scholarly journals In vivo cardiac electrical activity of nitric oxide in barium chloride treated male rats

2017 ◽  
Author(s):  
Abbas B. Q. Salihi ◽  
Mudhir S. Shekha ◽  
Peshraw S. Hamadamin ◽  
Ismail M. Maulood ◽  
Khder H. Rasul ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Electrical Activity ◽  
Barium Chloride ◽  
Male Rats ◽  
Treated Male ◽  
Cardiac Electrical Activity

In-vivo evaluation of reduced-lead-systems in noninvasive reconstruction and localization of cardiac electrical activity

2015 ◽  
Author(s):  
Matthijs JM Cluitmans ◽  
Joel Karel ◽  
Pietro Bonizzi ◽  
Monique MJ de Jong ◽  
Paul GA Volders ◽  
...  
Keyword(s):  
Electrical Activity ◽  
In Vivo Evaluation ◽  
Cardiac Electrical Activity

Activity-dependent feedback modulation of spike patterning of supraoptic nucleus neurons by endogenous adenosine

2006 ◽  
Vol 291 (1) ◽  
pp. R83-R90 ◽  
Author(s):  
P. M. Bull ◽  
C. H. Brown ◽  
J. A. Russell ◽  
M. Ludwig
Keyword(s):  
Electrical Activity ◽  
Hazard Function ◽  
Supraoptic Nucleus ◽  
Neuronal Excitability ◽  
Cell Activity ◽  
Male Rats ◽  
Firing Rates ◽  
Endogenous Adenosine

Neuropeptide secretion from the dendrites of hypothalamic magnocellular supraoptic nucleus (SON) neurons contributes to the regulation of neuronal activity patterning, which ultimately determines their peptide output from axon terminals in the posterior pituitary gland. SON dendrites also secrete a number of other neuromodulators, including ATP. ATP degrades to adenosine in the extracellular space to complement transported adenosine acting on pre- and postsynaptic SON A1 receptors to reduce neuronal excitability, measured in vitro. To assess adenosine control of electrical activity in vivo, we made extracellular single-unit recordings of the electrical activity of SON neurons in anesthetized male rats. Microdialysis application (retrodialysis) of the A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT) increased phasic vasopressin cell intraburst firing rates progressively over the first 5 s by 4.5 ± 1.6 Hz ( P < 0.05), and increased burst duration by 293 ± 64% ( P < 0.05). Hazard function plots were generated from interval interspike histograms and revealed that these effects were associated with increased postspike excitability. In contrast, CPT had no effect on the firing rates and hazard function plot profiles of continuously active vasopressin and oxytocin cells. However, CPT significantly increased clustering of spikes, as quantified by the index of dispersion, in oxytocin cells and continuously active vasopressin cells (by 267 ± 113% and 462 ± 67%, respectively, P < 0.05). Indeed, in 4 of 5 continuously active vasopressin cells, CPT induced a pseudophasic activity pattern. Together, these results indicate that endogenous adenosine is involved in the local control of SON cell activity in vivo.

Interactions between N-methyl-D-aspartate, nitric oxide and serotonin in the control of prolactin secretion in prepubertal male rats

1997 ◽  
pp. 99-106 ◽  
Author(s):  
E Aguilar ◽  
M Tena-Sempere ◽  
R Aguilar ◽  
D Gonzalez ◽  
L Pinilla
Keyword(s):  
Nitric Oxide ◽  
Nmda Antagonist ◽  
Prolactin Secretion ◽  
No Synthase ◽  
Male Rats ◽  
Serotonin Synthesis ◽  
Mk 801

The role of N-methyl-D-aspartate (NMDA) in the control of prolactin (PRL) secretion was analysed in prepubertal male rats. In experiment 1, males of different ages were decapitated after administration of NMDA or vehicle. In experiment 2, 30-day-old males were killed at different times after administration of vehicle, NMDA, MK-801 (a non-competitive NMDA antagonist) or NMDA plus MK-801. In experiment 3, 23-day-old males were sham-orchidectomized or orchidectomized. Orchidectomized males were or were not implanted with Silastic capsules containing different amounts of testosterone. On day 30, the animals were decapitated after administration of vehicle, NMDA or MK-801. In experiment 4, 30-day-old male rats were decapitated after being injected with vehicle, NMDA, Nw-nitro-L-arginine methyl ester (NAME) (an inhibitor of nitric oxide (NO) synthase), or NMDA plus NAME. Serum PRL concentrations, and dopamine pituitary and hypothalamic content were measured. In experiment 5, males pretreated with vehicle or NAME were killed after administration of the precursor of serotonin synthesis 5-hydroxytryptophan (5-HTP), the 5-HT1 receptor agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) or the 5-HT2 agonist (+/-) 2,5-dimethoxy-4-iodoamphetamine hydrochloride (DOI). Finally, the effects of NMDA, NAME and sodium nitroprusside (SNP) were tested in dispersed adenohypophyseal cells. We found that: (1) antagonism of NMDA receptors with MK-801 decreased PRL secretion in intact, orchidectomized and orchidectomized-testosterone treated male rats; (ii) NMDA inhibited PRL release in vivo through an increase in dopamine release and this effect was potentiated by NAME and prevented by testosterone; (iii) NMDA inhibited PRL, secretion in vitro and this effect was observed in presence of both SNP and NAME; (iv) NAME blocked the stimulatory effects of 5-HTP and DOI on PRL secretion. We conclude that endogenous glutamate stimulates PRL release and that NO might have a pivotal role in the mechanisms involved in the control of PRL release, inhibiting the release of dopamine and modulating the effects of NMDA and 5-HT.

