Potentiating effect of NH4Cl on vasoconstriction in rat aorta

Wakabayashi, Ichiro; Sakamoto, Kunihiro; Hatake, Kiyohiko; Masui, Hidehisa; Yoshimoto, Shusuke

doi:10.1016/0006-291x(91)90963-8

Cited by 11 publications

(8 citation statements)

References 19 publications

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“…There have been no reports available showing NH 4 Cl-induced depolarization of intact arteries. However, pretreatment of rat aortas with NH 4 Cl has been reported to increase contractile force induced by low concentrations of KCl, while the maximum contraction induced by high concentrations of KCl was not affected by NH 4 Cl [71]. This finding suggests that NH 4 Cl potentiates KCl-induced contraction through one common mechanism, namely depolarization.…”

Section: Phi Sensors In Vsmsupporting

confidence: 46%

“…depolarization with moderate elevation in extracellular K + (14.7 m M ) and preincubation with tetraethylammonium ions or BAY K8644, greatly potentiated the contractile action of NH 4 Cl [69], substantiating the central role of voltage-gated Ca 2+ channels. In rat aortas, a low concentration (10 m M ) of NH 4 Cl potentiated the contraction induced by KCl and phenylephrine, and this potentiation was not detectable in the presence of nifedipine or in the absence of external Ca 2+ [71]. In ferret pulmonary arterial SMs, cytosolic alkalinization by NH 4 Cl also caused an initial increase in both intracellular free Ca 2+ and pulmonary arterial pressure by predominantly increasing extracellular Ca 2+ influx and potentiated KCl-induced contraction [72].…”

Section: Phi Sensors In Vsmmentioning

confidence: 99%

“…On the other hand, NH 4 Cl-induced intracellular alkalinization just prior to stimulation with phenylephrine and high K + resulted in the potentiation of subsequent contraction of rat aorta [71, 77]. As timing of pH i changes in experiments is an important factor that requires careful consideration, the latter method is thought to generate results that are easier to interpret, since multiple pathways of cellular signal transduction are already fully active during the plateau phase and important processes that initiate cellular responses may be already terminated during a plateau of contraction.…”

Section: Control Of Vascular Contractility By Phi Signalsmentioning

confidence: 99%

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Intracellular pH as a Determinant of Vascular Smooth Muscle Function

2006

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Intracellular pH (pH_i) is a physiological parameter that is intimately linked to contractility, growth and proliferation of vascular smooth muscle (VSM). Regarding contractility, no general unifying concept of pH_i regulation but a rather complex relation between pH_i signals and vascular tone has been revealed so far. The modulation of vasotone by pH_i depends on the type of blood vessel as well as on the pattern of regulatory input signals. In addition, changes in pH_i have been recognized as an important cellular signal to determine the fate of cells in terms of proliferation or apoptosis. Cellular sensors for pH_i include a variety of ion transport systems which control intracellular Ca²⁺ gradients and are likely to serve as a link between pH_i and cell functions. Here we provide an overview on the potential targets and mechanisms that transduce pH_i signals in VSM. The role of pH_i-sensing signaling complexes and localized pH_i signaling as the basis of diversity of pH_i regulation of VSM function is discussed.

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Section: Phi Sensors In Vsmsupporting

confidence: 46%

Section: Phi Sensors In Vsmmentioning

confidence: 99%

Section: Control Of Vascular Contractility By Phi Signalsmentioning

confidence: 99%

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Intracellular pH as a Determinant of Vascular Smooth Muscle Function

2006

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“…3). 161 – 163 It was found that after inhibiting the effect of buffer pair (CO 2 /HCO 3 – ) on pH, NHE‐1 gene knockout led to cell acidification, and then decreased arterial tension, arterial media remodelling, blood pressure and Rho‐mediated VSMC sensitivity to calcium ions 164 . In PASMC, HIF‐1 could up‐regulate NHE‐1, and thus up‐regulate pHi, cause alkaline drift of cells, promote cell proliferation and mediate vascular remodelling 165 .…”

Section: Introductionmentioning

confidence: 99%

The mechanism of ions in pulmonary hypertension

Liu

fu²,

Tian

et al. 2021

Pulm. circ.

