Mechanisms Involved in the Stimulation of Aldosterone Production by Angiotensin Ii, Vasopressin and Endothelin

Woodcock, Elizabeth A.; Tanner, Jennifer K.; Caroccia, L.; Little, Peter J.

doi:10.1111/j.1440-1681.1990.tb01318.x

Cited by 20 publications

(6 citation statements)

References 14 publications

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“…In all responding cells, ET-1 provoked a biphasic increase in [Ca 2ϩ ] i consisting of an immediate and transient peak followed by a plateau phase. A similar effect of ET-1 has previously been described in human (30), rat (31), and rabbit glomerulosa cells (29). The abrupt arrest of the plateau phase of the response usually observed 2-4 min after application of ET-1 can be ascribed either to ET A receptor internalization or to PKA inactivation.…”

Section: Effect Of Et-1 On [Ca 2ϩ ] Isupporting

confidence: 75%

Activation of EndothelinA Receptors in Frog Adrenocortical Cells Stimulates Both Calcium Mobilization from Intracellular Stores and Calcium Influx through L-Type Calcium Channels

et al. 2005

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We have previously shown that endothelin (ET)-1 stimulates corticosterone and aldosterone secretion by the frog adrenal gland through activation of ETA receptors positively coupled to both the adenylyl cyclase and phospholipase C (PLC) pathways. The purpose of the present study was to investigate the involvement of calcium in ET-1-induced stimulation of corticosteroid secretion. Cytoautoradiographic labeling using [125I]ET-1 as a tracer revealed the presence of ET-1 binding sites on adrenocortical cells. Administration of graded concentrations of ET-1 in the vicinity of adrenocortical cells provoked a dose-dependent increase in cytosolic calcium concentrations ([Ca2+]i). ET-1 induced a biphasic response consisting of an immediate and transient peak of [Ca2+]i followed by a plateau phase. Preincubation of the cells with the calcium-ATPase inhibitor thapsigargin or the PLC inhibitor U-73122 reduced the amplitude of the transient phase. Administration of the calcium chelator EGTA or the protein kinase A inhibitor H-89 attenuated the plateau phase. The [Ca2+]i response to ET-1 was markedly reduced during concomitant administration of U-73122 and H-89. Preincubation of the cells with the L-type calcium channel blocker nifedipine attenuated the plateau phase. Corticosteroid secretion from perifused frog adrenal slices was almost completely suppressed by thapsigargin and reduced by nifedipine. Taken together, these data indicate that activation of ETA receptors in frog adrenocortical cells provokes immediate stimulation of PLC, which causes an early mobilization of calcium from intracellular stores, and activates adenylyl cyclase, which results in delayed calcium influx through L-type calcium channels. The resulting increase in [Ca2+]i plays a pivotal role in ET-1-induced corticosteroid secretion.

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Section: Effect Of Et-1 On [Ca 2ϩ ] Isupporting

confidence: 75%

Activation of EndothelinA Receptors in Frog Adrenocortical Cells Stimulates Both Calcium Mobilization from Intracellular Stores and Calcium Influx through L-Type Calcium Channels

et al. 2005

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“…However, the stimulation of aldosterone secretion appeared to be independent of the renin-angiotensin system, since it was observed also in vitro in dispersed ZG cells (2, 3, 1 1 ), and even after pretreatment with the angiotensin converting enzyme inhibitor captopril (46). Further studies have indeed shown that ET-1 directly stimulates aldosterone secretion, although less potently than angiotensin II, via a Ca2+-dependent mechanism (7,47). This stimulation is deemed to involve enhancement of the synthesis of prostaglandins, since in perfused slices of frog adrenal gland it was associated with a release of prostaglandins and was abolished by indomethacin (7).…”

Section: Discussionmentioning

confidence: 99%

Gene expression, localization, and characterization of endothelin A and B receptors in the human adrenal cortex.

