By Kazuo Kitamura, Kenji Kangawa, Tanenao Eto (auth.), Toshio Nishikimi MD, PhD (eds.)
Adrenomedullin was once chanced on in 1993 in an extract of human pheochromocytoma whereas tracking cAMP degrees in rat platelets. Adrenomedullin has attracted significant curiosity between cardiologists because of its impression at the cardiovascular method which incorporates a reduce in blood strain in vivo; an impression on vascular gentle muscle cells; raises cAMP degrees; in some way reduces blood strain and has a job within the pathogenesis of arteriosclerosis.
Adrenomedullin in heart problems is an updated assessment of the main suitable facets of adrenomedullin. It incorporates a extensive diversity of fields together with biochemistry, molecular biology, body structure, pharmacology, pathophysiology of heart problems and scientific functions of adrenomedullin to cardiovascular disease.
Toshio Nishikimi, MD, PhD, is an affiliate Professor within the division of high blood pressure and Cardiorenal medication, Dokkyo college college of drugs, Tochigi, Japan.
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Additional info for Adrenomedullin in Cardiovascular Disease
Rebuffat P, Forneris ML, Aragona F, Ziolkowska A, Malendowicz LK, and Nussdorfer GG. (2002) Adrenomedullin and its receptors are expressed in the zona glomerulosa of human adrenal gland: evidence that ADM enhances proliferation and decreases apoptosis in cultured ZG cells. Int J MolMed 9:119-124. Segawa K, Minami K, Sata T, Kuroiwa A, and Shigematsu A. (1996) Inhibitory effect of adrenomedullin on rat mesangial cell mitogenesis. Nephron 74:577-579. Shichiri M, Fukai N, Ozawa N, Iwasaki H, and Hirata Y (2003) Adrenomedullin is an autocrine/paracrine growth factor for rat vascular smooth muscle cells.
Our data strongly suggest that the mitogenic effect of AM on VSMCs is mediated via PTK/ERK pathway. It is of note that a cAMP antagonist (Rp-cAMP-S) and a highly selective PKA inhibitor (KT5720) failed to inhibit the mitogenic effect and ERK activation by AM, despite of the AM-mediated cAMP response. In our study, AM had no effect on either intracellular Ca2+ concentration ([Ca2+]i) or inositol 1,4,5,- 30 triphosphate formation, and a selective PKC inhibitor (GF109203X) and a dihydropyridine-sensitive Ca2+ channel blocker (nicardipine) failed to block AM-induced ERK activation.
2001). Although the effect of AP-2 may differ according to the species and the cell types, AP-2 is thought to participate in the transcriptional regulation of the AM gene. AM is known to stimulate cAMP production in various cells, and cAMP is thought to serve as a second messenger of the biological actions of AM. , 1999). Although it has not yet been proven, the consensus sequence of the cAMP responsive element existing in intron 1 at the nuclotide position of +347 may transmit this negative feedback signal.