Key result
External Ca2+ concentration positively modulated a component of ANP secreted by quiescent rat atria in vitro, independent of ryanodine-sensitive Ca2+ release.
External calcium concentration positively modulates stretch-augmented ANP secretion in quiescent rat atria without requiring ryanodine-sensitive calcium release from the sarcoplasmic reticulum.
Hypothesis-generating for Ca2+-dependent ANP secretion; human studies required before clinical relevance.
An in vitro noncontracting rat atrial preparation stretched at 37 degrees C by a distending pressure of 5.1 mmHg was used to examine effects of external Ca2+ concentration ([Ca2+]out, 0.05-3.0 mM) on secretion of immunoreactive atrial natriuretic peptide (ANP) in presence of saxitoxin (STX) and in presence or absence of ryanodine. Under these conditions, the time course of the amount (y) of ANP secreted per milligram dry atrium during 44 min could be approximated by a rate coefficient (k) according to the relation y = s[1 - e(-kt)], where s is the maximal amount secreted after a long time (t). Although k, the rate coefficient for stretch-augmented secretion, increased significantly as [Ca2+]out was raised, secretion inactivated progressively in a time- and [Ca2+]out-dependent manner. This time-dependent decrease was not prevented by ryanodine. We conclude that a component of ANP secreted by quiescent atria in vitro is positively modulated by [Ca2+]out and does not require ryanodine-sensitive Ca2+ release from sarcoplasmic reticulum. The [Ca2+]out-sensitive processes underlying time-dependent inactivation of secretion remain undetermined.
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Page et al. (1991) studied this question. External Ca2+ concentration ([Ca2+]out) was evaluated on Secretion of immunoreactive atrial natriuretic peptide (ANP). External Ca2+ concentration positively modulated a component of ANP secreted by quiescent rat atria in vitro, independent of ryanodine-sensitive Ca2+ release.
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