
H3 Receptor ◽  
Histamine H3

scholarly journals Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1407 ◽  
Author(s):  
You-Lin Tain ◽  
Julie Chan ◽  
Chien-Te Lee ◽  
Chien-Ning Hsu
Keyword(s):  
Methylation Status ◽  
Normal Diet ◽  
Male Offspring ◽  
Adult Offspring ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Male Adult ◽  
Methyl Donor ◽  
Adult Rat

Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or a high methyl-donor diet (H-MD) during gestation and lactation. Male offspring were assigned to four groups (n = 7–8/group): control, L-MD, H-MD, and H-MD rats were given melatonin (100 mg/L) with their drinking water throughout the period of pregnancy and lactation (H-MD+M). At 12 weeks of age, male offspring exposed to a L-MD or a H-MD diet developed programmed hypertension. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. A maternal L-MD diet and H-MD diet caused respectively 938 and 806 renal transcripts to be modified in adult offspring. The protective effects of melatonin against programmed hypertension relate to reduced oxidative stress, increased urinary NO2− level, and reduced renal expression of sodium transporters. A H-MD or L-MD diet may upset the balance of methylation status, leading to alterations of renal transcriptome and programmed hypertension. A better understanding of reprogramming effects of melatonin might aid in developing a therapeutic strategy for the prevention of hypertension in adult offspring exposed to an excessive maternal methyl-supplemented diet.

Serotonin2 receptors mediate respiratory recovery after cervical spinal cord hemisection in adult rats

2001 ◽  
Vol 91 (6) ◽  
pp. 2665-2673 ◽  
Author(s):  
Shi-Yi Zhou ◽  
Gregory J. Basura ◽  
Harry G. Goshgarian
Keyword(s):  
Spinal Cord ◽  
Receptor Antagonist ◽  
Phrenic Nerve ◽  
Cervical Spinal Cord ◽  
Sprague Dawley ◽  
Related Activity ◽  
Adult Rats ◽  
Cord Injury ◽  
Respiratory Recovery ◽  
Spinal Cord Hemisection

The aim of the present study was to specifically investigate the involvement of serotonin [5-hydroxytryptamine (5-HT2)] receptors in 5-HT-mediated respiratory recovery after cervical hemisection. Experiments were conducted on C2 spinal cord-hemisected, anesthetized (chloral hydrate, 400 mg/kg ip), vagotomized, pancuronium- paralyzed, and artificially ventilated female Sprague-Dawley rats in which CO2 levels were monitored and maintained. Twenty-four hours after spinal hemisection, the ipsilateral phrenic nerve displayed no respiratory-related activity indicative of a functionally complete hemisection. Intravenous administration of the 5-HT2A/2C-receptor agonist (±)-2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI) induced respiratory-related activity in the phrenic nerve ipsilateral to hemisection under conditions in which CO2 was maintained at constant levels and augmented the activity induced under conditions of hypercapnia. The effects of DOI were found to be dose dependent, and the recovery of activity could be maintained for up to 2 h after a single injection. DOI-induced recovery was attenuated by the 5-HT2-receptor antagonist ketanserin but not with the 5-HT2C-receptor antagonist RS-102221, suggesting that 5-HT2A and not necessarily 5-HT2C receptors may be involved in the induction of respiratory recovery after cervical spinal cord injury.

KELULUT HONEY SUPPLEMENTATION PREVENTS SPERM AND TESTICULAR OXIDATIVE DAMAGE IN STREPTOZOTOCIN-INDUCED DIABETIC RATS

2017 ◽  
Vol 79 (3) ◽  
Author(s):  
Siti Balkis Budin ◽  
Fatin Farhana Jubaidi ◽  
Siti Nur Farahana Mohd Noor Azam ◽  
Nur Liyana Mohamed Yusof ◽  
Izatus Shima Taib ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Sperm Quality ◽  
Diabetic Control ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
Control Groups ◽  
Sod Activity ◽  
Male Adult ◽  
Pathological Conditions ◽  
Sprague Dawley Rats

