Activation of 5-HT1A receptors attenuates tachycardia induced by restraint stress in rats

2008 ◽  
Vol 294 (1) ◽  
pp. R132-R141 ◽  
Author(s):  
Sukonthar Ngampramuan ◽  
Mathias Baumert ◽  
Mirza Irfan Beig ◽  
Naiphinich Kotchabhakdi ◽  
Eugene Nalivaiko
Keyword(s):  
Sympathetic Activity ◽  
Restraint Stress ◽  
Transient Increase ◽  
Dependent Manner ◽  
Initial Transient ◽  
Way 100635 ◽  
Medullary Raphe ◽  
Dose Dependent ◽  
Sustained Increase ◽  
Vagal Withdrawal

To better understand the central mechanisms that mediate increases in heart rate (HR) during psychological stress, we examined the effects of systemic and intramedullary (raphe region) administration of the serotonin-1A (5-HT1A) receptor agonist 8-hydroxy-2-(di- n-propylamino)tetraline (8-OH-DPAT) on cardiac changes elicited by restraint in hooded Wistar rats with preimplanted ECG telemetric transmitters. 8-OH-DPAT reduced basal HR from 356 ± 12 to 284 ± 12 beats/min, predominantly via a nonadrenergic, noncholinergic mechanism. Restraint stress caused tachycardia (an initial transient increase from 318 ± 3 to 492 ± 21 beats/min with a sustained component of 379 ± 12 beats/min). β-Adrenoreceptor blockade with atenolol suppressed the sustained component, whereas muscarinic blockade with methylscopolamine (50 μg/kg) abolished the initial transient increase, indicating that sympathetic activation and vagal withdrawal were responsible for the tachycardia. Systemic administration of 8-OH-DPAT (10, 30, and 100 μg/kg) attenuated stress-induced tachycardia in a dose-dependent manner, and this effect was suppressed by the 5-HT1A antagonist WAY-100635 (100 μg/kg). Given alone, the antagonist had no effect. Systemically injected 8-OH-DPAT (100 μg/kg) attenuated the sympathetically mediated sustained component (from +85 ± 19 to +32 ± 9 beats/min) and the vagally mediated transient (from +62 ± 5 to +25 ± 3 beats/min). Activation of 5-HT1A receptors in the medullary raphe by microinjection of 8-OH-DPAT mimicked the antitachycardic effect of the systemically administered drug but did not affect basal HR. We conclude that tachycardia induced by restraint stress is due to a sustained increase in cardiac sympathetic activity associated with a transient vagal withdrawal. Activation of central 5-HT1A receptors attenuates this tachycardia by suppressing autonomic effects. At least some of the relevant receptors are located in the medullary raphe-parapyramidal area.

Powerful depressor and sympathoinhibitory effects evoked from neurons in the caudal raphe pallidus and obscurus

1995 ◽  
Vol 268 (5) ◽  
pp. R1295-R1302 ◽  
Author(s):  
M. J. Coleman ◽  
R. A. Dampney
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Raphe Nuclei ◽  
Ventrolateral Medulla ◽  
Gamma Aminobutyric Acid ◽  
Medullary Raphe ◽  
Dose Dependent Decrease ◽  
Raphé Nuclei ◽  
Raphe Pallidus ◽  
Dose Dependent

Microinjection of glutamate into sites within the medullary raphe nuclei (pallidus and obscurus) at levels caudal to the obex resulted in a dose-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate in anesthetized rabbits. The depressor and sympathoinhibitory responses were similar in magnitude to those elicited from the previously described depressor region in the caudal ventrolateral medulla (CVLM) but had a shorter duration, in both intact and barodenervated animals. The bradycardia was not altered by barodenervation but was reduced after administration of propranolol or atropine and abolished after administration of both drugs. The neuroinhibitory compounds gamma-aminobutyric acid or muscimol had no effect on MAP or RSNA when injected into the caudal medullary raphe nuclei but evoked a pressor and sympathoexcitatory response when injected into the CVLM. The results indicate that neurons within the caudal raphe pallidus and obscurus can powerfully inhibit sympathetic activity, but unlike sympathoinhibitory neurons in the CVLM, they are not tonically active and are not capable of producing sustained changes in arterial pressure and sympathetic activity.

