Biphasic effects of Ca2+ on IP3 receptor function are common and widely
supposed to contribute to the complex Ca2+ signals recorded from intact
cells. I will present evidence from both functional and structural
analyses of IP3 receptors suggesting that IP3 controls the opening of the
channel by regulating Ca2+ binding to stimulatory and inhibitory
Ca2+-binding sites. Ca2+ entry across the plasma membrane also contributes
to the Ca2+ signals evoked by physiological stimuli. I will discuss recent
results from A7r5 vascular smooth muscle cells showing that vasopressin
reciprocally regulates Ca2+ entry through capacitative and
non-capacitative Ca2+ entry channels via a signalling cascade that
involves arachidonic acid, nitric oxide and
cGMP.
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