Median preoptic nucleus excitatory neurotransmitters in the maintenance of hypertensive state

Mourão, Aline A.; Mello, Aryanne B. Soares de; Moreira, Marina Conceição dos Santos; Rodrigues, Karla Lima; Lopes, Paulo Ricardo; Xavier, Carlos Henrique; Gomes, Rodrigo Mello; Freiria-Oliveira, André Henrique; Blanch, Graziela Torres; Colombari, Eduardo; Pedrino, Gustavo Rodrigues

doi:10.1016/j.brainresbull.2018.06.011

Cited by 5 publications

(6 citation statements)

References 70 publications

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“…Distinguishable to some extent from previous studies reflecting the effectiveness of KYNA in decreasing the amplitude of I h or heart rate [15,19,41], in the present study, we were unable to observe any adjustments of KYNA or KYNA-A4 on the amplitude and gating of I h activated by long-lasting membrane hyperpolarization. However, as GH 3 cells were continually exposed to KYNA, a further addition of ivabradine effectively suppressed the amplitude of I h .…”

Section: Discussioncontrasting

confidence: 87%

“…However, it needs to be mentioned that the inhibition by these compounds of I K(DR) in these cells might partly contribute to their effectiveness in their perturbations on spontaneous APs with high frequency, since it can lessen the strength of resurgent K + currents [57]. Of also note, awareness needs to be strengthened in attributing its aberrant use to the antagonistic effect on the NMDAR activity [8,12,14,15,53,58].…”

Section: Discussionmentioning

confidence: 99%

“…Previous work has demonstrated the ability of KYNA to decrease the amplitude of I h or heart rate [15,19,41]. For these reasons, we further investigated whether the presence of KYNA could perturb the amplitude and gating of I h in GH 3 cells [42].…”

Section: Inability Of Kyna To Modify Hyperpolarization-activated Cation Current (I H )mentioning

confidence: 95%

“…This compound, together with L-kynurenine, is thought to be an endogenous metabolite of L-tryptophan known to block N-methyl-D-aspartate receptor (NMDAR), and it has been frequently demonstrated to exert neuroprotective or anticonvulsant properties in the brain [2,3,[5][6][7][8][9][10][11][12][13]. This compound has been indeed disclosed to inhibit NMDARs at the glycine-binding site and it can noncompetitively inhibit α 7 -nicotinic acetylcholine receptor, and through this action, it might modulate glutamate release presynaptically [1,3,14,15].…”

Section: Introductionmentioning

confidence: 99%

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Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type K+ Current

Lin

Fang

et al. 2021

IJMS

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Kynurenic acid (KYNA, 4-oxoquinoline-2-carboxylic acid), an intermediate of the tryptophan metabolism, has been recognized to exert different neuroactive actions; however, the need of how it or its aminoalkylated amide derivative N-(2-(dimethylamino)ethyl)-3-(morpholinomethyl)-4-oxo-1,4-dihydroquinoline-2-carboxamide (KYNA-A4) exerts any effects on ion currents in excitable cells remains largely unmet. In this study, the investigations of how KYNA and other structurally similar KYNA derivatives have any adjustments on different ionic currents in pituitary GH3 cells and hippocampal mHippoE-14 neurons were performed by patch-clamp technique. KYNA or KYNA-A4 increased the amplitude of M-type K+ current (IK(M)) and concomitantly enhanced the activation time course of the current. The EC50 value required for KYNA- or KYNA-A4 -stimulated IK(M) was yielded to be 18.1 or 6.4 μM, respectively. The presence of KYNA or KYNA-A4 shifted the relationship of normalized IK(M)-conductance versus membrane potential to more depolarized potential with no change in the gating charge of the current. The voltage-dependent hysteretic area of IK(M) elicited by long-lasting triangular ramp pulse was observed in GH3 cells and that was increased during exposure to KYNA or KYNA-A4. In cell-attached current recordings, addition of KYNA raised the open probability of M-type K+ channels, along with increased mean open time of the channel. Cell exposure to KYNA or KYNA-A4 mildly inhibited delayed-rectifying K+ current; however, neither erg-mediated K+ current, hyperpolarization-activated cation current, nor voltage-gated Na+ current in GH3 cells was changed by KYNA or KYNA-A4. Under whole-cell, current-clamp recordings, exposure to KYNA or KYNA-A4 diminished the frequency of spontaneous action potentials; moreover, their reduction in firing frequency was attenuated by linopirdine, yet not by iberiotoxin or apamin. In hippocampal mHippoE-14 neurons, the addition of KYNA also increased the IK(M) amplitude effectively. Taken together, the actions presented herein would be one of the noticeable mechanisms through which they modulate functional activities of excitable cells occurring in vivo.

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Section: Discussioncontrasting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Inability Of Kyna To Modify Hyperpolarization-activated Cation Current (I H )mentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type K+ Current

Lin

Fang

et al. 2021

IJMS

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“…Circulating AngII provides an excitatory drive for MnPO neurons through neural sites that lack a functional blood-brain barrier, including the SFO/OVLT site. 87 MnPO drives small cell neurons of PVN through a glutamatergic pathway and participates in the regulation of arterial blood pressure and sympathetic nerve activity; 88 , 89 however, MnPO transmits signals to neuroendocrine cells in PVN to regulate glucocorticoid release. MnPO plays an important role in maintaining the sympathetic excitability of AngII.…”

Section: Osahs and Neuroendocrine Disordersmentioning

confidence: 99%

Recent Advances in Studies on the Role of Neuroendocrine Disorders in Obstructive Sleep Apnea–Hypopnea Syndrome-Related Atherosclerosis

Wang

Yanli

et al. 2021

NSS

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Cardiovascular disease is a common cause of death worldwide, and atherosclerosis (AS) and obstructive sleep apnea-hypopnea syndrome (OSAHS) critically contribute to the initiation and progression of cardiovascular diseases. OSAHS promotes endothelial injury, vascular smooth muscle cell (VSMC) proliferation, abnormal lipid metabolism, and elevated arterial blood pressure. However, the exact OSAHS mechanism that causes AS remains unclear. The nervous system is widely distributed in the central and peripheral regions. It regulates appetite, energy metabolism, inflammation, oxidative stress, insulin resistance, and vasoconstriction by releasing regulatory factors and participates in the occurrence and development of AS. Studies showed that OSAHS can cause changes in neurophysiological plasticity and affect modulator release, suggesting that neuroendocrine dysfunction may be related to the OSAHS mechanism causing AS. In this article, we review the possible mechanisms of neuroendocrine disorders in the pathogenesis of OSAHS-induced AS and provide a new basis for further research on the development of corresponding effective intervention strategies.

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Novel choline analog 2-(4-((1-phenyl-1H-pyrazol-4-yl)methyl)piperazin-1-yl)ethan-1-ol produces sympathoinhibition, hypotension, and antihypertensive effects

Menegatti

Carvalho

Lião

et al. 2019

Naunyn-Schmiedeberg's Arch Pharmacol

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Median preoptic nucleus excitatory neurotransmitters in the maintenance of hypertensive state

Cited by 5 publications

References 70 publications

Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type K+ Current

Effective Activation by Kynurenic Acid and Its Aminoalkylated Derivatives on M-Type K+ Current

Recent Advances in Studies on the Role of Neuroendocrine Disorders in Obstructive Sleep Apnea–Hypopnea Syndrome-Related Atherosclerosis

Novel choline analog 2-(4-((1-phenyl-1H-pyrazol-4-yl)methyl)piperazin-1-yl)ethan-1-ol produces sympathoinhibition, hypotension, and antihypertensive effects

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