Atrial natriuretic peptide(ANP) is a hormone with potent natriuretic, diuretic and relaxing properties on vascular smooth muscle. Specific chemical modulator in response for the ANP secretion has not been found yet. Therefore, we have investigated the role of Ca^(2+) responsible for the regulation of ANP induced by protein kinase C(PKC) on mechanically stretch-induced ANP secretion in the rat atria. The results obtained were as follows ;
1. ANP secretion and ANP concentration were increased to more in Ca^(2+) -free buffer than in the Kreb-Henseleit buffer on mechanically stretch-induced ANP secretion(p $lt; 0.05), but extracellular fluid translocation(ECF) was not significant. Phorbol 12-myristate 13-acetate(PMA, 10^(-7)M) induced ANP secretion and ANP concentration in Ca^(2+)-free buffer shown to more accentuate on mechanically stretch-induced ANP secretion than in the Ca^(2+)-free buffer(p $lt; 0.05), but ECF translocation was not significant.
2. In the presence of ryanodine(3 × 10^(-6)M), PMA(10^(-7)M) induced ANP secretion and ANP concentration in the Kreb-Henseleit buffer were shown to more increase on mechanically stretch-induced ANP secretion than in the ryanodine(3 × 10^(-6)M) with the Kreb-Henseleit buffer(p $lt; 0.05), but ECF translocation was not significant.
3. In the presence of ryanodine(3 × 10^(-6)M), PMA(10^(-7)M) induced ANP secretion and ANP concentration in the Ca^(2+)-free buffer was shown to more increase on mechanically stretch-induced ANP secretion than in the ryanodine(3 × 10^(-6)M) with the Ca^(2+)-free buffer on mechanically induced ANP secretion(p $lt; 0.05), but ECF translocation was not significant.
The results suggest that PKC-induced ANP secretion may not be related to the change of Ca^(2+) on mechanically induced ANP secretion in the rat atria.
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