Previous studies found that Kelulut Honey produced by Trigona spp. bees is able to prevent oxidative damage in various pathological conditions.  Thus, the present study aimed to determine whether Kelulut Honey could prevent the sperm and testicular damage in streptozotocin-induced diabetic rats. Male Adult male Sprague-Dawley rats were divided into four groups: Non-Diabetic (NDM), Non-Diabetic with Kelulut Honey supplementation (NDMKH), Diabetic without supplementation (DM) and Diabetic with Kelulut Honey supplementation (DMKH).  Kelulut honey was given at the dose of 2.0 g/kg weight daily via gavage for 28 consecutive days. Results showed that sperm quality produced by diabetic rats supplemented with Kelulut honey significantly improved compared to the diabetic control groups (p<0.05). SOD activity and GSH level increased significantly (p<0.05) whereas PC and MDA levels significantly decreased in sperm and testis of DMKH rats when compared to DM rats (p<0.05). Histological observation showed obvious increase in spermatozoa in the lumen of epididymis and increased spermatogenic cells density in the testis of DMKH group.  In conclusion, Kelulut Honey has a potential in preventing the damage of sperm and testis in diabetic rats.

scholarly journals Hydro ethanol extract of Holarrhena floribunda stem bark exhibits anti-anaphylactic and anti-oedematogenic effects in murine models of acute inflammation

2020 ◽  
Author(s):  
Stephen Antwi ◽  
Daniel Oduro-Mensah ◽  
David Darko Obiri ◽  
Newman Osafo ◽  
Aaron Opoku Antwi ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Serotonin Receptor ◽  
Acute Inflammation ◽  
Late Phase ◽  
Ethanol Extract ◽  
Stem Bark ◽  
Bark Extract ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Anti Inflammatory

Abstract Background: Holarrhena floribunda stem bark has anecdotal use in Ghanaian folk medicine for management of inflammatory conditions. This study was conducted to investigate the in vivo anti-inflammatory activity of the bark extract using models of acute inflammation in male Sprague Dawley rats, C57BL/6 mice and 36 ICR mice. Methods: A 70 % hydro-ethanol extract of the stem bark (HFE) was evaluated at doses of 5–500 mg/kg bw. Local anaphylaxis was modelled by the pinnal cutaneous anaphylactic test. Systemic anaphylaxis or sepsis were modeled by compound 48/80 or lipopolysaccharide, respectively. Clonidine-induced catalepsy was used to investigate effect on histamine signaling. Anti-oedematogenic effect was assessed by induction with carrageenan. Effects on mediators of biphasic acute inflammation were studied using histamine and serotonin (early phase) or prostaglandin E2 (late phase).Results: HFE demonstrated anti-inflammatory and/or anti-oedematogenic activity comparable to standard doses of aspirin and diclofenac (inhibitors of cyclooxygenases-1 and -2), chlorpheniramine (histamine H1-receptor antagonist), dexamethasone (glucocorticoid receptor agonist), granisetron (serotonin receptor antagonist) and sodium cromoglycate (inhibitor of mast cell degranulation). All observed HFE bioactivities increased with dose.Conclusions: The data provide evidence that the extract of H. floribunda stem bark has anti-anaphylactic and anti-oedematogenic effects; by interfering with signalling or metabolism of histamine, serotonin and prostaglandin E2 which mediate progression of inflammation. The anti-inflammatory and antihistaminic activities of HFE may be relevant in the context of management of COVID-19.

Cholecystokinin satiety involves CCKA receptors perfused by the superior pancreaticoduodenal artery

1998 ◽  
Vol 274 (5) ◽  
pp. R1390-R1396 ◽  
Author(s):  
James E. Cox
Keyword(s):  
Receptor Antagonist ◽  
Food Deprivation ◽  
Jugular Vein ◽  
Sucrose Intake ◽  
Sprague Dawley ◽  
Pancreaticoduodenal Artery ◽  
Cholecystokinin Octapeptide ◽  
Sprague Dawley Rats ◽  
Within Subjects ◽  
Ccka Receptors

Three experiments compared the potency of the type A cholecystokinin (CCKA)-receptor antagonist devazepide for increasing intake of 30% sucrose when injected into the superior pancreaticoduodenal (SPD) artery (SPD group) or jugular vein (IV group). In experiment 1, 15 min of sucrose intake in adult, male Sprague-Dawley rats after 6 h of food deprivation was increased by devazepide (20 μg/kg) administered into the SPD artery whether given alone or in conjunction with cholecystokinin octapeptide (CCK-8, 2 μg/kg ip). Devazepide had no effect in the IV group. In experiment 2, injection of 8, 20, and 50 μg/kg of devazepide into the SPD artery increased sucrose intake of nondeprived rats. Only the highest dose was effective in the IV group. On subsequent tests, administration of 1 μg/kg of CCK-8 significantly suppressed intake only in the SPD group. In experiment 3, nondeprived rats with SPD artery and jugular vein catheters were tested in a within-subjects design. Devazepide (20 μg/kg) increased sucrose intake after injection into the SPD artery, but not into the jugular vein. In experiment 4, intraduodenal devazepide (8, 20, and 50 μg/kg) had no effect. These results indicate that CCKA receptors within the SPD arterial bed mediate the satiating action of CCK, consistent with local action of duodenal CCK.