Involvement of the 5-HT3 receptor in CRH-induced defecation in rats

1998 ◽  
Vol 274 (5) ◽  
pp. G827-G831 ◽  
Author(s):  
Keiji Miyata ◽  
Hiroyuki Ito ◽  
Shin Fukudo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Restraint Stress ◽  
Dependent Manner ◽  
Corticotropin Releasing Hormone ◽  
Receptor Antagonists ◽  
Releasing Hormone ◽  
The Central Nervous System ◽  
Dose Dependent

We evaluated the possibility that serotonin (5-HT) mediates defecation induced by corticotropin-releasing hormone (CRH) exogenously administered or released from the central nervous system by stress via the 5-HT3 receptor in rats. Intracerebroventricular (ICV) injection of CRH (1, 3, and 10 μg/rat) dose dependently increased the number of stools excreted in rats, whereas intravenous (IV) injection of up to 100 μg/kg CRH did not affect defecation. α-Helical CRH-(9—41) and 5-HT3 receptor antagonists ramosetron and azasetron inhibited CRH (10 μg icv)-induced defecation in a dose-dependent manner with ED50 values of 4.3 μg/kg iv, 3.8 μg/kg po, and 70.4 μg/kg po, respectively. α-Helical CRH-(9—41) also inhibited CRH-induced defecation by ICV injection with an ED50 value of 0.078 μg/rat. In contrast, ramosetron and azasetron injectied ICV had no effect on CRH-induced defecation. α-Helical CRH-(9—41), ramosetron, and azasetron reduced defecation caused by restraint stress with ED50 values of 0.32, 3.6, and 19.7 μg/kg iv, respectively. These results indicate that CRH exogenously administered or released from the central nervous system by stress peripherally promotes the release of 5-HT, which in turn stimulates defecation through the 5-HT3 receptor.

scholarly journals EVALUATION OF ANTIDEPRESSANT ACTIVITY OF ETHANOLIC EXTRACT OF LAGERSTROEMIA SPECIOSA LEAVES IN ALBINO WISTAR RATS

2019 ◽  
pp. 68-74
Author(s):  
VANITA KANASE ◽  
SUNITA VISHWAKARMA
Keyword(s):  
Oxidative Stress ◽  
Normal Saline ◽  
Restraint Stress ◽  
Wistar Rats ◽  
Ethanolic Extract ◽  
Antidepressant Activity ◽  
Control Group ◽  
Dependent Manner ◽  
Lagerstroemia Speciosa ◽  
Dose Dependent