scholarly journals Comparative Review of the Algorithms for Removal of Electrocardiographic Interference from Trunk Electromyography

Sensors ◽  
2020 ◽  
Vol 20 (17) ◽  
pp. 4890
Author(s):  
Lin Xu ◽  
Elisabetta Peri ◽  
Rik Vullings ◽  
Chiara Rabotti ◽  
Johannes P. Van Dijk ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Biceps Brachii ◽  
Signal To Noise Ratio ◽  
Surface Emg ◽  
Cardiac Electrical Activity ◽  
Emg Signal ◽  
Comparative Review ◽  
Electrocardiogram Ecg ◽  
High Pass

Surface electromyogram (EMG) is a noninvasive measure of muscle electrical activity and has been widely used in a variety of applications. When recorded from the trunk, surface EMG can be contaminated by the cardiac electrical activity, i.e., the electrocardiogram (ECG). ECG may distort the desired EMG signal, complicating the extraction of reliable information from the trunk EMG. Several methods are available for ECG removal from the trunk EMG, but a comparative assessment of the performance of these methods is lacking, limiting the possibility of selecting a suitable method for specific applications. The aim of the present study is therefore to review and compare the performance of different ECG removal methods from the trunk EMG. To this end, a synthetic dataset was generated by combining in vivo EMG signals recorded on the biceps brachii and healthy or dysrhythmia ECG data from the Physionet database with a predefined signal-to-noise ratio. Gating, high-pass filtering, template subtraction, wavelet transform, adaptive filtering, and blind source separation were implemented for ECG removal. A robust measure of Kurtosis, i.e., KR2 and two EMG features, the average rectified value (ARV), and mean frequency (MF), were then calculated from the processed EMG signals and compared with the EMG before mixing. Our results indicate template subtraction to produce the lowest root mean square error in both ARV and MF, providing useful insight for the selection of a suitable ECG removal method.

Lamprey GnRH-III Acts on Its Putative Receptor via Nitric Oxide to Release Follicle-Stimulating Hormone Specifically

2002 ◽  
Vol 227 (9) ◽  
pp. 786-793 ◽  
Author(s):  
W.H. Yu ◽  
S. Karanth ◽  
C.A. Mastronardi ◽  
S. Sealfon ◽  
C. Dean ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cultured Cells ◽  
Follicle Stimulating Hormone ◽  
The Other ◽  
Male Rats ◽  
Other Hand ◽  
Lh Rh ◽  
Stimulating Hormone

Lamprey gonadotropin-releasing hormone-III (I-GnRH-III), the putative follicle-stimulating hormone (FSH)-releasing factor (FSHRF), exerts a preferential FSH-releasing activity in rats both in vitro and in vivo. To test the hypothesis that I-GnRH-III acts on its own receptors to stimulate gonadotropin release, the functional activity of this peptide at mammalian (m) leutinizing hormone (LH)RH receptors transfected to COS cells was tested. I-GnRH-III activated m-LHRH receptors only at a minimal effective concentration (MEC) of 10–6 M, whereas m-LHRH was active at a MEC of 10–9 M, at least 1,000 times less than that required for I-GnRH-III. In 4-day monolayer cultured cells, I-GnRH-III was similarly extremely weak in releasing either LH or FSH, and, in fact, it released LH at a lower concentration (10–7 M) than that required for FSH release (10–6 M). In this assay, m-LHRH released both FSH and LH significantly at the lowest concentration tested (10–10 M). On the other hand, I-GnRH-III had a high potency to selectively release FSH and not LH from hemipituitaries of male rats. The results suggest that the cultured cells were devoid of FSHRF receptors, thereby resulting in a pattern of FSH and LH release caused by the LHRH receptor. On the other hand, the putative FSH-releasing factor receptor accounts for the selective FSH release by I-GnRH-III when tested on hemipituitaries. Removal of calcium from the medium plus the addition of EGTA, a calcium chelator, suppressed the release of gonadotropins induced by either I-GnRH-III or LHRH, indicating that calcium is required for the action of either peptide. Previous results showed that sodium nitroprusside, a releaser of nitric oxide (NO), causes the release of both FSH and LH from hemipituitaries incubated in vitro. In the present experiments, a competitive inhibitor of NO synthase, L-NG-monomethyl-l-arginine (300 μM) blocked the action of I-GnRH-III or partially purified FSHRF. The results indicate that I-GnRH-III and FSHRF act on putative FSHRF receptors by a calcium-dependent NO pathway.

