Studies on the relationship between the catecholamine distribution in the atrium and the specific granules present in atrial muscle cells: 1. Isolation of a purified specific granule subfraction

Bold, Adolfo J. de; Bencosme, Sergio A.

doi:10.1093/cvr/7.3.351

Cited by 23 publications

(4 citation statements)

References 14 publications

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“…The granules were similar to those found in other organs that secrete peptide hormones [13,14]. The first hint that ANP secretion might be physiologically regulated was observed by De Bold [15] who showed that atrial granularity decreased significantly in rats on 2% NaCl plus mineralocorticoids while granularity increased in both water restricted or NaCl restricted rats.…”

Section: Atrial Distensionsupporting

confidence: 76%

Mechanisms of atrial natriuretic peptide secretion from the atrium

Dietz

2005

Cardiovascular Research

155

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Since the discovery of atrial natriuretic peptide (ANP) more than 20 years ago, numerous studies have focused on the mechanisms regulating ANP secretion. From a physiological standpoint, the most important factor governing ANP secretion is mechanical stretching of the atria, which normally occurs when extracellular fluid volume or blood volume is elevated. In addition, the ability of several vasoconstrictors to increase ANP secretion can be traced to their indirect effects on atrial stretch via increases in cardiac preload or afterload. Whether vasoconstrictors such as angiotensin II and vasopressin have a direct positive or negative effect on ANP secretion has not been determined with certainty. Two paracrine factors derived from endothelial cells play important roles in modulating ANP secretion. Endothelin, a potent vasoconstrictor, stimulates ANP secretion and augments stretch induced ANP secretion. The dramatic increase in ANP release produced by cardiac ischemia appears to be mediated in part by endothelin. Nitric oxide (NO), an important vasodilator, is also produced by endothelial cells and inhibits ANP secretion acting through cyclic GMP as an intracellular messenger. Several recent studies have helped to define the cellular mechanism contributing to regulation of ANP secretion including stretch-activated ion channels, prostaglandins, cytochrome P450, G proteins and cell calcium. A number of steps in the cellular transduction of the ANP signal remain to be resolved. The release of ANP in disease states such as myocardial infarction and heart failure appears to be related to both mechanical and cellular events.

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Section: Atrial Distensionsupporting

confidence: 76%

Mechanisms of atrial natriuretic peptide secretion from the atrium

Dietz

2005

Cardiovascular Research

155

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“…The heavier ANF peak probably represent mature granules (49), whereas the lighter fraction, which sediments in the region of the Golgi marker galactosyl transferase, probably represents ANF immunoreactivity associated with Golgi complex components. However, the highest purification of G o ␣ took place in a region of the gradient that is of lighter density than either the Golgi marker or ANF, thus suggesting that the association between ANF and G o ␣ is not quantitatively as important as the association of G o ␣ with lower density subcellular elements.…”

Section: Discussionmentioning

confidence: 99%

Participation of G Proteins in Natriuretic Peptide Hormone Secretion from Heart Atria

Bensimon¹,

Chang²,

Bold³

et al. 2004

Endocrinology

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The involvement of G proteins in the mechanism underlying the increased atrial natriuretic factor (ANF) secretion observed after atrial muscle stretch (stretch-secretion coupling) was assessed using a combined pharmacological, immunocytochemical, and tissue fractionation approach. It was found that G(i/o) inhibition by pertussis toxin (PTX) abolished stretch-secretion coupling without affecting baseline secretion through a mechanism that is independent of G(q) signaling agonists. Mastoparan-7, a G(i/o) agonist, significantly increased ANF secretion even in the absence of muscle stretch through a PTX-sensitive mechanism. By confocal and electron immunocytochemistry, ANF and G(o) partially colocalized, whereas ultracentrifugation analysis suggested the presence of two populations of granules, one of which was partially associated with G(o), as demonstrated by Western blotting. PTX did not affect basal or endothelin-1-stimulated ANF secretion, in line with the view that endothelin-1 signals mainly through G(q). It is concluded there are at least two types of regulated secretory processes in atrial cardiocytes: one is acutely responsive to muscle stretch and is PTX sensitive, and the other is G(q)mediated and PTX insensitive and may be responsible for changes in secretion after chronic changes in the neuroendocrine environment.

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“…Regardless of salt, when BP values are low, it is clear that the renin-angiotensin-aldosterone and sympathetic nervous systems are key for restoring homeostasis. 108 With volume expansion, natriuretic peptides initially described by de Bold and Bencosme 109,110 also have been proposed as important for maintenance of BP. Although several important hormonal and cytokine systems have been implicated and intensively studied by laboratories across the world, 111,112 we will focus this review on another factor, collectively referred to as the cardiotonic steroids (CTS; also called endogenous digitalis-like substances), 113 which are emerging as a class of hormones mechanistically linked to natriuresis.…”

Section: Molecular Physiological and Pathophysiological Studiesmentioning

confidence: 99%