Objective: The objective of the study was to evaluate the antidepressant activity of ethanolic extract of dried leaves of Lagerstroemia speciosa L. (EELS) on acute restraint stress (ARS)-induced depression-like behavior and biochemical alterations in albino Wistar rats. Methods: Thirty rats were randomly divided into five experimental groups. Group-I (normal control) rats received normal saline (2.0 ml/kg, p.o.) daily for 14 days; Group-II (stress control) rats received normal saline (2.0 ml/kg, p.o.) daily for 14 days and subjected to restraint stress on the 13th day. Group-III (standard drug-treated) rats received imipramine (15 mg/kg, p.o.) daily for 14 days and subjected to restraint stress on the 13th day. Groups-IV and V rats were treated with EELS (100 mg/kg and 300 mg/kg, p.o.) daily for 14 days subjected to ARS on the 13th day. Stress-like behavior was assessed by subjecting the rats to behavioral paradigms such as tail-suspension test (TST) and open field test (OFT), 40 min post-restraint stress procedure. Pretest of 10 min for forced swim test (FST) was also given to each rat simultaneously. Then, 23.5 h later, the relevant samples were administered and the main test performed 30 min later. Oxidative stress parameters such as superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and extent of lipid peroxidation (LPO) were analyzed in restraint stress-induced animals and control group, following FST on the 15th day. Statistical Analysis: Expression of data was done as a mean standard error of the mean. The normally distributed data were subjected to one-way analysis of variance followed by Dunnett’s test. *p<0.05 was considered statistically significant. Results: It was observed that L. speciosa L. showed a significant dose-dependent decrease in duration of immobility time in TST and FST when compared with the control group in a dose-dependent manner. The results of OFT also showed a dose-dependent increase in locomotor activity. In addition to behavioral tests, EELS also normalized oxidative stress markers such as CAT, SOD, MDA, and LPO in a dose-dependent manner. Conclusion: The results suggest that the ethanolic extract of L. speciosa L. leaves possesses significant antidepressant property, may be recommended as a supplement for the antidepressant activity.

scholarly journals Breath Hydrogen Produced by Ingestion of Commercial Hydrogen Water and Milk

2009 ◽  
Vol 4 ◽  
pp. BMI.S2209 ◽  
Author(s):  
Akito Shimouchi ◽  
Kazutoshi Nose ◽  
Makoto Yamaguchi ◽  
Hiroshi Ishiguro ◽  
Takaharu Kondo
Keyword(s):  
Baseline Level ◽  
Area Under The Curve ◽  
Distilled Water ◽  
Dependent Manner ◽  
Breath Hydrogen ◽  
Milk Intolerance ◽  
Maximal Level ◽  
Hydrogen Water ◽  
Dose Dependent ◽  
Sustained Increase

Objective To compare how and to what extent ingestion of hydrogen water and milk increase breath hydrogen in adults. Methods Five subjects without specific diseases, ingested distilled or hydrogen water and milk as a reference material that could increase breath hydrogen. Their end-alveolar breath hydrogen was measured. Results Ingestion of hydrogen water rapidly increased breath hydrogen to the maximal level of approximately 40 ppm 10–15 min after ingestion and thereafter rapidly decreased to the baseline level, whereas ingestion of the same amount of distilled water did not change breath hydrogen (p < 0.001). Ingestion of hydrogen water increased both hydrogen peaks and the area under the curve (AUC) of breath hydrogen in a dose-dependent manner. Ingestion of milk showed a delayed and sustained increase of breath hydrogen in subjects with milk intolerance for up to 540 min. Ingestion of hydrogen water produced breath hydrogen at AUC levels of 2 to 9 ppm hour, whereas milk increased breath hydrogen to AUC levels of 164 ppm hour for 540 min after drinking. Conclusion Hydrogen water caused a rapid increase in breath hydrogen in a dose-dependent manner; however, the rise in breath hydrogen was not sustained compared with milk.

Calcium entry in rat parotid acini: activation by carbachol and aluminum fluoride

1990 ◽  
Vol 258 (4) ◽  
pp. C654-C661 ◽  
Author(s):  
L. M. Mertz ◽  
V. J. Horn ◽  
B. J. Baum ◽  
I. S. Ambudkar
Keyword(s):  
Fluid Transport ◽  
Fluid Secretion ◽  
Transient Increase ◽  
Protein Activation ◽  
Initial Transient ◽  
Entry Pathway ◽  
G Protein Activation ◽  
Rat Parotid ◽  
Two Phases ◽  
Sustained Increase