Effect of the nitric oxide level in the medial preoptic area on male copulatory behavior in rats

1998 ◽  
Vol 274 (1) ◽  
pp. R243-R247 ◽  
Author(s):  
Yoshikazu Sato ◽  
Hiroki Horita ◽  
Toshie Kurohata ◽  
Hideki Adachi ◽  
Taiji Tsukamoto
Keyword(s):  
Nitric Oxide ◽  
Preoptic Area ◽  
Copulatory Behavior ◽  
Medial Preoptic Area ◽  
In Vivo Microdialysis ◽  
Male Rats ◽  
Nitric Oxide Level ◽  
Synthase Inhibitor ◽  
Male Copulatory Behavior

We investigated the influence of the extracellular nitric oxide (NO) level on male copulatory behavior. We confirmed the changes of nitrite ([Formula: see text]) and nitrate ([Formula: see text]) in the medial preoptic area (MPOA) by administration of the NO precursorl-arginine (l-Arg, 10 mM) or the NO synthase inhibitor N G-monomethyl-l-arginine (l-NMMA, 10 mM) via a dialysis probe. [Formula: see text] and[Formula: see text] were measured simultaneously by an in vivo microdialysis method coupled with the Griess reaction.l-Arg induced significant elevations of extracellular [Formula: see text]and [Formula: see text].l-NMMA significantly reduced[Formula: see text] and[Formula: see text] levels. We observed male copulatory behavior during infusion ofl-Arg orl-NMMA. The mount rate of male rats significantly increased during infusion ofl-Arg in the MPOA. Administration of l-NMMA reduced the mount rate. These findings suggested that the elevation of extracellular NO in the MPOA facilitates male copulatory behavior of rats, whereas the decrease of NO reduces their copulatory behavior.

scholarly journals Nitric Oxide–cGMP Pathway Modulation in an Experimental Model of Hypoxic Pulmonary Hypertension

2021 ◽  
pp. 107424842110141
Author(s):  
Melanie Reinero ◽  
Maurice Beghetti ◽  
Piergiorgio Tozzi ◽  
Ludwig K von Segesser ◽  
Michele Samaja ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Soluble Guanylate Cyclase ◽  
Morphological Changes ◽  
Male Rats ◽  
No Donor ◽  
Cgmp Pathway ◽  
Modulatory Sites ◽  
Ventricle Hypertrophy

Manipulation of nitric oxide (NO) may enable control of progression and treatment of pulmonary hypertension (PH). Several approaches may modulate the NO-cGMP pathway in vivo. Here, we investigate the effectiveness of 3 modulatory sites: (i) the amount of l-arginine; (ii) the size of plasma NO stores that stimulate soluble guanylate cyclase; (iii) the conversion of cGMP into inactive 5′-GMP, with respect to hypoxia, to test the effectiveness of the treatments with respect to hypoxia-induced PH. Male rats (n = 80; 10/group) maintained in normoxic (21% O2) or hypoxic chambers (10% O2) for 14 days were subdivided in 4 sub-groups: placebo, l-arginine (20 mg/ml), the NO donor molsidomine (15 mg/kg in drinking water), and phoshodiesterase-5 inhibitor sildenafil (1.4 mg/kg in 0.3 ml saline, i.p.). Hypoxia depressed homeostasis and increased erythropoiesis, heart and right ventricle hypertrophy, myocardial fibrosis and apoptosis inducing pulmonary remodeling. Stimulating anyone of the 3 mechanisms that enhance the NO-cGMP pathway helped rescuing the functional and morphological changes in the cardiopulmonary system leading to improvement, sometimes normalization, of the pressures. None of the treatments affected the observed parameters in normoxia. Thus, the 3 modulatory sites are essentially similar in enhancing the NO-cGMP pathway, thereby attenuating the hypoxia-related effects that lead to pulmonary hypertension.

scholarly journals Kvβ1.1 (AKR6A8) senses pyridine nucleotide changes in the mouse heart and modulates cardiac electrical activity

