Endothelin‐1 stimulates sodium‐dependent calcium efflux from bovine adrenal chromaffin cells in culture

Yoshizumi, Masanori; Tsuchiya, Koichiro; Hirose, Masao; Kitagawa, Tetsuya; Kujime, Toshihide; Shimizu, Eiji; Niwa, Yasuharu; Minakuchi, Kazuo; Takahashi, Toshiaki

doi:10.1038/sj.bjp.0702047

Cited by 7 publications

(6 citation statements)

References 24 publications

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“…In cultured bovine adrenal chromaffin cells, ET-1 (305), but not ET-3 (422), increases [Ca 2+ ] i via uptake of extracellular Ca 2+ and evokes catecholamine release. This response to ET-1 is abolished by BQ123, but not BQ788, consistent with an ET A -mediated effect.…”

Section: Endothelin and Humoral Systemsmentioning

confidence: 99%

“…Furthermore, nifedipine only partially inhibits the response that is completely abrogated by further addition of agents that block Ca 2+ entry via voltage-independent cation channels (422). ET B agonists also stimulate Ca 2+ efflux from cells preloaded with 45 Ca 2+ and increase NO generation (305). NOS blockade prevents both the rise in NO and Ca 2+ efflux.…”

Section: Endothelin and Humoral Systemsmentioning

confidence: 99%

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Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

373

459

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Endothelin (ET) peptides and their receptors are intimately involved in the physiological control of systemic blood pressure and body Na homeostasis, exerting these effects through alterations in a host of circulating and local factors. Hormonal systems affected by ET include natriuretic peptides, aldosterone, catecholamines, and angiotensin. ET also directly regulates cardiac output, central and peripheral nervous system activity, renal Na and water excretion, systemic vascular resistance, and venous capacitance. ET regulation of these systems is often complex, sometimes involving opposing actions depending on which receptor isoform is activated, which cells are affected, and what other prevailing factors exist. A detailed understanding of this system is important; disordered regulation of the ET system is strongly associated with hypertension and dysregulated extracellular fluid volume homeostasis. In addition, ET receptor antagonists are being increasingly used for the treatment of a variety of diseases; while demonstrating benefit, these agents also have adverse effects on fluid retention that may substantially limit their clinical utility. This review provides a detailed analysis of how the ET system is involved in the control of blood pressure and Na homeostasis, focusing primarily on physiological regulation with some discussion of the role of the ET system in hypertension.

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Section: Endothelin and Humoral Systemsmentioning

confidence: 99%

Section: Endothelin and Humoral Systemsmentioning

confidence: 99%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

373

459

View full text Add to dashboard Cite

show abstract

“… 45 There is evidence that ET B receptor‐induced increases in cGMP and NO in bovine chromaffin cells mediate increases in calcium efflux from the cells, which suggests that ET plays a role in re‐establishing resting levels of intracellular calcium after stimulation. 43 …”

Section: Mechanisms By Which Et May Affect Adrenal Functionmentioning

confidence: 99%

Endothelin Regulation of Adrenal Function

Hinojosa‐Laborde

Lange

1999

Clin Exp Pharma Physio

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1. The goal of the present review is to recount the evidence that endothelin (ET) has a significant influence on the peripheral sympathetic nervous system by regulating the function of the adrenal medulla. 2. The presence of an active ET system in the adrenal medulla has been clearly demonstrated. Endothelin protein, mRNA, binding sites and ET-converting enzyme have been identified in adrenal tissue and medullary chromaffin cells, suggesting that this peptide may contribute to the regulation of adrenal medullary function. 3. Studies investigating the function of ET in the adrenal gland have demonstrated that ET has a stimulatory effect on the adrenal medulla. Endothelin elicits an increase in catecholamine release from perfused intact adrenal glands as well as from cultured chromaffin cells. This effect has been shown to be mediated by ETA and ETB receptors. 4. The mechanism by which ET causes an increase in catecholamine release from the adrenal medulla appears to be independent of cholinergic activation of chromaffin cells. Endothelin has been shown to act directly at chromaffin cells to increase intracellular calcium, which results in catecholamine release. 5. Endothelin can indirectly affect catecholamine release by its effect on adrenal blood flow. Studies indicate that ET has both vasoconstrictor and vasodilator effects in the adrenal gland, which suggests a role for ET in the regulation of adrenal blood flow. Endothelin has also been proposed to participate in the selective contraction of the adrenomedullary veins, which enhances the discharge of catecholamines from the adrenal gland during activation.

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“…Our previous study has suggested that NO plays an inhibitory role in catecholamine secretion from the dog adrenal gland (17). Stimulation of ET B receptors is demonstrated to induce NO and cyclic GMP production in the rat adrenal medulla (10) and bovine adrenal chromaffin cells (6). It was also reported that the inhibitory effect of S6c on the nerve stimulation-evoked norepinephrine efflux was susceptible to NOS inhibition in the dog kidney (11).…”

Section: R1054mentioning

confidence: 95%

“…These findings suggest that NO interferes with the cholinergic control of adrenal catecholamine secretion. Stimulation of ET B receptors is reported to enhance NO production in bovine adrenal chromaffin cells (6) and the rat adrenal medullary cells (10). It is therefore possible that ET B receptors play an inhibitory role in adrenal catecholamine secretion via NO production.…”

mentioning

confidence: 99%

Role of ET_B receptors and nitric oxide in adrenal catecholamine secretion in anesthetized dogs

Hosokawa

Nagayama

Masada

et al. 1999

American Journal of Physiology-Regulatory, Integrative and Comp

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We examined the effects of sarafotoxin 6c (S6c), an endothelin-B (ET(B)) receptor agonist, on adrenal catecholamine secretion in response to cholinergic stimuli in pentobarbital sodium-anesthetized dogs. Drugs were administered intra-arterially into the adrenal gland through the phrenicoabdominal artery. Infusion of S6c attenuated increases in adrenal catecholamine output induced by splanchnic nerve stimulation. The inhibitory effect of S6c on the catecholamine secretion response was suppressed with a selective ET(B) receptor antagonist N-cis 2, 6-dimethylpiperidinocarbonyl-L-gamma-methylleucyl-D-1-methoxycarbonyl tryptophanyl-D-norleucine (BQ-788), a nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester, and a neuronal NOS inhibitor 7-nitroindazole monosodium salt (7-NINA). Similar results were obtained with the catecholamine secretion response induced by injection of ACh. 7-NINA alone did not affect these catecholamine secretion responses. These results suggest that ET(B) receptors play an inhibitory role in adrenal catecholamine secretion by activating neuronal NOS, whereas neuronal NOS is unlikely to be involved in regulation of adrenal catecholamine secretion in the absence of simultaneous ET(B) receptor stimulation.

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Endothelin‐1 stimulates sodium‐dependent calcium efflux from bovine adrenal chromaffin cells in culture

Cited by 7 publications

References 24 publications

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Endothelin Regulation of Adrenal Function

Role of ET_B receptors and nitric oxide in adrenal catecholamine secretion in anesthetized dogs

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Endothelin‐1 stimulates sodium‐dependent calcium efflux from bovine adrenal chromaffin cells in culture

Cited by 7 publications

References 24 publications

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Endothelin Regulation of Adrenal Function

Role of ETB receptors and nitric oxide in adrenal catecholamine secretion in anesthetized dogs

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Product

Resources

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Role of ET_B receptors and nitric oxide in adrenal catecholamine secretion in anesthetized dogs