Aldosterone causes vasoconstriction in coronary arterioles of rats via angiotensin II type-1 receptor: Influence of hypertension

Kushibiki, Motoi; Yamada, Masahiro; Oikawa, Koichi; Tomita, Hirofumi; Osanai, Tomohiro; Okumura, Ken

doi:10.1016/j.ejphar.2007.06.017

Cited by 25 publications

(17 citation statements)

References 31 publications

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“…With regard to the coronary circulation, aldosterone produces dose-dependent vasoconstriction in vivo in open-chest dogs [121], in vitro in isolated perfused rat hearts [122], and in isolated coronary arterioles [123]. Interestingly, this non-genomic effect of aldosterone is blunted by inhibition of AT 1 receptors [123;124] and endothelial denudation [123], but is unaffected by blockade of mineralocorticoid receptors with spironolactone [121;123]. Coronary effects of aldosterone also appear to be augmented in disease states such as hypertension [123] and to worsen contractile function during cardiac ischemia [121].…”

Section: Neurohumoral Modulation Of Coronary Flow In Metsmentioning

confidence: 99%

“…Interestingly, this non-genomic effect of aldosterone is blunted by inhibition of AT 1 receptors [123;124] and endothelial denudation [123], but is unaffected by blockade of mineralocorticoid receptors with spironolactone [121;123]. Coronary effects of aldosterone also appear to be augmented in disease states such as hypertension [123] and to worsen contractile function during cardiac ischemia [121]. Although clinical trials have established a beneficial effect of aldosterone antagonism on cardiovascular morbidity and mortality in myocardial infarction and heart failure [55;125], pathophysiologic consequences of elevated coronary mineralocorticoid receptor stimulation in MetS have not been examined.…”

Section: Neurohumoral Modulation Of Coronary Flow In Metsmentioning

confidence: 99%

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Heart of the matter: Coronary dysfunction in metabolic syndrome

Berwick¹,

Dick²,

Tune³

2012

Journal of Molecular and Cellular Cardiology

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Metabolic syndrome (MetS) is a collection of risk factors including obesity, dyslipidemia, insulin resistance/impaired glucose tolerance, and/or hypertension. The incidence of obesity has reached pandemic levels, as ~20–30% of adults in most developed countries can be classified as having MetS. This increased prevalence of MetS is critical as it is associated with a two-fold elevated risk for cardiovascular disease. Although the pathophysiology underlying this increase in disease has not been clearly defined, recent evidence indicates that alterations in the control of coronary blood flow could play an important role. The purpose of this review is to highlight current understanding of the effects of MetS on regulation of coronary blood flow and to outline the potential mechanisms involved. In particular, the role of neurohumoral modulation via sympathetic α-adrenoceptors and the renin-angiotensin-aldosterone system (RAAS) are explored. Alterations in the contribution of end-effector K+, Ca2+, and transient receptor potential (TRP) channels are also addressed. Finally, future perspectives and potential therapeutic targeting of the microcirculation in MetS are discussed.

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Section: Neurohumoral Modulation Of Coronary Flow In Metsmentioning

confidence: 99%

Section: Neurohumoral Modulation Of Coronary Flow In Metsmentioning

confidence: 99%

Heart of the matter: Coronary dysfunction in metabolic syndrome

Berwick¹,

Dick²,

Tune³

2012

Journal of Molecular and Cellular Cardiology

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“…However, the nature of the acute effect of aldosterone on vascular function is still in dispute. In coronary and renal arteries of animals 2–4 and forearm arteries of humans 5, acute administration of aldosterone elicits concentration-dependent vasoconstrictor responses. It was demonstrated that the aldosterone-induced vasoconstriction was independent of the mineralocorticoid receptor but dependent on activation of phospholipase C and protein kinase C, and a subsequent calcium mobilization thorough voltage-dependent calcium channels 2,3.…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide-mediated Dilation of Arterioles to Intraluminal Administration of Aldosterone