Entry of extracellular Ca2+ into the cytosol of exocrine cells plays an important role in the process of fluid transport, especially during periods of prolonged secretion. However, in parotid acinar cells, the process of Ca2+ entry and the identity of factors which regulate it remain obscure. In this report, we demonstrate that AlF-4, like carbachol, activates Ca2+ entry into dispersed rat parotid acini. In physiological Ca2(+)-containing (1.28 mM) medium, both agents elicit three phases of cytosolic Ca2+ change, an initial transient increase (intracellular Ca2+ dependent) followed sequentially by a decrease (intra- and extracellular Ca2+ dependent) and a small sustained increase (extracellular Ca2+ dependent). Cytosolic Ca2+ concentration ([Ca2+]i) during the last two phases is influenced by variations in extracellular [Ca2+]. Elevation of extracellular [Ca2+], at any time after the initial transient increase, results in a rise of cytosolic [Ca2+], thus demonstrating the existence of a Ca2+ entry pathway during the two later phases. These data suggest the likelihood that in parotid acini, G protein activation is involved in stimulating this Ca2+ entry pathway. Because in AlF-4-treated acini entry into the cytosol is detectable only after the initial intracellular Ca2+ release phase, we suggest that this Ca2+ entry process does not accompany initial intracellular Ca2+ mobilization. Furthermore, the sustained cytosolic [Ca2+] elevation which can be observed 15-30 min after initial stimulation of acini is likely determined by this Ca2+ entry process which, in physiological conditions, could support sustained fluid secretion.

Histamine- and stress-induced prolactin secretion: importance of vasopressin V1- and V2-receptors

1994 ◽  
Vol 131 (4) ◽  
pp. 391-397 ◽  
Author(s):  
Andreas Kjær ◽  
Ulrich Knigge ◽  
Jørgen Warberg
Keyword(s):  
Receptor Antagonist ◽  
Propionic Acid ◽  
Arginine Vasopressin ◽  
Restraint Stress ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Dependent Manner ◽  
Selective Blockade ◽  
Combined Administration ◽  
Dose Dependent

Kjær A, Knigge U, Warberg J. Histamine- and stress-induced prolactin secretion: importance of vasopressin V1- and V2-receptors. Eur J Endocrinol 1994;131:391–7. ISSN 0804–4643 We investigated the involvement of arginine vasopressin (AVP) V1- and V2-receptors in the prolactin (PRL) secretory response to histamine (HA) or restraint stress stimulation in conscious male rats by selective blockade of AVP receptors using different antagonists. Histamine (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated PRL secretion 10–14-fold. Pretreatment with the selective V1- receptor antagonists [1-(p-t-butyl-β-mercapto-β, β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-d-arginine] vasopressin or [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine]vasopressin inhibited the PRL response to HA and restraint stress in a dose-dependent manner with maximal inhibition of 60%. The effect of the two antagonists was identical when equipotent antivasopressor doses were administered. The selective V2-receptor antagonist [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-d-isoleucine-4-isoleucine-8-arginine]vasopressin was unable to inhibit the PRL response significantly. Combined administration of the V1-receptor antagonist [1-(p-t-butyl-β-mercapto-β, β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-d-arginine]vasopressin and the V2-receptor antagonist inhibited the PRL response to HA to the same extent as that observed when the V1antagonist was administered alone. None of the antagonists used had any effect on basal PRL secretion. We conclude that AVP seems to play a role in the mediation of HA- and restraint stressinduced secretion of PRL, and that the AVP receptor involved is primarily of the V1 -type or similar to this. Andreas Kjær, Department of Medical Physiology, Division of Endocrinology and Metabolism, The Panum Institute (Building 12.3), University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark

Inhibitory effects of excess sympathetic activity on parasympathetic vasodilation in the rat masseter muscle

2007 ◽  
Vol 293 (2) ◽  
pp. R729-R736 ◽  
Author(s):  
Hisayoshi Ishii ◽  
Takeharu Niioka ◽  
Hidekazu Watanabe ◽  
Hiroshi Izumi
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Masseter Muscle ◽  
Lingual Nerve ◽  
Dependent Manner ◽  
Tonic Activity ◽  
Inhibitory Effects ◽  
Cervical Sympathetic ◽  
Dose Dependent ◽  
Stimulation Of

