Capacitative calcium entry in parotid acinar cells

Abstract

The intracellular Ca2+ indicator, fura-2, was used to monitor changes in cytosolic [Ca2+] in parotid acinar cells. When parotid cells were incubated in a medium containing low [Ca2+], and [Ca2+] was restored to the physiological range, there was a small increase in cytosolic [Ca2+]. If, however, the cells were first activated by a muscarinic agonist, and receptor activation was terminated before the addition of Ca2+ by the addition of a pharmacological excess of the muscarinic-receptor antagonist atropine, the initial increase in cytosolic [Ca2+] was faster and transiently larger than in the control cells which had not been previously stimulated. This suggested that a stimulation of Ca2+ entry occurred owing to the prior emptying of the agonist-regulated intracellular Ca2+ pool. This extra Ca2+ influx seen in pool-depleted cells persisted even when the interval between the addition of atropine and Ca2+ was increased from 1 to 20 min. Also, when the pool was allowed to refill by adding atropine in the presence of extracellular Ca2+, and Ca2+ was then sequentially removed and restored, the rise in cytosolic [Ca2+] after the addition of extracellular Ca2+ was not rapid, and resembled the increase seen in unstimulated cells. These results indicate that, when the agonist-sensitive Ca2+ pool is emptied by an agonist, Ca2+ influx across the plasma membrane is increased. This influx of Ca2+ occurs independently of the concentrations of inositol phosphates and probably of any second messengers linked directly to receptor activation. It appears rather to be a consequence of the empty state of the Ca2+ pool. Further, we suggest that, whenever the agonist-sensitive Ca2+ pool is emptied by agonist activation, the plasma-membrane permeability to Ca2+ will be increased, and this may account, at least in part, for the phenomenon of receptor-activated Ca2+ entry.

Relaxation of rat thoracic aorta induced by the Ca2+‐ATPase inhibitor, cyclopiazonic acid, possibly through nitric oxide formation

“…Therefore, calmodulin antagonists have been proposed as useful tools for identifying the type of NO synthase involved in relaxation (Schini & Vanhoutte, 1992). In this respect, in the present experiments, it was found that the calmodulin inhibitors selectively abolished endothe-5 4 lium-dependent relaxation and increase in cyclic GMP formation induced by CPA as well as by ACh, without affecting the endothelium-independent nitroprusside-induced respon- Ca-free (Merritt & Rink, 1987;Pandol et al, 1987;Takemura & Putney, 1989;Kwan et al, 1990;Mertz et al, 1990; :opiazonic acid 1990; Demaurex et al, 1992;Low et al, 1992 brane Ca2"' channels subsequent to depletion by CPA of stored Ca2" may activate NO synthase.…”

Calcium Signaling in Airway Smooth Muscle

“…It is probable that localized SR calcium depletion could limit agonist-elicited SR quantal release. Calcium influx can occur through a variety of mechanisms, including voltage-and receptor-operated membrane channels, and store-operated calcium entry (SOCE) (1,6,(26)(27)(28)(29). Calcium influx by SOCE is triggered by depletion of the intracellular stores and may be influenced by the second messenger systems eliciting calcium release (30).…”

Regulation of store-operated Ca2+entry by CD38 in human airway smooth muscle

“…In the last case, store-operated Ca 2ϩ entry (SOCE) is triggered by depletion of SR Ca 2ϩ stores (6,41,42,49,55,56). We and others have shown that different transient receptor potential channel (TRPC) isoforms are expressed in ASM (6,58).…”