Differential effects of endogenous and exogenous nitric oxide on the release of endothelin‐1 from the intact perfused rat adrenal gland in situ

Hinson, J. P.; Kapas, S.; Cameron, L.A.

doi:10.1016/0014-5793(95)01467-5

Cited by 21 publications

(9 citation statements)

References 18 publications

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“…Similar observations have been made for other vasoactive peptides. Neuropeptide Y gene expression and release is upregulated by NO on a transcriptional level in vitro [13] whereas endothelin-1 release is attenuated by NO in vitro [14]. The effect of NO-induced adrenomedullin production is considerably more pronounced on mRNA than on peptide level as demonstrated by two independent methods for mRNA quantification.…”

Section: Discussionmentioning

confidence: 86%

Nitric Oxide Stimulates Adrenomedullin Secretion and Gene Expression in Endothelial Cells

Dötsch

Schoof²,

Hänze³

et al. 2002

Pharmacology

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Adrenomedullin, a peptide with vasorelaxant activity, stimulates nitric oxide (NO) synthesis. We tested whether or not NO regulates the function of the adrenomedullin system. Human umbilical vein endothelial cells (HUVEC) were incubated with the NO donors sodium nitroprusside (SNP), morpholinosydnonimine (SIN-1) and the phospodiesterase V inhibitor zaprinast. In HUVEC, adrenomedullin concentration in the supernatant was measured by radioimmunoassay and mRNA expression was studied by Northern blot and competitive quantitative PCR. SNP, SIN-1, and zaprinast (100 µmol/l each) significantly increased adrenomedullin concentration in the supernatant of HUVEC twofold. The same concentrations increased adrenomedullin mRNA expression four- to tenfold. Similar results were obtained by both quantitative PCR and Northern blot. Thus, NO donor exposure in vitro increases both adrenomedullin secretion and mRNA expression in a dose-dependent manner.

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Section: Discussionmentioning

confidence: 86%

Nitric Oxide Stimulates Adrenomedullin Secretion and Gene Expression in Endothelial Cells

Dötsch

Schoof²,

Hänze³

et al. 2002

Pharmacology

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“…In perfused rat adrenal gland (the precise source of ET-1 within the adrenal was not determined), ACTH increased adrenal vein ET-1 content (290); this effect has been ascribed to ACTH-induced increases in adrenal blood flow (81). In the same experimental model, NOS inhibition increased, while l -arginine decreased, ET-1 release through an apparently cGMP-independent mechanism (288). …”

Section: Endothelin and Humoral Systemsmentioning

confidence: 98%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

368

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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“…We postulated that NO secretion by endothelial cells would change ECE-1 protein expression as previously described [38, 39]. In order to evaluate this hypothesis, cells were treated with insulin (data not shown) or bradykinin, both known to increase NO production and secretion, and with L-NAME, which blocks NO production (fig.…”

Section: Discussionmentioning

confidence: 99%

Increased Expression of Endothelin-Converting Enzyme-1c Isoform in Response to High Glucose Levels in Endothelial Cells

et al. 2004

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Endothelin-1 (ET-1) is both a potent vasoconstrictor and mitogenic factor that has been implicated as a cause of the micro- and macrovascular complications of diabetes mellitus. The pathway by which the high-glucose environment of diabetes mediates increased levels of endothelins has not been completely elucidated but appears to involve endothelin-converting enzyme (ECE-1), which converts inactive big ET-1 to active ET-1 peptide. To determine the effect of high glucose concentrations on the expression of ECE-1, hybrid endothelial cells (EA.hy926) and human umbilical vein endothelial cells (HUVEC) were both grown in various glucose concentrations. There was a 2-fold increase in ECE-1 immunoreactivity in the EA.hy926 cell line growing in medium containing 22.2 versus 5.5 mmol/l glucose after 24 h, which rose to greater than 20-fold after 5 days. Similar results were seen with HUVEC. Bradykinin or NG-nitro-L-arginine methyl ester did not change the effect of high glucose on ECE-1 protein expression. High glucose induced a 72 and 41% increase in total protein kinase C (PKC) activity in both EA.hy926 cells and HUVEC, respectively, and a 39, 49 and 109% elevation in PKC β1, β2 and δ expression, respectively, in EA.hy926 cells. The increase in ECE-1 expression was inhibited in both cell cultures by GF109203X (5 µmol/l), a general PKC inhibitor, while addition of 10 nmol/l phorbol myristic acid to EA.hy926 cells or HUVEC growing on medium containing 5.5 mmol/l glucose increased ECE-1 expression to a level similar to that of cells conditioned in high glucose. Human ECE-1 protein exists in four different isoforms, termed 1a, 1b, 1c and 1d. Northern blot analysis revealed that only ECE-1c isoform mRNA levels increased. Immunohistochemical staining of EA.hy926 cells grown in high glucose concentrations demonstrated an increase in the ECE-1c isoform, which occurred mainly in the plasma membrane. These results showed that the PKC pathway may play an important role in the glucose-mediated induction of ECE-1 expression. The main isoform to increase in response to high glucose was ECE-1c. This enzyme may be one of the factors contributing to the elevated ET-1 peptide levels observed in diabetes.

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Differential effects of endogenous and exogenous nitric oxide on the release of endothelin‐1 from the intact perfused rat adrenal gland in situ

Cited by 21 publications

References 18 publications

Nitric Oxide Stimulates Adrenomedullin Secretion and Gene Expression in Endothelial Cells

Nitric Oxide Stimulates Adrenomedullin Secretion and Gene Expression in Endothelial Cells

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Increased Expression of Endothelin-Converting Enzyme-1c Isoform in Response to High Glucose Levels in Endothelial Cells

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