The present study was designed to examine the effect of sympathetic tonic activity on parasympathetic vasodilation evoked by the trigeminal-mediated reflex in the masseter muscle in urethane-anesthetized rats. Sectioning of the superior cervical sympathetic trunk (CST) ipsilaterally increased the basal level of blood flow in the masseter muscle (MBF). Electrical stimulation of the peripheral cut end of the CST for 2 min using 2-ms pulses ipsilaterally decreased in a dependent manner the intensity (0.5–10 V) and frequency (0.1–5 Hz) of the MBF. The CST stimulation for 2 min at <0.5 Hz with 5 V using 2-ms pulses seems to be comparable with the spontaneous activity in the CST fibers innervating the masseter vasculature, because this stimulation restored the basal level of the MBF to the presectioned values. Parasympathetic vasodilation evoked by electrical stimulation of the central cut end of the lingual nerve in the masseter muscle was markedly reduced by CST stimulation for 2 min with 5 V using 2-ms pulses in a frequency-dependent manner (0.5–5 Hz). Intravenous administration of phentolamine significantly reduced the vasoconstriction induced by CST stimulation in a dose-dependent manner (0.1–1 mg/kg), but pretreatment with either phentolamine or propranolol failed to affect the sympathetic inhibition of the parasympathetic vasodilation. Our results suggest that 1) excess sympathetic activity inhibits parasympathetic vasodilation in the masseter muscle, and 2) α- and β-adrenoceptors do not contribute to sympathetic inhibition of parasympathetic vasodilation, and thus some other types of receptors must be involved in this response.

Glibenclamide prevents coronary vasodilation induced by beta 1-adrenoceptor stimulation in dogs

1994 ◽  
Vol 266 (1) ◽  
pp. H84-H92 ◽  
Author(s):  
T. Narishige ◽  
K. Egashira ◽  
Y. Akatsuka ◽  
Y. Imamura ◽  
T. Takahashi ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Electromagnetic Flowmeter ◽  
Left Ventricular ◽  
K Channel ◽  
Dependent Manner ◽  
Coronary Vasodilation ◽  
Intracoronary Infusion ◽  
Before And After ◽  
Dose Dependent ◽  
Sustained Increase

This study aimed to determine whether a putative ATP-sensitive K(+)-channel blocker, glibenclamide (Glb), prevents metabolic coronary vasodilation associated with increased myocardial oxygen consumption (MVO2) caused by beta 1-adrenoceptor stimulation in anesthetized open-chest dogs. Isoproterenol (Iso) was infused selectively into the left circumflex coronary artery before and after Glb. Coronary blood flow (CBF) by an electromagnetic flowmeter, regional myocardial function by sonomicrometers, and left ventricular and arterial pressures were continuously measured. An intracoronary infusion of Iso (10 ng.kg-1 x min-1) resulted in the sustained increase in CBF as well as in the myocardial inotropic and chronotropic state. Glb (10, 30, and 100 micrograms/min ic) attenuated the Iso-induced increase in CBF in a dose-dependent manner, whereas inotropic and chronotropic responses to Iso were not affected by Glb. After beta 1-blockade with bisoprolol (0.3 mg/kg), which completely inhibited inotropic and chronotropic responses to Iso, the Iso-induced increase in CBF, presumably mediated by vascular beta 2-receptor stimulation, was not affected by Glb. Intracoronary denopamine (0.1 microgram.kg-1 x min-1), a beta 1-selective agonist, increased CBF, which was almost completely abolished by Glb. The increases in MVO2 induced by Iso or denopamine were similar before and after Glb, indicating that attenuation of the Iso- or denopamine-induced increase in CBF by Glb did not result from the decrease in MVO2. These results indicate that Glb prevented the increase in CBF associated with increased MVO2 caused by beta 1-adrenoceptor stimulation. It is suggested that ATP-sensitive K+ channels may play an important role in metabolic coronary vasodilation in dogs.