2017 ◽  
Vol 312 (3) ◽  
pp. H571-H583 ◽  
Author(s):  
Jared Tur ◽  
Kalyan C. Chapalamadugu ◽  
Christopher Katnik ◽  
Javier Cuevas ◽  
Aruni Bhatnagar ◽  
...  
Keyword(s):  
Action Potential ◽  
Electrical Activity ◽  
Action Potential Duration ◽  
Ex Vivo ◽  
Physiological Role ◽  
Pyridine Nucleotide ◽  
Mouse Heart ◽  
Wild Type ◽  
Cardiac Electrical Activity

The present study investigates the physiological role of Kvβ1 subunit for sensing pyridine nucleotide (NADH/NAD+) changes in the heart. We used Kvβ1.1 knockout (KO) or wild-type (WT) mice and established that Kvβ1.1 preferentially binds with Kv4.2 and senses the pyridine nucleotide changes in the heart. The cellular action potential duration (APD) obtained from WT cardiomyocytes showed longer APDs with lactate perfusion, which increases intracellular NADH levels, while the APDs remained unaltered in the Kvβ1.1 KO. Ex vivo monophasic action potentials showed a similar response, in which the APDs were prolonged in WT mouse hearts with lactate perfusion; however, the Kvβ1.1 KO mouse hearts did not show APD changes upon lactate perfusion. COS-7 cells coexpressing Kv4.2 and Kvβ1.1 were used for whole cell patch-clamp recordings to evaluate changes caused by NADH (lactate). These data reveal that Kvβ1.1 is required in the mediated inactivation of Kv4.2 currents, when NADH (lactate) levels are increased. In vivo, isoproterenol infusion led to increased NADH in the heart along with QTc prolongation in wild-type mice; regardless of the approach, our data show that Kvβ1.1 recognizes NADH changes and modulates Kv4.2 currents affecting AP and QTc durations. Overall, this study uses multiple levels of investigation, including the heterologous overexpression system, cardiomyocyte, ex vivo, and ECG, and clearly depicts that Kvβ1.1 is an obligatory sensor of NADH/NAD changes in vivo, with a physiological role in the heart. NEW & NOTEWORTHY Cardiac electrical activity is mediated by ion channels, and Kv4.2 plays a significant role, along with its binding partner, the Kvβ1.1 subunit. In the present study, we identify Kvβ1.1 as a sensor of pyridine nucleotide changes and as a modulator of Kv4.2 gating, action potential duration, and ECG in the mouse heart.

Mechanisms of inhibitory action of kainic acid on prolactin secretion in male rats

1996 ◽  
Vol 151 (1) ◽  
pp. 159-167 ◽  
Author(s):  
L Pinilla ◽  
D Gonzalez ◽  
M Tena-Sempere ◽  
R Aguilar ◽  
E Aguilar
Keyword(s):  
Nitric Oxide ◽  
Kainic Acid ◽  
Inhibitory Action ◽  
Prolactin Secretion ◽  
Kainate Receptors ◽  
Male Rats ◽  
Endogenous Nitric Oxide ◽  
Oxide Synthase

Abstract Activation of excitatory N-methyl-d-aspartate and kainate receptors evokes multiple and diverse neuroendocrine changes. We have previously shown that kainic acid (KA), an agonist of kainate receptors, inhibits prolactin (PRL) secretion in male rats when given systemically. In the present studies we have characterized this inhibitory action. KA inhibited in vivo PRL secretion in neonatal, prepubertal and adult male rats. This inhibition was independent of gonadal secretion and was evident in male rats whether intact, orchidectomized, or orchidectomized and treated with testosterone. In addition, KA inhibited PRL secretion in male rats rendered hyperprolactinaemic by neonatal administration of oestradiol benzoate. The decrease in serum PRL levels after KA administration was accompanied by an increase in pituitary concentrations of dopamine, and the KA effect on PRL disappeared in males pretreated with domperidone, an antagonist of dopaminergic receptors. These findings strongly suggest that an increase in dopamine release was involved in the effects of KA. Also, KA inhibited in vitro PRL secretion by adenohypophysial dispersed cells and this effect was blocked by 6,7-dinitroquinoxaline, a kainate receptor antagonist, which indicates that the pituitary is also a possible site of action of KA. Nw-nitro-l-arginine-methyl ester, a blocker of nitric oxide synthase, reduced the effects of KA in vivo and slightly stimulated PRL release in vitro. We conclude that the inhibitory action of KA is independent of the age of the animal, the gonadal status and the prevailing PRL levels. The action of KA is probably mediated by an increase in dopamine secretion and by a direct effect at the pituitary level. Finally, the effect of KA on PRL secretion is partially dependent on endogenous nitric oxide. Journal of Endocrinology (1996) 151, 159–167

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