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Agonist-Dependent Depolarization

There are several potential mechanisms for agonist-induced depolarization (1) ATP (via the P2x receptor) and carbachol reportedly open nonspecific cation [Pg.229]

2-nitro-4-carboxyphenyl-N, N-diphenylcarbamate (NCDC, a phospholipase C inhibitor) in rabbit basilar artery (Clark and Garland, 1993). These results suggest that agonist-dependent depolarization does not depend on Ca + influx, activation of protein kinase C, or activation of phospholipase C. There is also a feedback mechanism for depolarization increases in [Ca +]i, per se, appear to inhibit depolarization by [Ca2+]j-dependent activation of K a (BK) channels (Brayden and Nelson, 1992). [Pg.229]

Agonists Induce Higher Force Than Expected from the Degree of Depolarization [Pg.229]

Endothelial-derived relaxing factor (EDRF) (e.g., nitric oxide) and the atrial natriuretic factor(s) increase [cGMP] in smooth muscle. They relax arterial smooth muscle by three mechanisms decreasing [Ca +Jj, decreasing the [Ca2+]i sensitivity of phosphorylation, and uncoupling force from myosin phosphorylation (the latter two are pharmacomechanical mechanisms  [Pg.229]

cGMP-Dependent H)q erpolarization Resulting in Decreased Ca + Influx [Pg.230]

See other pages where Agonist-Dependent Depolarization is mentioned: [Pg.229]    [Pg.229]    [Pg.229]    [Pg.229]    [Pg.231]    [Pg.229]    [Pg.229]    [Pg.229]    [Pg.229]    [Pg.231]    [Pg.229]    [Pg.614]    [Pg.86]    [Pg.19]    [Pg.296]    [Pg.658]    [Pg.313]    [Pg.275]    [Pg.225]    [Pg.226]    [Pg.271]    [Pg.388]    [Pg.82]    [Pg.208]    [Pg.38]    [Pg.89]    [Pg.96]    [Pg.245]    [Pg.62]    [Pg.1786]    [Pg.137]    [Pg.56]    [Pg.329]    [Pg.379]    [Pg.380]    [Pg.436]    [Pg.486]    [Pg.508]    [Pg.386]    [Pg.487]    [Pg.242]    [Pg.184]    [Pg.66]    [Pg.73]    [Pg.219]    [Pg.88]    [Pg.296]    [Pg.658]    [Pg.56]    [Pg.64]    [Pg.184]    [Pg.173]   


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Calcium channels agonist-dependent depolarization

Depolarization

Depolarizer (

Depolarizers

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