Bay K 8644, a voltage-sensitive calcium channel agonist, facilitates secretion of atrial natriuretic polypeptide from isolated perfused rat hearts

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Effects of Bay K 8644, a voltage-sensitive calcium channel agonist, on atrial natriuretic polypeptide (ANP) secretion from isolated rat hearts perfused with Krebs-Henseleit solution were investigated. After a ninetymin period for stabilization, coronary sinus effluents were collected every two min and ANP levels were measured by radioimmunoassay. The basal secretory rate of ANP was 1.65 ± 0.15 ng/min (mean ± standard error). Bay K 8644 stimulated ANP secretion dose-dependently. This stimulatory action was blocked by simultaneous administration of nifedipine, its competitive antagonist. Heart rate was also increased by Bay K 8644 administration. In the gel filtration study, the major secretory form of ANP corresponded to α-rat ANP, a 28-amino acid peptide. These results suggest that voltage-sensitive calcium channels are involved in two principal biological properties, contraction and ANP secretion, of atrial cardiocytes.

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    Surprisingly, Ni2+, an effective inhibitor of the Na+–Ca2+ exchanger, greatly attenuated extracellular Na+ depletion-induced intracellular Ca2+ increase but not ANP secretion (Seul et al., 2003). In fact, the role of intracellular Ca2+ in ANP secretion is controversial: an increase of ANP secretion by increasing intracellular Ca2+ and by decreasing intracellular Ca2+ has both been proposed (Ito et al., 1988; Saito et al., 1986; Schiebinger, 1989; de Bold and de Bold, 1989; Matsubara et al., 1988). The reason behind this discrepancy is not clear yet.

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    Whereas increases in Ca2+ have been demonstrated to evoke exocytosis in a number of secretory cell types, there is no clear consensus regarding a role for Ca2+ in ANP secretion. Studies using perfused rat heart or isolated atria have reported that Ca2+ has a positive role [41,42], no involvement or even a negative role in ANP release [13,43,44]. For example, ANP release was shown to be amplified by the Ca2+ channel agonist Bay K8644 in paced rat atria [45] but not effective at modulating release from quiescent atria or myocyte cultures, suggesting that basal and or stimulated release are differentially regulated [46,47].

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