A calmodulin antagonist (W-7) and a protein kinase C inhibitor (H-7) have no effect on atrial natriuretic peptide release induced by atrial stretch

Ishida, Akihiro; Tanahashi, Tamotsu; Okumura, Kenji; Hashimoto, Hidekazu; Itō, Takayuki; Ogawa, Kouichi; Satake, Tatsuo

doi:10.1016/0024-3205(88)90445-6

Cited by 15 publications

(6 citation statements)

References 24 publications

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“…Release was inhibited by W-7, a calmodulin antagonist, and H-7, a protein kinase C inhibitor. By contrast, when secretion was stimulated by atrial stretch, it was not inhibited by either W-7 or H-7 (Ishida et al, 1988).…”

Section: Action Of Neuromimetics On Anp Releasecontrasting

confidence: 50%

“…The presence of more than one mechanism could help to clarify the complicated picture of secretion of this hormone. Phenylephrine, an alpha 1-adrenergic agonist which activates the polyphosphoinositide system, and consequently both the diacylglycerol-protein kinase C system and the Ca2+-Ca2+ receptor system, has been reported to stimulate A " release in a dosedependent manner (Ishida et al, 1988). Release was inhibited by W-7, a calmodulin antagonist, and H-7, a protein kinase C inhibitor.…”

Section: Action Of Neuromimetics On Anp Releasementioning

confidence: 98%

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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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Section: Action Of Neuromimetics On Anp Releasecontrasting

confidence: 50%

Section: Action Of Neuromimetics On Anp Releasementioning

confidence: 98%

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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“…Isoprenaline (a P-adrenoreceptor agonist) has been reported variously to increase (Ruskoaho and Leppaluoto, 1988) and have no effect upon ANP release (Sonnenberg et al, 1984;Currie and Newman, 1986). Similarly phenylephrine (an a-adrenoreceptor agonist) has been reported by some groups to increase release (Currie and Newman, 1986;Ishida et al, 1988;Onwochei and Rapp, 1988) and by others to have no effect (Ferrari and Agnoletti, 1989). Acetylcholine has also been reported to increase ANP release (Sonnenberg et al, 1984), although other groups have again reported no change (Garcia et al, 1986).…”

Section: Discussionmentioning

confidence: 91%

“…For example, there is conflicting evidence concerning the involvement of a-and padrenoreceptors (Sonnenberg et al, 1984;Currie and Newman, 1986;Ishida et al, 1988;Onwochei and Rapp, 1988;Ruskoaho and Leppaluoto, 1988;Ferrari and Agnoletti, 1989), opioid receptors (Tang et al, 1987;Ferrari and Agnoletti, 19891, and acetylcholine receptors (Garcia et al, 1986;Sonnenberg et al, 1984) when release is stimulated. Furthermore, the precise roles of protein kinase C (Ishida et al, 1988;Matsubara et al, 1988) and calcium (Blochetal, 1988;De Bold and De Bold, 1988;Saito et al, 1986;Page et al, 1991) in ANP release remains to be clarified. Although interpretation of these findings is complicated by the different types of preparations used, a n independent ultrastructural measure of granule exocytosis would aid our understanding of the factors affecting ANP release and the mechanisms involved at the level of the individual my ocyte .…”

mentioning

confidence: 96%

Stretch and anesthetic dependency of atrial natriuretic peptide release demonstrated by an ultrastructural assay

Newman¹,

Severs²

1993

Journal Cellular Physiology

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Using an ultrastructural assay developed to quantify the secretion of atrial natriuretic peptide-containing granules, release of the hormone, in response to different degrees of atrial distension, is directly demonstrated at the cellular level. The ultrastructural assay developed uses an in situ tannic acid perfusion technique to arrest the exocytosis of atrial granules in the anesthetized rat. Secretory granules, which retain the capacity to undergo exocytosis throughout a 30-minute tannic acid perfusion, accumulate at the cell surface in a state of fusion with the plasma membrane, with the core contents retained. Quantification of arrested granules thus provides a measure of the rate of granule release and allows the responses to different stimuli to be assessed. By altering the height of the perfusate, perfusion pressure and hence the degree of distension of the right atrium can be increased, and this causes a proportional rise in the release of secretory granules from individual myocytes. An anesthetic regime incorporating fentanyl citrate was found to increase significantly the rate of granule release, and this was further augmented by atrial distension. Quantification of the numbers of cytoplasmic granules under the same conditions did not reveal a reduction in granules. This is thought to be because only a small pool of granules is recruited for exocytosis, and granule production may continue during the perfusion period. Our assay of atrial secretory granule release allows the effect of a variety of stimulatory and inhibitory agents to be assessed directly at the cellular level and provides an independent comparison with previous biochemical data from whole animal and isolated organ studies.

