Stretch-stimulated ANF secretion: Are the ATP-sensitive potassium channels the missing link?

Abstract

See article by Saegusa et al. [9] (pages 60–68) in this issue . In 1981, de Bold et al. reported that the administration of atrial extracts to rats induced diuresis and natriuresis [1]. Soon afterwards, the substance with diuretic and natriuretic properties present in the atrial extracts was identified as the atrial natriuretic peptide (ANF) [2]. This important discovery led to the new concept that the heart was not only a mechanical pump but also an endocrine organ. Since the characterization of ANF, many reports appeared in the literature describing a wide spectrum of biological actions displayed by this peptide supported by the wide distribution of the receptors in different tissues and cell types. Other natriuretic peptides were also characterized: BNP and CNP. The family of natriuretic peptides plays a relevant role in the regulation of sodium and water as well as in cardiovascular homeostasis. ANF is synthesized, stored and secreted by mammalian atrial cardiocytes. The peptide is continuously released from the heart but appropriate mechanical (atrial stretch) or neuroendocrine (endothelin-1 or α1 adrenergic stimulation) stimuli enhance the rate of release with or without a concomitant increase in the synthesis [3]. Although many factors modulate the release of ANF, the major physiological stimulus is atrial stretch evoked by hemodynamic changes. Stretch secretion coupling results in an immediate increase of ANF secretion, but this … *Tel.: +54 11 4964 8268x37. Email address: lbianc{at}ffyb.uba.ar