Search PubMed⌕ Search

Biomedical subjects

Chao-Shu Tang

Publications and source records attributed to Chao-Shu Tang.

At least 37 records · Page 2Linked to original sources
PubMed2005

Adrenomedullin induces heme oxygenase-1 gene expression and cGMP formation in rat vascular smooth muscle cells.

Adrenomedullin (ADM) is a potent vasodilatory peptide. It regulates blood pressure by increasing cyclic adenosine monophosphate (cAMP) and guanosine-3',5'-monophosphate (cGMP). We sought to investigate the effect of ADM on heme oxygenase-1 (HO-1) gene expression and cGMP formation in cultured rat vascular smooth muscle cells (VSMCs). ADM treatment, 10(-9) and 10(-8) mol/L, increased cGMP production, and it increased the intracellular cGMP content of platelets coincubated with VSMCs. It increased cGMP content by 158.8% and 273.5%, respectively; increased HO-1 activity by 49.5% and 87%, respectively; augmented HO-1 protein levels by 66% and 126%, respectively; upregulated the steady-state level of HO-1 mRNA by 73% and 159%, respectively, and increased HO-1 mRNA transcription synthesis by four- and seven-fold, respectively. These results suggest that ADM induces HO-1 gene expression and cGMP formation in rat VSMCs.

Adrenomedullin↗
PubMed2005

Protective effects of intermedin/adrenomedullin2 on ischemia/reperfusion injury in isolated rat hearts.

Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene-related peptide (CT/CGRP) family identified from human and other vertebrate tissues. Preprointermedin can generate a 47-amino acid mature peptide (IMD(1-47)) and a shorter 40-amino acid one (IMD(8-47)) by proteolytic cleavage. The present study was designed to determine the protective effect of IMD on cardiac ischemia/reperfusion (I/R) injury and its possible mechanism. Isolated rat hearts were perfused on a Langendorff apparatus and subjected to 45-min global ischemia and 30-min reperfusion. Cardiac function was measured. The release of myocardial protein and lactate dehydrogenase (LDH) and the formation of malondialdehyde (MDA) were assayed. Myocardial cAMP content was determined by radioimmunoassay (RIA). Cardiac I/R induced a marked inhibition of cardiac function and myocardial injury. Reperfusion with IMD significantly attenuated the I/R injury. Compared with I/R alone, perfusion with 10(-8)mol/L IMD(1-47) and IMD(8-47) induced a 36% and 33% increase in Delta left ventricular pressure (DeltaLVP), 30% and 28% in maximal rate of increase of LV pressure (+LVdP/dt max), and 34% and 31% in maximal rate of decrease of LV pressure (-LVdP/dt max), respectively (all P<0.01) but an approximately 58% and 51% decrease in LV diastolic pressure, respectively (P<0.01). In addition, perfusion with IMD markedly attenuated the leakage of LDH, total protein and myoglobin from myocardia compared with I/R alone. The contents of ventricular myocardia cAMP after reperfusion with 10(-8)mol/L IMD(1-47) and IMD(8-47) were 130% and 91% higher, respectively, than that with I/R alone (all P<0.01). However, formations of myocardial MDA were 52% and 50% lower than that with I/R alone (all P<0.01), respectively. Interestingly, the above IMD effects were similar to those of adrenomedullin (10(-8)mol/L). These results suggest that IMD, like adrenomedullin, exerts cardio-protective effects against myocardial I/R injury.

Adrenomedullin↗
PubMed2005

Effect of relaxin on myocardial ischemia injury induced by isoproterenol.