Rossi¹,

Albertin²,

Belloni³

et al. 1994

J. Clin. Invest.

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Compelling evidence indicates that the endothelium-derived potent vasoconstrictor endothelin-1 (ET-1) stimulates aldosterone secretion by interacting with specific receptors. Although two different ET-1 receptors have been identified and cloned, the receptor subtype involved in mediating aldosterone secretion is still unknown. Accordingly, we wished to investigate whether the genes of ET-1 and of its receptors A and B are expressed in the normal human adrenal cortex. We designed specific primers for ET-1 and the ETA and ETB receptors genes and developed a reverse transcription polymerase chain reaction (RT-PCR) with chemiluminescent quantitation of the cDNA. In addition, we carried out 'I ET-1 displacement studies with cold ET-1, ET-3 and the specific ETA and ETB ligands BQ123 and sarafotoxin 6C. Localization of each receptor subtype was also investigated by autoradiography. Binding experiments were first individually analyzed by Scatchard and Hofstee plot and then coanalyzed by the nonlinear iterative curve fitting program Ligand. Histologically normal adrenal cortex tissue, obtained from kidney cancer patients (n = 7), and an aldosterone-producing adenoma (APA), which is histogenetically derived from the zona glomerulosa (ZG) cells, were studied. Results showed that the ET-1, ETA and ETB mRNA can be detected by RT-PCR in all adrenal cortices as well as in the APA. The best fitting of the 125I ET-1 displacement binding data was consistently provided by a two-site model both in the normal adrenal cortex (F = 22.1, P < 0.0001) and in the APA (F = 18.4, P < 0.0001). In the former the density (B..n) of the ETA and ETB subtype was 2.6±0.5 pmol/mg protein (m±SEM) and 1.19±0.6, respectively. The dissociation constant (Kd) of ET-1, S6C,

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“…4) suggests a possible role of ET in the regulation of adrenocortical function, especially in the zona glomerulosa. This is supported by the fact that the addition of ET-1 stimulates aldosterone secretion in vitro from the adrenocortical tissue of various animal species [29, [90][91][92][93][94]. However, no data are available in man.…”

Section: Adrenal Glandmentioning

confidence: 99%

Recent Advances in Endothelin Research on Cardiovascular and Endocrine Systems.

Naruse¹,

Naruse²,

Demura³

1994

Endocr J

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IntroductionSince the quite exciting discovery in 1988 of endothelin (ET) in the culture medium of aortic endothelial cells by Yanagisawa and coworkers [1], evidence has accumulated to support its important roles in the regulation of blood pressure and body fluid homeostasis and its pathophysiological significance in various cardiovascular diseases. The discovery of ET and the opponent substances including nitric oxide [2] and natriuretic peptides [3] during the last decade was epoch-making in the field of "Cardiovascular Endocrinology". Because of its impressive potency and the long duration of its pressor action [1], the roles of ET in the regulation of cardiovascular homeostasis have been extensively studied.However, the co-expression or close localization of ET and its receptors in various tissues other than the vascular vessels suggest non-vascular roles of ET [4][5][6]. In the present review, we firstly integrate the information relevant to its physiological role in blood pressure regulation and possible pathogenic role in hypertension.We secondarily focus on the possible roles of ET in the endocrine system, especially in the pituitary and adrenal.Substantial review articles on ET in the kidney [7,8], ET and the heart [9], the growth regulating properties of ET [10], and ET in bronchial diseases [11, 12] have been published. Structure of ET and ET ReceptorThe molecular and biochemical aspects of ET family peptides and ET receptors have been reviewed by Masaki and Yanagisawa [13] and others [14][15][16]. We here describe the fundamentals. ET PeptidesThe ET molecule consists of 21 amino acid residues with two intramolecular disulfide bonds between cystein residues at 1 and 15 and 3 and 11, respectively. The ring structure and the hydrophobic amino acid residues at the C-terminus are indispensable to its full biological activities. There are three distinct isof orms of ET: ET-1, . The difference in the amino acid sequence is seen in the ring structure, while they share the same sequence in the linear C-terminal portion. Interspecies differences are minimal [13][14][15][16]. Interestingly, the amino acid sequence of a family of rare snake venoms, the sarafotoxins, is very similar to the sequence of ET [16], composing the ET-sarafotoxin family and suggesting the importance of the peptide in evolution.PreproET-1, the precursor of the peptide, is synthesized through the gene transcription and translation. Expression of the preproET-1 mRNA in the endothelial cells is stimulated by various humoral and physical factors: thrombin, TGF-f3, interleukin-1, TNF-a, angiotensin II (Ang II), vasopressin, and shear stress (for review see [13][14][15] produced.In addition, the existence of ET was also shown by immunoassay in a variety of tissues other than the vascular endothelium [22]. The ET-1 content is the highest in the posterior pituitary and the lung followed by the anterior pituitary, brain, and adrenal gland. The ET-3 content is highest in the posterior and anterior pituitaries.The ET-1 content is significantly hi...

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Mechanisms Involved in the Stimulation of Aldosterone Production by Angiotensin Ii, Vasopressin and Endothelin

Cited by 20 publications

References 14 publications

Activation of EndothelinA Receptors in Frog Adrenocortical Cells Stimulates Both Calcium Mobilization from Intracellular Stores and Calcium Influx through L-Type Calcium Channels

Activation of EndothelinA Receptors in Frog Adrenocortical Cells Stimulates Both Calcium Mobilization from Intracellular Stores and Calcium Influx through L-Type Calcium Channels

Gene expression, localization, and characterization of endothelin A and B receptors in the human adrenal cortex.

Recent Advances in Endothelin Research on Cardiovascular and Endocrine Systems.

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