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Pulmonary hypertension（PH）is a kind of hemodynamic and pathophysiological state, in which the pulmonary artery pressure (PAP) rises above a certain threshold. The main pathological manifestation is pulmonary vasoconstriction and remodelling progressively. More and more studies have found that ions play a major role in the pathogenesis of PH. Many vasoactive substances, inflammatory mediators, transcription-inducing factors, apoptosis mediators, redox substances and translation modifiers can control the concentration of ions inside and outside the cell by regulating the activity of ion channels, which can regulate vascular contraction, cell proliferation, migration, apoptosis, inflammation and other functions. We all know that there are no effective drugs to treat PH. Ions are involved in the occurrence and development of PH, so it is necessary to clarify the mechanism of ions in PH as a therapeutic target for PH. The main ions involved in PH are calcium ion (Ca2+), potassium ion (K+), sodium ion (Na+) and chloride ion (Cl–). Here, we mainly discuss the distribution of these ions and their channels in pulmonary arteries and their role in the pathogenesis of PH.

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“…In porcine coronary arteries and rat aortas, intracellular alkalinization induced a rise in intracellular Ca 2+ that was attenuated by nifedipine, an inhibitor of L-type voltage-gated Ca 2+ channels. 137,138 Alkalinization also increased intracellular Ca 2+ levels in ferret PASMCs and potentiated contraction in response to potassium chloride, 5 indicating that L-type voltage-gated Ca 2+ channels contributed to pHmediated Ca 2+ entry. Furthermore, intracellular alkalinization inhibited voltage-gated K + currents, resulting in depolarization of canine PASMCs, 139 which may serve as one of the mechanisms by which an alkaline shift in pH activates L-type Ca 2+ channels.…”

Section: Ca 2+ Signalingmentioning

confidence: 97%

Na⁺/H⁺ Exchange and Hypoxic Pulmonary Hypertension

Huetsch

Shimoda

2015

Pulm. circ.

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Intracellular pH (pH i ) homeostasis is key to the functioning of vascular smooth muscle cells, including pulmonary artery smooth muscle cells (PASMCs). Sodium-hydrogen exchange (NHE) is an important contributor to pH i control in PASMCs. In this review, we examine the role of NHE in PASMC function, in both physiologic and pathologic conditions. In particular, we focus on the contribution of NHE to the PASMC response to hypoxia, considering both acute hypoxic pulmonary vasoconstriction and the development of pulmonary vascular remodeling and pulmonary hypertension in response to chronic hypoxia. Hypoxic pulmonary hypertension remains a disease with limited therapeutic options. Thus, this review explores past efforts at disrupting NHE signaling and discusses the therapeutic potential that such efforts may have in the field of pulmonary hypertension.

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Potentiating effect of NH4Cl on vasoconstriction in rat aorta

Cited by 11 publications

References 19 publications

Intracellular pH as a Determinant of Vascular Smooth Muscle Function

Intracellular pH as a Determinant of Vascular Smooth Muscle Function

The mechanism of ions in pulmonary hypertension

Na⁺/H⁺ Exchange and Hypoxic Pulmonary Hypertension

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Potentiating effect of NH4Cl on vasoconstriction in rat aorta

Cited by 11 publications

References 19 publications

Intracellular pH as a Determinant of Vascular Smooth Muscle Function

Intracellular pH as a Determinant of Vascular Smooth Muscle Function

The mechanism of ions in pulmonary hypertension

Na+/H+ Exchange and Hypoxic Pulmonary Hypertension

Contact Info

Product

Resources

About

Na⁺/H⁺ Exchange and Hypoxic Pulmonary Hypertension