ArticleProceedings of the National Academy of Sciences of the United States of America2005
Receptor-induced depletion of phosphatidylinositol 4,5-bisphosphate inhibits inwardly rectifying K+ channels in a receptor-specific manner.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 82 citations in OpenAlex.
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- Direct modulation of TRPC ion channels by Gα proteins.Frontiers in physiology · 2024Review
- Selective Inhibition of Pulmonary Vein Excitability by Constitutively Active GIRK Channels Blockade in Rats.International journal of molecular sciences · 2023Article
- Involvement of CaCellular and molecular neurobiology · 2023Article
- Ionic signalling mechanisms involved in neurokinin-3 receptor-mediated augmentation of fear-potentiated startle response in the basolateral amygdala.The Journal of physiology · 2022Article
- Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022Review
- Roles of PLCβ, PIPJournal of cellular physiology · 2022Article
- Ionic and signaling mechanisms involved in neurotensin-mediated excitation of central amygdala neurons.Neuropharmacology · 2021Article
- Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH.American journal of physiology. Cell physiology · 2021Article
- Involvement of TRPC5 channels, inwardly rectifying KThe Journal of physiology · 2021Article
- Phosphoinositides: Roles in the Development of Microglial-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- PIPProceedings of the National Academy of Sciences of the United States of America · 2020Review
- Distinct functional properties of two electrogenic isoforms of the SLC34 Na-Pi cotransporter.Physiological reports · 2019Article
- PIPeLife · 2018Article
- Endothelial GqPCR activity controls capillary electrical signaling and brain blood flow through PIPProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Lipid signaling to membrane proteins: From second messengers to membrane domains and adapter-free endocytosis.The Journal of general physiology · 2018Review
- Does PKC activation increase the homologous desensitization of μ opioid receptors?British journal of pharmacology · 2015Article
- Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Phosphatidylionsitol 4,5-bisphosphate (PIP(2)), a substrate of phospholipase C, has recently been recognized to regulate membrane-associated proteins and act as a signal molecule in phospholipase C-linked Gq-coupled receptor (GqPCR) pathways. However, it is not known whether PIP(2) depletion induced by GqPCRs can act as receptor-specific signals in native cells. We investigated this issue in cardiomyocytes where PIP(2)-dependent ion channels, G protein-gated inwardly rectifying K(+) (GIRK) and inwardly rectifying background K(+) (IRK) channels, and various GqPCRs are present. The GIRK current was recorded by using the patch-clamp technique during the application of 10 microM acetylcholine. The extent of receptor-mediated inhibition was estimated as the current decrease over 4 min while taking the GIRK current (I(GIRK)) value during a previous stimulation as the control. Each GqPCR agonist inhibited I(GIRK) with different potencies and kinetics. The extents of inhibition induced by phenylephrine, angiotensin II, endothelin-1, prostaglandin F2alpha, and bradykinin at supramaximal concentrations were (mean +/- SE) 32.1 +/- 0.6%, 21.9 +/- 1.4%, 86.4 +/- 1.6%, 63.7 +/- 4.9%, and 5.7 +/- 1.9%, respectively. GqPCR-induced inhibitions of I(GIRK) were not affected by protein kinase C inhibitor (calphostin C) but potentiated and became irreversible when the replenishment of PIP(2) was blocked by wortmannin (phosphatidylinositol kinase inhibitor). Loading the cells with PIP(2) significantly reduced endothelin-1 and prostaglandin F2alpha-induced inhibition of I(GIRK). On the contrary, GqPCR-mediated inhibitions of inwardly rectifying background K(+) currents were observed only when GqPCR agonists were applied with wortmannin, and the effects were not parallel with those on I(GIRK). These results indicate that GqPCR-induced inhibition of ion channels by means of PIP(2) depletion occurs in a receptor-specific manner.
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