ArticleThe Journal of pharmacology and experimental therapeutics2009
Role of protein kinase Czeta and calcium entry in KCl-induced vascular smooth muscle calcium sensitization and feedback control of cellular calcium levels.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Enhanced KCl-mediated contractility and CaAmerican journal of physiology. Heart and circulatory physiology · 2020Article
- Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease.Biochemical pharmacology · 2018Review
- Physiological vs. pharmacological signalling to myosin phosphorylation in airway smooth muscle.The Journal of physiology · 2017Article
- Chemerin-induced arterial contraction is GVascular pharmacology · 2017Article
- Metabolic Stress-Induced Activation of AMPK and Inhibition of Constitutive Phosphoproteins Controlling Smooth Muscle Contraction: Evidence for Smooth Muscle Fatigue?Frontiers in physiology · 2017Article
- Protein Kinase C as Regulator of Vascular Smooth Muscle Function and Potential Target in Vascular Disorders.Advances in pharmacology (San Diego, Calif.) · 2017Review
- The effects of Ginseng Java root extract on uterine contractility in nonpregnant rats.Physiological reports · 2014Article
- Sealing of transected neurites of rat B104 cells requires a diacylglycerol PKC-dependent pathway and a PKA-dependent pathway.Cellular and molecular neurobiology · 2013Article
- Contribution of transient and sustained calcium influx, and sensitization to depolarization-induced contractions of the intact mouse aorta.BMC physiology · 2012Article
- Rho-kinase inhibition attenuates calcium-induced contraction in β-escin but not Triton X-100 permeabilized rabbit femoral artery.Journal of muscle research and cell motility · 2011Article
- Active tension adaptation at a shortened arterial muscle length: inhibition by cytochalasin-D.American journal of physiology. Heart and circulatory physiology · 2011Article
- Failure of Bay K 8644 to induce RhoA kinase-dependent calcium sensitization in rabbit blood vessels.British journal of pharmacology · 2010Article
- Carbachol-induced rabbit bladder smooth muscle contraction: roles of protein kinase C and Rho kinase.American journal of physiology. Renal physiology · 2009Article
- Calcium-independent phospholipase A2 participates in KCl-induced calcium sensitization of vascular smooth muscle.Cell calcium · 2009Article
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2 authors at 1 institution in 1 country.
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Abstract
The degree of tonic force (F) maintenance induced in vascular smooth muscle upon K(+) depolarization with 110 mM KCl can be greatly reduced by inhibition of rhoA kinase (ROCK). We explored the possibility that a protein kinase C (PKC) isotype may also play a role in causing KCl-induced Ca(2+) sensitization. In isometric rings of rabbit artery, the PKC inhibitors, Go-6983 (3-[1-[3-(dimethylamino)propyl]-5-methoxy-1H-indol-3-yl]-4-(1H-indol-3-yl)-1H-pyrrole-2,5-dione), GF-109203X (2-[1-(3-dimethylaminopropyl)indol-3-yl]-3-(indol-3-yl) maleimide), and a cell-permeable (myristoylated) pseudosubstrate inhibitor of PKCzeta (PI(PKCzeta)) inhibited KCl-induced tonic F. A myristoylated pseudosubstrate inhibitor of PKCalpha/beta that inhibited phorbol dibutyrate-induced F slightly potentiated KCl-induced tonic F and attenuated 30 mM KCl-induced F. Although the ROCK inhibitor, H-1152 [(S)-(+)-2-methyl-1-[(4-methyl-5-isoquinolinyl)-sulfonyl]-hexahydro-1H-1,4-diazepine dihydrochloride], reduced basal phosphorylation of myosin light-chain phosphatase-targeting subunit at Thr853 (MYPT1-pT853), 3 and 10 muM GF-109203X inhibited only KCl-stimulated phosphorylation, not basal MYPT1-pT853. In fura-2-loaded tissues, GF-109203X and PI(PKCzeta) elevated basal [Ca(2+)](i) (calcium) and potentiated KCl-induced tonic increases in calcium while reducing KCl-induced tonic increases in F. Blockade by nifedipine of Ca(2+) entry through voltage-operated Ca(2+) channels reduced KCl-induced Ca(2+) sensitization and KCl-stimulated but not basal MYPT1-pT853. These data together support a model in which ROCK and PKCzeta are constitutively active and function in "resting" muscle to regulate the basal levels of MYPT1-pT853 and calcium, respectively. In this model, KCl-induced increases in calcium activate PKCzeta to feed forward and cause additional MYPT1-pT853 above that induced by constitutive ROCK, permitting Ca(2+) sensitization and strong F maintenance. Active PKCzeta also feeds back to attenuate the degree of KCl-induced increases in calcium.
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