Haemodynamic Responses to Rat Adrenomedullin in Anaesthetized Spontaneously Hypertensive Rats

Ishiyama, Yuichiro; Kïtamura, Kazuo; Ichiki, Yoshinari; Sakata, Junichiro; Kida, Osamu; Kangawa, Kenji; Eto, Tanenao

doi:10.1111/j.1440-1681.1995.tb02075.x

Cited by 37 publications

(20 citation statements)

References 17 publications

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“…This finding was compatible with the previous report that AM and CGRP exerted a potent vasodilator action via cAMP (7). Although HR was increased by both peptides, implying that reflexive sympathetic activation occurs as a result of both treatments, CI was increased by AM (23,24) but not by CGRP (15,16), in agreement with previous reports. This finding was probably due to the difference in cardiac-afterload reduction between the AM and CGRP groups.…”

Section: Discussionsupporting

confidence: 92%

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

et al. 2002

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Section: Discussionsupporting

confidence: 92%

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

et al. 2002

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“…2,11,12 The hypotensive effect of AM observed in those studies was shown to be largely secondary to direct vasodilatation, 11,12 which was further demonstrated by ex vivo studies with isolated rat aorta and with perfused rat mesenteric artery. 13,14 The mechanisms by which AM dilates blood vessels are not completely understood; however, based on the numerous articles published to date, it is clear that AM directly dilates blood vessels of the systemic and pulmonary circulation in an endothelium-dependent or independent manner.…”

Section: Vasodilator Action Of Ammentioning

confidence: 80%

Adrenomedullin

Kato

Tsuruda

Kita

et al. 2005

ATVB

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145

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Abstract-Adrenomedullin (AM) is a vasodilator peptide having a wide range of biological actions such as reduction of oxidative stress and inhibition of endothelial cell apoptosis. The AM gene is expressed in vascular walls, and AM was found to be secreted from cultured vascular endothelial cells, smooth muscle cells, and adventitial fibroblasts. Plasma AM levels in patients with arteriosclerotic vascular diseases are elevated in possible association with the severity of the disease. When administered over a relatively short period, AM dilates blood vessels via an endothelium-dependent or independent mechanism. Experiments in vitro have shown that AM exerts multiple actions on cultured vascular cells, which are mostly protective or inhibitory against vascular damage and progression of arteriosclerosis. Key Words: adrenomedullin Ⅲ vasodilatation Ⅲ endothelium Ⅲ smooth muscle cell Ⅲ arteriosclerosis C ardiovascular diseases secondary to arteriosclerosis of blood vessels are currently among the leading causes of death in developed countries. A number of factors, both humoral and mechanical, have been shown to modulate vascular function in humans as well as in experimental animals. 1 Blood vessel dysfunction resulting from an imbalance of those factors accelerates the process of vascular remodeling and atherosclerosis. 1 Vasoconstrictors including angiotensin II and endothelins not always but mostly act as proatherogenic factors, whereas vasodilators, either peptides or non-peptides, such as natriuretic peptides, nitric oxide (NO), and prostaglandin (PG) I 2 , have antiatherogenic properties. 1 In 1993, a new vasodilator peptide, adrenomedullin (AM), was isolated from the tissue extract of a human pheochromocytoma by monitoring cAMP levels in rat platelets. 2 Substantial levels of the AM peptide and gene expression were detected in the cardiovascular tissues including blood vessels. As listed in the Table, AM was found to exert a wide range of biological actions related to vascular functions in cultured cells, with which observations in vivo have been mostly accordant. Ever since the discovery of AM, efforts have been made to clarify the role of this bioactive peptide in blood vessels and a substantial amount of basic and clinical data has been accumulated. In this review, after summarizing the biochemical and pharmacological features of AM, we discuss its role in blood vessels, which is assumed to be protective, or inhibitory against the progression of vascular damage and remodeling. Biochemistry of AMHuman AM is a 52-aa peptide with a ring structure formed by a disulfide bond and amidated tyrosine at the C terminus ( Figure 1), both essential for binding to receptors and biological activity. 2-4 Based on sequence homology, AM is thought to belong to the calcitonin gene-related peptide (CGRP) superfamily. [2][3][4] Cloning of the cDNA encoding AM revealed the AM precursor peptide preproAM to comprise 185 amino acids, with the C terminus followed by a pair of basic amino acids, Arg-Arg, a typical processing signal (...

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“…The increased vasodilation was associated with a slight increase in glomerular filtration rate and natriuresis in the renal system (8). In the cardiovascular system, Ishiyama et al (9) reported that the Adm peptide, in addition to producing a fall in blood pressure, elicited an increase in cardiac index and stroke volume without a subsequent change in heart rate.…”

Section: Adrenomedullin (Adm)mentioning

confidence: 99%

Adrenomedullin Gene Expression Is Developmentally Regulated and Induced by Hypoxia in Rat Ventricular Cardiac Myocytes

Cormier¹,

Nguyen

Claycomb

1998

Journal of Biological Chemistry

209

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Adrenomedullin is a recently discovered hypotensive peptide that is expressed in a variety of cell and tissue types. Using the technique of differential display, the adrenomedullin gene was observed to be differentially expressed in developing rat heart. Reverse transcription-polymerase chain reaction analysis revealed that the level of adrenomedullin mRNA was significantly higher in adult ventricular cardiac muscle as compared with embryonic day 17 ventricular cardiac muscle. Adrenomedullin receptor mRNA was constitutively expressed throughout development of the ventricular heart. Two potential hypoxia-inducible factor-1 (HIF-1) consensus binding sites were identified in the mouse adrenomedullin promoter at -1095 and -770 nucleotides from the transcription start site. Exposure of cultured adult rat ventricular cardiac myocytes to hypoxia (1% O 2 ) resulted in a significant, time-dependent increase in adrenomedullin mRNA levels. Transfection studies revealed that the 5-flanking sequence of adrenomedullin was capable of mediating a hypoxia-inducible increase in transcription. Mutation of the putative HIF-1 consensus binding sites revealed that the major regulatory sequence that mediates the hypoxia-inducible transcriptional response is located at -1095. These data demonstrate that the adrenomedullin gene is developmentally regulated in ventricular cardiomyocytes, that adrenomedullin transcription can be induced by hypoxia, and that this response is primarily mediated by HIF-1 consensus sites in the adrenomedullin promoter.

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Haemodynamic Responses to Rat Adrenomedullin in Anaesthetized Spontaneously Hypertensive Rats

Cited by 37 publications

References 17 publications

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

Regional Hemodynamic Effects of Adrenomedullin in Wistar Rats: A Comparison with Calcitonin Gene-Related Peptide.

Adrenomedullin

Adrenomedullin Gene Expression Is Developmentally Regulated and Induced by Hypoxia in Rat Ventricular Cardiac Myocytes

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