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transducer  (ADInstruments)


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    Structured Review

    ADInstruments transducer
    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal <t>transducer</t> and activator of transcription.
    Transducer, supplied by ADInstruments, used in various techniques. Bioz Stars score: 96/100, based on 351 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/disposable+transducer+mlt0670/Disposable+BP+Transducer/pmc12981474-61-7-11
    Average 96 stars, based on 351 article reviews
    transducer - by Bioz Stars, 2026-09
    96/100 stars

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    1) Product Images from "Early administration of renin–angiotensin system inhibitors improves survival and cardiac remodeling in heart failure with preserved ejection fraction"

    Article Title: Early administration of renin–angiotensin system inhibitors improves survival and cardiac remodeling in heart failure with preserved ejection fraction

    Journal: PLOS One

    doi: 10.1371/journal.pone.0339600

    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal transducer and activator of transcription.
    Figure Legend Snippet: The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal transducer and activator of transcription.

    Techniques Used: In Vivo, Activity Assay, Expressing, Protein-Protein interactions

    Related Articles

    other:

    Article Title: Maternal renal dysfunction in sheep is associated with salt insensitivity in female offspring
    Article Snippet: Arterial blood pressure and heart rates were continuously measured with the animal standing throughout the experiment using pressure transducers (MLT0670 Disposable BP Transducer, ADInstruments Pty Ltd, Australia) placed beside the cage at the level of the heart.

    Article Title: Mechanisms of neonatal increase in glomerular filtration rate.
    Article Snippet: Arterial pressure and heart rate of all animals were monitored and recorded continuously using pressure transducers (MLT0670 Disposable BP Transducer; ADInstruments) connected to a Powerlab system and stored for analysis (Powerlab Chart 5, ADInstruments).



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    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal <t>transducer</t> and activator of transcription.
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    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal <t>transducer</t> and activator of transcription.
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    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal <t>transducer</t> and activator of transcription.
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    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal <t>transducer</t> and activator of transcription.
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    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal <t>transducer</t> and activator of transcription.
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    The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal transducer and activator of transcription.

    Journal: PLOS One

    Article Title: Early administration of renin–angiotensin system inhibitors improves survival and cardiac remodeling in heart failure with preserved ejection fraction

    doi: 10.1371/journal.pone.0339600

    Figure Lengend Snippet: The decrease in NO levels in vivo following the ingestion of HFD and L-NAME decreased the activity of the NO-sGC-cGMP pathway. cGMP-activated PKG has hypotensive, anti-inflammatory, and anti-fibrotic effects; therefore, decreased activity of the NO-sGC-cGMP pathway may lead to inflammation, hypertrophy, and apoptosis, leading to the development of HFpEF. Furthermore, the decrease in NO levels in vivo converts Ang I to Ang II; hence, a decrease in NO activates RAS. Ang II increased by RAS activity increases TGF-β expression, which consequently activates the MAPK signaling pathway, leading to fibroblast proliferation, ECM overdeposition, and fibrosis. Ang II also activates the PI3K-Akt and JAK-STAT signaling pathways, which may trigger inflammation, hypertrophy, and apoptosis, leading to HFpEF development. Early administration of the RAS inhibitors Cap and Sac/Val may suppress downstream signaling by inhibiting RAS, thereby reducing inflammation and fibrosis and preventing the onset of HFpEF. NO: nitric oxide; HFD: high-fat diet; L-NAME: NG-Nitro-L-arginine methyl ester; sGC: soluble guanylate cyclase; cGMP: cyclic guanosine monophosphate; PKG: protein kinase G; Ang I: angiotensin I; Ang II: angiotensin II; RAS: renin-angiotensin system; TGF-β: transforming growth factor-β; MAPK: mitogen-activated protein kinase; ECM: extracellular matrix; PI3K: phosphatidylinositol-3 kinase; Akt: serine/threonine protein kinase; JAK: janus kinase; STAT: signal transducer and activator of transcription.

    Article Snippet: The cannula was then connected to a transducer (MLT0670, BP transducer, AD Instruments, Oxford, UK), and blood pressure was continuously monitored for 10 min using the PowerLab® system (AD Instruments), with the average value calculated [ ].

    Techniques: In Vivo, Activity Assay, Expressing, Protein-Protein interactions