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“…This finding may be explained by previously reported observations that the stretch-secretion coupling mechanism is different and independent from other stimulussecretion mechanisms. 21 Known second messenger systems such as phosphatidyl inositol bisphosphate, protein kinase C, and cyclic adenosine 3',5' monophosphate, which are mechanisms of adrenergic stimulusresponse coupling, 22 do not appear to play a role in stretch-mediated secretion.…”

Section: Discussionmentioning

confidence: 99%

Alterations in the secretion of atrial natriuretic factor in atria from aged rats.

1992

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We measured plasma atrial natriuretic factor levels and atrial natriuretic factor secretion by isolated left atria from aging rats to determine the secretory response to stretch and adrenergic stimulation. Systolic arterial pressure and right atrial pressure were measured in vivo. Twenty-four hours later, atria were removed and studied in vitro in a perifusion system. After removal, stabilization at 0.7 g tension, and equilibration for 65 minutes, atria were stretched by increasing external tension for 20 minutes. After reequilibration atria were perifused with phenylephrine, 10~: M, for an additional 30 minutes. Right atrial pressure was not different between young (3 months) and aged (16-24 months) rats. Aged rats had higher plasma atrial natriuretic factor levels (52±8 versus 21±6 pmol/l;p<0.05) than young rats. Basal atrial natriuretic factor secretory rate in vitro was greater in atria from aged rats than young rats (875±35 versus 402±22 pg/min; p<0.05). Atria from aged rats had an increased response to phenylephrine compared with young rats (1,687±143 versus 788±113 pg/min; p<0.05) when means were adjusted for basal secretory rate. The secretory response to stretch was less than that of young rats (673 ±37 versus 773±27 pg/min), although this difference was not significant (p=0.07). Atrial natriuretic factor secretion in response to adrenergic stimulation is increased with aging, and these secretory responses may contribute to increased plasma levels that occur during aging. In contrast to increased adrenergic responses, atrial natriuretic factor secretion after external stretch is not increased in aging rats. (Hypertension 1992,20:85-88) KEY WORDS • atrial natriuretic peptides • age factors • phenylephrine • rat studies P lasma levels of atrial natriuretic factor (ANF) are elevated in healthy elderly people compared with young individuals, 1 " 5 but the factors responsible for these increased levels have not been determined. Previous data have suggested that direct alterations in atrial dimension play an important role in the regulation of ANF secretion. 6 A number of clinical conditions such as essential hypertension, 7 congestive cardiomyopathy, 89 chronic renal failure, 10 rapid volume expansion, 1112 and tachycardia syndromes 13 are associated with increases in both atrial pressure and ANF secretion. This suggests that direct atrial stretch can stimulate ANF secretion. In addition, secretion of ANF is greatly increased by adrenergic stimulation in vitro.14 To evaluate changes in atria that occur with aging and their possible contributions to altered ANF secretion, we measured changes in ANF secretion in atria from aging rats to determine the secretory response to stretch and adrenergic stimulation. Supported by a fellowship support grant from the Hartford Foundation, by grant HL-18575 from the National Heart, Lung, and Blood Institute, and by support from the American Heart Association and its Indiana Affiliate, Inc. J.D. performed this work during the tenure of a Clinician-Scientist Award from the...

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A calmodulin antagonist (W-7) and a protein kinase C inhibitor (H-7) have no effect on atrial natriuretic peptide release induced by atrial stretch

Cited by 15 publications

References 24 publications

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

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

Stretch and anesthetic dependency of atrial natriuretic peptide release demonstrated by an ultrastructural assay

Alterations in the secretion of atrial natriuretic factor in atria from aged rats.

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