Heylen

Huang²,

Sun³

et al. 2009

Journal of Cardiovascular Pharmacology

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The nature of the rapid action of aldosterone on blood vessels, whether endothelium-dependent dilation or smooth muscle-dependent constriction is predominant, is still in dispute. In this study, we administered aldosterone intraluminally or extraluminally to isolated mesenteric and cerebral arterioles of male Wistar rats. Extraluminal administration of aldosterone (10 −11 or 10 −7 M) elicited a transient vasodilatation. The peak response appeared at ~5 minutes. In contrast, intraluminal administration of aldosterone elicited a greater and sustained dilation. When aldosterone (10 −12 to 10 −7 M) was administered extraluminally in a cumulative manner, dose-dependent vasodilator responses were elicited, except a reduced dilation was observed to 10 −7 M aldosterone. The dilations were significantly inhibited by spironolactone (10 −7 M), a mineralocorticoid receptor antagonist or L-NAME (3×10 −4 M), a NO synthesis inhibitor. In endothelium-denuded vessels, extraluminal aldosterone induced a dose-dependent vasoconstrictor response. Scavenging superoxide with Tempol (10 −4 M) sustained the extraluminal aldosterone (10 −11 or 10 −7 M)-induced dilation; whereas inhibition of NO synthesis or removal of the endothelium abolished intraluminal aldosterone-induced dilation. Dilation to 10 −7 M aldosterone was significantly enhanced after inhibition of NAD(P)Hoxidase with apocynin (10 −5 M). Furthermore, in the presence of endothelial dysfunction, induced by chronic inhibition of NO synthesis, intraluminal administration of aldosterone failed to dilate the arterioles. We conclude that in physiological conditions, acute elevation of aldosterone will evoke mainly an endothelium-dependent, nitric oxide-mediated dilation.

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“…As a second common signaling mechanism, IGF1R and redox-dependent activation of kinases like RHOA kinase was described, which support VSMC migration (Montezano et al 2008). Furthermore, aldosteroneinduced rapid vasoconstriction in coronary arterioles was dependent on AT1 and possibly AT1 dimer formation but in this case, spironolactone was not able to block the effect of aldosterone (Kushibiki et al 2007. While aldosterone-dependent phosphorylation of ERK1/2, JNK and NFκB requires AT1, angII-dependent activation of NFκB requires MR (Lemarie et al 2008).…”

Section: At1mentioning

confidence: 99%

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Nongenomic effects via the mineralocorticoid receptor

Ruhs

Nolze

Hübschmann

et al. 2017

Journal of Endocrinology

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The mineralocorticoid receptor (MR) belongs to the steroid hormone receptor family and classically functions as a ligand-dependent transcription factor. It is involved in water-electrolyte homeostasis and blood pressure regulation but independent from these effects also furthers inflammation, fibrosis, hypertrophy and remodeling in cardiovascular tissues. Next to genomic effects, aldosterone elicits very rapid actions within minutes that do not require transcription or translation and that occur not only in classical MR epithelial target organs like kidney and colon but also in nonepithelial tissues like heart, vasculature and adipose tissue. Most of these effects can be mediated by classical MR and its crosstalk with different signaling cascades. Near the plasma membrane, the MR seems to be associated with caveolin and striatin as well as with receptor tyrosine kinases like EGFR, PDGFR and IGF1R and G proteincoupled receptors like AT1 and GPER1, which then mediate nongenomic aldosterone effects. GPER1 has also been named a putative novel MR. There is a close interaction and functional synergism between the genomic and the nongenomic signaling so that nongenomic signaling can lead to long-term effects and support genomic actions. Therefore, understanding nongenomic aldosterone/MR effects is of potential relevance for modulating genomic aldosterone effects and may provide additional targets for intervention.

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Aldosterone causes vasoconstriction in coronary arterioles of rats via angiotensin II type-1 receptor: Influence of hypertension

Cited by 25 publications

References 31 publications

Heart of the matter: Coronary dysfunction in metabolic syndrome

Heart of the matter: Coronary dysfunction in metabolic syndrome

Nitric Oxide-mediated Dilation of Arterioles to Intraluminal Administration of Aldosterone

30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Nongenomic effects via the mineralocorticoid receptor

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