Interaction between stretch and hormonally stimulated atrial natriuretic peptide secretion

Schiebinger, Rick J.; Greening, Karen

doi:10.1152/ajpheart.1992.262.1.h78

Cited by 17 publications

(11 citation statements)

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“…Therefore, as a marker for stimulation of the fetal gene program that is a virtually universal finding in cardiac hypertrophy, 30 we measured ANP release for 1 hour after Ang II or androgen addition to the cultures. Figure 5 demonstrates that Ang II augments ANP release from myocytes.…”

Section: Functional Analysis Of Signal Transduction By the Androgen Rmentioning

confidence: 99%

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

et al. 1998

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Background-The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain.Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response. Methods and Results-We used reverse transcription-polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [ 3 H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion. Conclusions-Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.(Circulation. 1998;98:256-261.)

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Section: Functional Analysis Of Signal Transduction By the Androgen Rmentioning

confidence: 99%

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

et al. 1998

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“…The modulating role of the EE has recently been demonstrated by studies showing that the removal of the endocardium results in a negative inotropic effect on myocardial contraction (1,3,6). Another function of the EE is the release of endothelial-derived relaxing factor (EDRF) and of endothelin, which seem to be involved in the secretion of atrial natriuretic factor from atrial myocytes (7)(8)(9).…”

mentioning

confidence: 99%

Ca2+ influx through stretch-activated cation channels activates maxi K+ channels in porcine endocardial endothelium.

Hoyer

Distler

Haase

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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The endocardial endothelium is an important modulator of myocardial function. The present study demonstrates the existence of a stretch-activated Ca2+-permeable cation channel and of a Ca2+-activated K+ channel in the endocardial endothelium of the porcine right atrium. The stretch-activated channel is permeable for K+, Na+, Ca2+, and Ba2+, with mean conductances of z32 pS for the monovalent cations and -13 pS for divalent cations. The Ca2+-activated K+ channel has a mean conductance of 192 pS in symmetrical KCI solution. Channel activity is strongly dependent on membrane potential and the cytosolic Ca2+ concentration. Halfmaximal activation occurs at a cytosolic Ca2+ concentration of -5 pM. The influx of Ca2+ through the stretch-activated channel is sufficient to activate the Ca2+-activated K+ channel in cell-attached patches. Upon activation of the stretchactivated channel, the cytosolic Ca2+ concentration increases, at least locally, to values of =0.5 #M, as deduced from the open probability of the Ca2+-dependent K+ channel that was activated simultaneously. The stretch-activated channels are capable of inducing an intracellular Ca2+ signal and may have a role as mechanosensors in the atrial endothelium, possibly activated by atrial overload.The cavitary side of the atrial and ventricular wall of the heart is covered by the endocardial endothelium (EE). A monolayer of endothelial cells adheres to a basal membrane overlying layers of collagen and elastic fibers (1). There is growing evidence that the EE modulates myocardial function (2, 3) and the vascular endothelium regulates vascular function (4, 5) in similar ways. The modulating role of the EE has recently been demonstrated by studies showing that the removal of the endocardium results in a negative inotropic effect on myocardial contraction (1,3,6). Another function of the EE is the release of endothelial-derived relaxing factor (EDRF) and of endothelin, which seem to be involved in the secretion of atrial natriuretic factor from atrial myocytes (7-9).Studies in vascular endothelium have demonstrated that the EDRF release is not only regulated by various humoral factors but also by physical stimuli such as shear stress or flow (10, 11). For instance, increased shear stress or flow induces an increased release of EDRF by the endothelium and a subsequent vasodilation (10). A mechanism through which shear stress could be coupled to EDRF release and vasodilation may be the activation of stretch-activated cation channels (SACs) that act as "mechanotransducers" (12). The SACs presumably act as a gate to Ca2+ influx into endothelial cells (12)(13)(14) and, therefore, might trigger the intracellular formation of EDRF by Ca2+-dependent synthetases (15, 16).The endothelial release of EDRF has also been shown to be regulated by the cell membrane potential (17). Hyperpolarization induced by activation of K+ channels has been demonstrated to enhance Ca2+ influx into endothelial cells and the release of EDRF.In contrast, to our knowledge, the electrophysiologi...

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“…An ability to target both granular and secretagogue-activated pools of ANP could explain why endothelin is such a potent secretagogue for A". Independence of a secondary pool from the main regulated granule pool could also explain why phenylephrine and other drugs such as phorbol esters, which activate protein kinase C directly, have an additive effect upon stretch-activated release (Schiebinger and Greening, 1992;Ruskahao, 19921, which does not appear to share this protein kinase C dependence.…”

Section: Are There Two Pools Of Anp?mentioning

confidence: 99%

Effect of neuromimetics upon the release of atrial natriuretic peptide granules: Are multiple pathways involved in secretion?

Newman

Severs

1996

J. Cell. Physiol.

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The release of atrial natriuretic peptide (ANP) in response to the application of neurohumoral agonists (neuromimetics) is directly demonstrated and quantified at the cellular level, using an ultrastructural assay developed to quantify secretion. The assay uses an in situ tannic acid perfusion technique to arrest the exocytosis of atrial secretory granules in the anesthetized rat. The animal is perfused with the neuromimetic, and secretory granules, which retain the capacity to undergo exocytosis throughout the subsequent 30 min tannic acid perfusion, accumulate at the cell surface in a state of fusion with the plasma membrane. Quantification of arrested granules thus provides a measure of the rate of granule release and allows the responses to different agents to be assessed. The actions of three different agents were investigated: isoproterenol, phenylephrine, and acetylcholine. In previously published studies, investigations of the actions of these agents on ANP release has produced unclear and sometimes contradictory results. Using our ultrastructural assay, it was found that during the 30 min perfusion period neither isoprenaline nor phenylephrine caused a significant change in the rate of secretory granule release, whereas acetylcholine significantly decreased the rate of granule release. A new model of secretion is proposed to integrate these findings with previous results and help clarify the complex picture of atrial natriuretic peptide release.

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Interaction between stretch and hormonally stimulated atrial natriuretic peptide secretion

Cited by 17 publications

References 0 publications

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes

Ca2+ influx through stretch-activated cation channels activates maxi K+ channels in porcine endocardial endothelium.

Effect of neuromimetics upon the release of atrial natriuretic peptide granules: Are multiple pathways involved in secretion?

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