BQ123, an ETA-receptor antagonist, attenuates hypoxic pulmonary hypertension in rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1327-H1331 ◽  
Author(s):  
S. T. Bonvallet ◽  
M. R. Zamora ◽  
K. Hasunuma ◽  
K. Sato ◽  
N. Hanasato ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Receptor Antagonist ◽  
Resistance Index ◽  
Sprague Dawley ◽  
Hypoxic Pulmonary Hypertension ◽  
Mean Pressure ◽  
Eta Receptor ◽  
Medial Wall Thickness ◽  
Eta Receptor Antagonist

To investigate the role of endothelin-1 (ET-1) in the pathogenesis of hypoxic pulmonary hypertension, we studied the effects of a recently described endothelin-receptor antagonist (ETA), BQ123, on the development of this process. Intraperitoneal osmotic pumps were placed into 8-wk-old Sprague-Dawley rats that received either saline or BQ123 (0.15 mg/h). The rats were maintained in room air normoxia or placed in a hypobaric chamber (380 Torr) for 2 wk to induce hypoxic pulmonary hypertension. There were no hemodynamic differences between normoxic rats treated with either saline or BQ123. However, treatment with BQ123 attenuated the hypoxia-induced increase in pulmonary arterial mean pressure and total pulmonary resistance index by 60 and 87% respectively. There was also a reduction in hypoxia-induced right ventricular hypertrophy in the BQ123 group. Histological studies performed using a barium-gelatin fixation technique in hypoxic BQ123-treated animals demonstrated a decrease in medial wall thickness in arteries corresponding to the respiratory and terminal bronchioles, respectively. Similarly, there was a significant reduction in the degree of muscularization of more distal vessels at the level of alveolar ducts in BQ123-treated hypoxic rats. We conclude that the ETA-receptor antagonist BQ123 attenuates the development of hypoxic pulmonary hypertension in rats in vivo, thereby suggesting a possible contributing role for ET-1 and the ETA receptor in the pathogenesis of this process.

Nociceptin in rVLM mediates electroacupuncture inhibition of cardiovascular reflex excitatory response in rats

2005 ◽  
Vol 98 (6) ◽  
pp. 2056-2063 ◽  
Author(s):  
Melissa M. Crisostomo ◽  
Peng Li ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Pressor Response ◽  
Inhibitory Effect ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Nociceptin Receptor

Electroacupuncture (EA) at Neiguan-Jianshi acupoints through an opioid mechanism inhibits the cardiovascular pressor response induced by mechanical stimulation of the stomach. Because nociceptin also may regulate cardiovascular activity through its action in the brain stem, we hypothesized that this neuromodulator serves a role in the EA-related inhibitory effect. Blood pressure in ventilated male Sprague-Dawley rats (400–600 g) anesthetized by ketamine and α-chloralose was measured during balloon inflation of the stomach. Gastric distension with 6–8 ml of air induced consistent pressor reflexes of 26 ± 1 mmHg that could be repeated every 10 min for 100 min. When nociceptin (10 nM) was microinjected into the rostral ventrolateral medulla (rVLM), the pressor response induced by gastric distension was inhibited by 68 ± 6%. Thirty minutes of EA also decreased the reflex response by 75 ± 11%; microinjection of saline into the rVLM did not alter the inhibitory effect of EA. In contrast, microinjection of a nociceptin receptor antagonist into the rVLM promptly reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not influence the EA-like inhibitory effect of nociceptin on the distension-induced pressor reflex (22 ± 1 to 8 ± 2 mmHg). Furthermore, a μ-opioid receptor agonist microinjected into the rVLM after microinjection of a nociceptin receptor antagonist during EA promptly reversed the nociceptin receptor antagonist-related inhibition of the EA effect. Thus, in addition to the classical opioid system, nociceptin, through opioid receptor-like-1 receptor stimulation in the rVLM, participates in the modulatory influence of EA on reflex-induced increases in blood pressure.

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