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- W1999738210 abstract "A trial natriuretic peptide (ANP) is synthesized and stored within atrial myocytes, and released in response to increased atrial pressure. It possesses vasodilator properties and inhibits the renin-angiotensin-aldosterone system. Little is known about the mechanism of release of ANP. Radioimmunoassay of ANP has shown that its concentration is elevated in patients with congestive heart failure and during paroxysm of supraventricular tachycardia. Experimentally, ANP concentrations can be increased by either left atrial or right atrial distension, suggesting that stretch of the atrial myocytes is the stimulus for release.1,2 The increase of ANP levels during paroxysmal tachycardia suggests that the rate of atrial contraction is an additional stimulus for release. Schiebinger and Linden3 showed that rapid pacing of suspended rat atria increases ANP secretion and concluded that the frequency of atrial contraction directly influences the rate of ANP secretion. To test whether atrial contraction is a prerequisite for ANP secretion, we measured the ANP concentration in patients with atrial paralysis paced with ventricular-demand (VVI) units." @default.
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- W1999738210 date "1989-03-01" @default.
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- W1999738210 title "Relation of atrial natriuretic peptide release to atrial contraction" @default.
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- W1999738210 doi "https://doi.org/10.1016/0002-9149(89)90268-3" @default.
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