Biomedical subjects

Chun-Shui Pan

Publications and source records attributed to Chun-Shui Pan.

21 records · Page 2Linked to original sources

PubMed2004

Effects of adrenomedullin on cell proliferation in rat adventitia induced by aldosterone.

OBJECTIVE: Aldosterone is involved in cardiovascular diseases such as hypertension and heart failure by inducing sodium retention and vascular remodeling, which is characterized by fibroblast proliferation and migration in adventitia. It is well known that aldosterone stimulates vascular smooth muscle cells and fibroblasts to produce and secrete adrenomedullin (ADM), a multiple functional peptide with an important cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion and its mRNA expression in rat aortic adventitia to study the paracrine/autocrine interaction between endogenous ADM and aldosterone. METHODS: ADM produced and secreted from adventitia stimulated by aldosterone in the absence or presence of spironolactone, RU486 or spironolactone together with RU486 were detected by radioimmunoassay, proliferation in adventitia cells was evaluated by the level of [H]-thymine incorporation, and preproADM gene expression was measured by semi-quantitative reverse transcriptase polymerase chain reaction. RESULTS: Adventitial ADM secretion and mRNA expression stimulated by aldosterone were concentration-dependent as was the inhibitive effect of ADM on aldosterone-induced proliferation. The induction of aldosterone in ADM secretion was mediated by mineralocorticoid receptor. Antagonists of specific receptors of calcitonin gene-related peptide (CGRP) receptor type 1 and ADM both potentiated the proliferation effect induced by aldosterone; and thiorphan, an inhibitor of the enzyme for ADM degradation, inhibited the adventitial [H]-thymine incorporation induced by aldosterone. ADM inhibited the activity of extracellular signal related kinase (ERK) stimulated by aldosterone. CONCLUSION: Aldosterone stimulates adventitia to produce and secrete ADM, which in turn, antagonizes the aldosterone-induced proliferation in adventitia.

Adrenomedullin↗

PubMed2004

Relationship between the contents of adrenomedullin and distributions of neutral endopeptidase in blood and tissues of spontaneously hypertensive rats.

Adrenomedullin (ADM) is a multifunctional peptide with important roles in the cardiovascular system, especially in the adjustment of cardiovascular and renal homeostasis. ADM is present in plasma, organs and tissues, and its activity increases during hypertension. It remains unknown whether the clearance of this peptide is altered during hypertension. Neutral endopeptidase (NEP) is the major enzyme in ADM's degradation. We observed the activity and distribution of NEP and the expression of its mRNA in the plasma, cardiac ventricle, aorta, jejunum and kidney of spontaneously hypertensive rats (SHRs) in order to study the possible role of NEP in elevating tissue ADM concentrations during hypertension. ADM and NEP were diffuse in all tissues studied. The level of tissue ADM was generally higher in SHR tissues than in control tissues, except in the renal medulla, and its mRNA expression was higher in all tissues. Plasma NEP activity, general NEP activity and the expression of NEP mRNA in the left ventricle, aorta and jejunum in SHRs was lower than that of controls, and the level of ADM was inversely correlated with NEP activity. NEP activity and mRNA and protein expression in SHR kidneys were higher than in control kidneys; moreover, the ADM content was positively correlated with NEP activity in the renal cortex. NEP activity in the lung of SHRs did not differ from that of controls. Thus, in SHRs, the local concentration and action of ADM in the tissues may be differentially regulated by NEP.

Adrenomedullin↗

PubMed2004

Ghrelin protects myocardium from isoproterenol-induced injury in rats.

AIM: To investigate the cardiac protective effects of ghrelin in rat with myocardial injury induced by isoproterenol (ISO). METHODS: Rats were subcutaneously injected ISO 40 mg/kg/d with or without ghrelin 1 or 10 nmol/kg/d for 2 d. Hemodynamic parameters including mean arterial blood pressure and left ventricular pressure were measured at 12 h after the last injection with ISO and/or ghrelin. Plasma lactate dehydrogenase (LDH) activity, plasma and myocardial contents of malondialdehyde (MDA), and conjugated diene were measured. Plasma ghrelin and endothelin-1 levels were assayed using radioimmunoassay methods. Endothelin-1 and ghrelin mRNA were determined using RT-PCR. RESULTS: About 45 % (5/11) of rats after treatment with ISO alone died during experimental periods. However, no rats died after administration with ghrelin 10 nmol/kg/d (0/11, P<0.05). Ghrelin also obviously ameliorated the hemodynamic disturbance in rats induced by ISO. The plasma LDH activity, contents of myocardial and plasma MDA, and conjugated diene level in plasma in ISO+G10 nmol/kg/d group were decreased by 28 %, 34 %, 73 %, and 38 % compared with those of ISO group (all P<0.01) respectively. ISO-induced endothelin-1 mRNA over-expression was inhibited and endothelin-1 level in plasma were inhibited by ghrelin 1 and 10 nmol/kg/d. The ghrelin levels in plasma and ghrelin mRNA in myocardium were increased in the rats after injection of ISO. The plasma ghrelin level was further increased after ghrelin administration. CONCLUSION: Ghrelin has a protective effect against ISO-induced myocardial injury.

Animals↗