Direct pituitary inhibition of prolactin secretion by dopamine and noradrenaline in sheep

1989 ◽  
Vol 123 (3) ◽  
pp. 393-402 ◽  
Author(s):  
G. B. Thomas ◽  
J. T. Cummins ◽  
B. W. Doughton ◽  
N. Griffin ◽  
G. A. Smythe ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Prolactin Secretion ◽  
Plasma Prolactin ◽  
Dependent Manner ◽  
Dopamine Receptor Antagonist ◽  
Peripheral Plasma ◽  
Series Of Experiments ◽  
Dose Dependent ◽  
Inhibitory Regulation ◽  
Sustained Increase

ABSTRACT The effects of dopamine, noradrenaline and 3,4-dihydroxyphenylacetic acid (DOPAC) on the release of prolactin were examined in ovariectomized ewes. Infusion of dopamine (0·5 or 1 μg/kg per min for 2 h i.v.) reduced plasma prolactin concentrations in a dose-dependent manner, whereas DOPAC (5 or 10 μg/kg per min for 2 h i.v.) had no effect. In a further series of experiments, ovariectomized hypothalamo-pituitary disconnected ewes were given dopamine or noradrenaline (each at 0·5 or 1 μg/kg per min for 2 h i.v.), and both amines reduced mean plasma concentrations of prolactin with similar potency in a dose-dependent manner. These effects were blocked by treatment with pimozide and prazosin respectively. During the infusion of dopamine, the peripheral plasma concentrations of DOPAC and 3,4-dihydroxyphenylethyleneglycol (DHPG) were increased (DOPAC, 22 ± 7 (s.e.m.) to 131 ± 11 nmol/l; DHPG, 2·9 ± 0·3 to 6·4 ± 0·2 nmol/l), but plasma concentrations of dopamine and noradrenaline did not change. Finally, administration of domperidone, a specific dopamine receptor antagonist that does not cross the blood-brain barrier, resulted in a sustained increase in plasma prolactin concentrations in ovariectomized ewes. We conclude that the secretion of prolactin from the pituitary gland is under dual inhibitory regulation by both dopamine and noradrenaline in the sheep. Journal of Endocrinology (1989) 123, 393–402

Elicitation of supramaximal thermogenesis by aminophylline in the rat

1982 ◽  
Vol 53 (1) ◽  
pp. 16-20 ◽  
Author(s):  
L. C. Wang ◽  
E. C. Anholt
Keyword(s):  
Receptor Binding ◽  
Cold Exposure ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Sympathetic Activity ◽  
Dependent Manner ◽  
Overnight Fasting ◽  
Dose Dependent ◽  
Sympathetic Discharge ◽  
Fasted Rats

Previous studies in rats indicate that maximal thermogenesis during severe cold exposure is suppressed by overnight fasting. Since fasting depresses sympathetic activity and the activity of adrenergic receptors, both of which affect substrate mobilization in cold, the present study attempted to restore maximal thermogenesis in fasted rats by exogenous sympathomimetics and a hypoxanthine (aminophylline). In overnight-fasted rats, exogenous sympathomimetics had no effect in further enhancing maximal thermogenesis induced by exposure to severe cold (in He-O2 at -10 degrees C), indicating maximization of endogenous sympathetic discharge and saturation of adrenergic receptor binding during severe cold exposure. In contrast, aminophylline (1.25–37.5 mg/kg ip) elicited “supramaximal thermogenesis” beyond control maximums in both fasted (+19.4%) and fed +14.4%) conditions in a dose-dependent manner, resulting in improved cold tolerance and prevention of hypothermia. Since aminophylline acts distally to adrenergic receptors to increase intracellular adenosine 3′,5′-cyclic monophosphate concentration, it is possible that such increases could enhance substrate mobilization to support supramaximal thermogenesis in severe cold.

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