Glucocorticoids induce endothelin release from vascular smooth muscle cells but not endothelial cells

Kanse, Sandip M.; Benito-Orfila, M.A.; Takahashi, Katsuaki; Warren, J. B.; Ghatei, Mohammed A.; Bloom, S.R.

doi:10.1016/0167-0115(91)90122-w

Cited by 14 publications

(16 citation statements)

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“…From day 1 through to day 4, however, plasma natriuretic peptide concentrations (and endothelin-1 levels) tended to be reduced compared with control data -presumably as a consequence of the sustained improvements in hemodynamic function. The transient increase in plasma endothelin-1 levels may conceivably relate to stimulation by factors such as cortisol, 29 which shows a concomitant tendency to rise in the present study, or to a reduction in shear stress and/or tissue oxygen concentrations after the AMinduced fall in blood pressure (from already reduced levels)-both of which are reported to enhance endothelin secretion. 30,31 The acute rise in endothelin is unlikely to be owing to a direct effect of AM, given that the peptide has been shown to inhibit endothelin production in vascular smooth muscle cells.…”

Section: Chronic Effects Of Adrenomedullin In Sheep With Experimentalmentioning

confidence: 47%

Long-Term Adrenomedullin Administration in Experimental Heart Failure

et al. 2002

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Abstract-Short-term administration of adrenomedullin, a recently discovered peptide with potent vasodilator, natriuretic, and aldosterone-inhibitory actions, has beneficial effects in experimental and clinical heart failure. The effects of prolonged adrenomedullin administration have not previously been assessed in this setting. Consequently, in 16 sheep with pacing-induced heart failure, we infused either adrenomedullin (10 ng/kg per minute; nϭ8) or a vehicle control (Hemaccel; nϭ8) for 4 days. Compared with control data, infusion of adrenomedullin persistently increased circulating levels of the peptide (by Ϸ9.5 pmol/L; PϽ0.001), in association with prompt (15 minutes) and sustained (4 days) increases in cardiac output (day 4, 27%), and reductions in peripheral resistance (30%), mean arterial pressure (13%), and left atrial pressure (24%; all, PϽ0.001). Adrenomedullin also significantly enhanced urinary sodium excretion (day 4, 3-fold; PϽ0.05), creatinine excretion (1.2-fold; PϽ0.001), and creatinine clearance (1.4-fold; PϽ0.001) over the 4 days of treatment, whereas urine volume and cAMP excretion tended to be elevated (both, 0.1ϾPϾ0.05). Plasma renin activity was increased (PϽ0.05), whereas aldosterone levels were reduced in a sustained fashion (PϽ0.01). Plasma endothelin rose transiently (hours 1 to 6) after initiation of treatment (PϽ0.05). Despite substantial cardiac unloading, plasma concentrations of the natriuretic peptides were not significantly different from control. In conclusion, long-term administration of adrenomedullin induces pronounced and sustained cardiovascular and renal effects in experimental heart failure, including reductions in cardiac preload and afterload, as well as augmentation of cardiac output, sodium excretion, and glomerular filtration. These findings support the concept of adrenomedullin as a protective hormone during hemodynamic compromise with therapeutic potential in heart failure.

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Section: Chronic Effects Of Adrenomedullin In Sheep With Experimentalmentioning

confidence: 47%

Long-Term Adrenomedullin Administration in Experimental Heart Failure

et al. 2002

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“…Dexaméthasone potentiates the production of inositol triphosphate, a second messenger of angiotensin II and arginine vasopressin [29], and sup presses the atrial natriuretic factor-mediated response in vascular smooth muscle cells [30]. In addition, dexamethasone treatment has been found to lead to endothelin release from vascular smooth muscle cells [31]. Compara ble effects in this regard, however, have not been con firmed in vivo.…”

Section: Discussionmentioning

confidence: 99%

Dependence of Elevated Mesenteric Arteriolar Tone on Glucocorticoids in Spontaneously Hypertensive Rats

Suzuki¹,

Zweifach²,

Schmid-Schönbein³

1995

Int J Microcirc

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This study is designed to explore the effect of adrenal glucocorticoids on arteriolar behavior under steady state conditions in spontaneously hypertensive rats (SHR) compared with their normotensive controls, the Wistar Kyoto (WKY) rats. Mesenteric arterioles were observed by intravital microscopy under general anesthesia and arteriolar diameters were measured. At the end of each experiment, papaverine was topically applied to determine maximum diameter of the vessels for which arteriolar tone was computed. The adrenal contribution to the atypical arteriolar tone in SHR was explored by subjecting them to bilateral adrenalectomy with or without glucocorticoid replacement therapy. Adrenalectomy led to a reduction in the elevated blood pressure in SHR to normotensive levels, which could be restored to its hypertensive level by treatment with dexamethasone. Adrenalectomy had no significant effect on blood pressure in WKY rats, although administration of dexamethasone but not aldosterone did lead to an elevation of the blood pressure in sham-operated WKY. Arteriolar tone in SHR was set at a higher steady state level than in WKY rats. In adrenalectomized SHR, tone fell to the levels observed in WKY rats. This decrease in arteriolar tone in the adrenalectomized SHR could in turn be restored to the hypertensive levels with dexamethasone but not aldosterone. Our results suggest that the enhancement of arteriolar tone, as well as the high blood pressure in SHR, may be related to the above normal levels of adrenal glucocorticoids present in the bloodstream.

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“…For instance, in patients with Cushing's disease, hypertension is a common condition. Furthermore, glucocorticoids are involved in the regulation of endothelin-1 (ET-1) transcription [7], release [8], action [9] and receptor expression [10,11]. This endothelial-derived peptide possesses a potent vasoconstricting activity [12] and is related to both vascular complications in hypertension [13] and poor prognosis in patients with ischemic heart disease [14].…”

Section: Introductionmentioning

confidence: 99%

Endothelin-1 Plasma Concentrations in Depressed Patients and Healthy Controls

Lederbogen

Weber²,

Colla³

et al. 1999

Neuropsychobiology

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Depression and cardiovascular morbidity are known to be associated. So far, however, the pathophysiological link between these conditions is unclear. We tested the hypothesis that in depressed hypercortisolemic patients endothelin-1 (ET-1) plasma concentrations are increased and contribute to the cardiovascular risk. Diurnal plasma concentrations of cortisol and ET-1 were measured in 29 healthy controls and 22 depressed patients. ANCOVA did not reveal a significant effect of diagnosis or age upon ET-1 concentrations. However, only in depressed patients, cortisol plasma concentrations tended to be positively related to ET-1 concentrations. We conclude that ET-1 is not increased in depressed patients, but within this group, hypercortisolemia may be associated with increased ET-1 concentrations.

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Glucocorticoids induce endothelin release from vascular smooth muscle cells but not endothelial cells

Cited by 14 publications

References 0 publications

Long-Term Adrenomedullin Administration in Experimental Heart Failure

Long-Term Adrenomedullin Administration in Experimental Heart Failure

Dependence of Elevated Mesenteric Arteriolar Tone on Glucocorticoids in Spontaneously Hypertensive Rats

Endothelin-1 Plasma Concentrations in Depressed Patients and Healthy Controls

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