Key result
Histamine pretreatment reduced net transsarcolemmal Ca2+ flux into porcine carotid artery smooth muscle in response to 40 mM KCl, with CPA-insensitive mechanisms dominating the desensitization.
Why the study?
Does cyclopiazonic acid (CPA) abolish the transient attenuation of the increase in [Ca2+]i in histamine-desensitized porcine carotid artery smooth muscle exposed to KCl?
Population
Porcine carotid artery smooth muscle (PCASM)
Comparison
40 mM KCl in the presence of cyclopiazonic acid… vs Tissues not treated with CPA
Design
Preclinical
Authors
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Histamine desensitization of vascular Ca2+ flux occurs via CPA-insensitive pathways in porcine arteries; leaves open relevance to human smooth-muscle regulation.
Does cyclopiazonic acid (CPA) abolish the transient attenuation of the increase in [Ca2+]i in histamine-desensitized porcine carotid artery smooth muscle exposed to KCl?
Histamine pretreatment reduces net transsarcolemmal Ca2+ flux into porcine carotid artery smooth muscle in response to KCl, primarily through CPA-insensitive mechanisms rather than SR Ca2+ depletion.
Wardle et al. (1998) studied this question. Cyclopiazonic acid (CPA) vs. Tissues not treated with CPA was evaluated on Rate of force generation and [Ca2+]i in response to 40 mM KCl. Histamine pretreatment reduced net transsarcolemmal Ca2+ flux into porcine carotid artery smooth muscle in response to 40 mM KCl, with CPA-insensitive mechanisms dominating the desensitization.
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