The omnipresent 6-kDa polypeptide relaxin (RLX) is emerging as a multifunctional endocrine and paracrine factor in a broad range of target tissues including cardiovascular tissues. To explore the pathophysiological roles of RLX in ischemic cardiovascular diseases, we studied the changes in RLX mRNA level in the myocardium and the effect of RLX supplements in rats with isoproterenol (ISO)-induced myocardial injury. In ISO-treated rats, RLX levels in myocardia and plasma increased 3.7- and 6.9-fold, respectively (P<0.01), the mRNA level increased significantly in myocardia compared with controls. Co-administration of RLX (0.2 and 2.0 microg/kg/d) and ISO increased left-ventricular pressure development and decreased left ventricular end-diastolic pressure (LVDEP) (all P<0.01). Malondialdehyde content in myocardia and lactate dehydrogenase and creatine phosphokinase activities in plasma in RLX-treated rats decreased markedly compared with that in ISO-treated alone rats (P<0.01 or P<0.05). In the high-dose RLX group, fibroblastic hyperplasia was relieved in myocardia, hydroxyproline level was lower, by 33% (P<0.05), and endothelin content in plasma was lower, by 31% (P<0.01) than in the ISO-alone group. Compared with control group, any indexes in sham rats treated with high-dose RLX were unaltered (all P>0.05). These results showed an up-regulation of myocardial RLX during ISO-induced myocardial ischemia injury and the protective effect of RLX on ISO-induced cardiac inhibition and fibrosis, which suggests that RLX could be an endogenous cardioprotective factor in ischemic heart diseases.

Animals↗
PubMed2005

Blood pressure responses of endothelin-1 1-31 within the rostral ventrolateral medulla through conversion to endothelin-1 1-21.

Endothelin-1 1-31 (ET-1 1-31), a novel member of the endothelin family comprising 31 amino acids and derived from the selective hydrolysis of big ET-1 by chymase, directly activates endothelin receptors or converts to ET-1 1-21 by ET converting enzyme (ECE). The cardiovascular effects of central ET-1 1-31 are not identified. The present study was designed to investigate the cardiovascular actions of ET-1 1-31 within the rostral ventrolateral medulla (RVLM) in anesthetized rats. Bilateral injection of ET-1 1-31 (0.5, 1, and 2 pmol for each side) into the rostral ventrolateral medulla produced an initial pressor and/or a long-lasting hypotensive action but did not affect HR. Unilateral microinjection of 2 and 4 pmol of ET-1 1-31 into the rostral ventrolateral medulla only produced a significant (P < 0.05) transient increase in blood pressure by an average of 13 and 12 mm Hg, respectively, whereas unilateral microinjection of 8 pmol of ET-1 1-31 produced a sustained fall in blood pressure (from 92 +/- 6 to 69 +/- 8 mm Hg, P < 0.05). The transient pressor effect of unilaterally injecting ET-1 1-31 (4 pmol) into the rostral ventrolateral medulla was completely abolished by pretreatment with either ETA receptor antagonist BQ123 (83 +/- 2 versus 84 +/- 5 mm Hg, P > 0.05) or ET converting enzyme inhibitor phosphoramidon (99 +/- 5 versus 99 +/- 7 mm Hg, P > 0.05) but not ETB receptor antagonist IRL1038 (89 +/- 6 versus 96 +/- 7 mm Hg, P < 0.05). In addition, prior injection of phosphoramidon also completely abolished the long-lasting hypotension of intra-RVLM ET-1 1-31 (8 pmol) but did not modify the depressor action of intra-RVLM ET-1 1-21 (from 100 +/- 6 to 76 +/- 8 mm Hg, P < 0.05). In conclusion, the current results suggest that the cardiovascular effects of intra-RVLM ET-1 1-31 might be the result of conversion of ET-1 1-31 to ET-1 1-21 through activation of ETA receptors.

Animals↗
PubMed2005

Taurine inhibits ischemia/reperfusion-induced compartment syndrome in rabbits.

AIM: To investigate effects of taurine on ischemia/reperfusion (I/R)-induced compartment syndrome in rabbit hind limbs. METHODS: Rabbits underwent femoral artery occlusion after ligation of branches from terminal aorta to femoral artery. After a 7-h ischemia, reperfusion was established with the use of heparinized polyethylene shunts. Rabbits received taurine (1g/kg) or normal saline (control) by iv infusion 10 min before shunt placement. During reperfusion, anterior compartment pressure (ACP) was monitored continuously in the left lower extremity. Gastrocnemius muscle triphenyltetrazolium chloride (TTC) level, taurine content and myeloperoxidase activity were assayed. Oxidative stress was induced in the in vitro gastrocnemius muscle slices by free radical generating systems (FRGS), and the malondialdehyde content was measured in presence or absence of taurine. RESULTS: After 7 h of ischemia, none of the parameters that we measured were different from those before ischemia, except that TTC reduction decreased by 80%. In the control group, after 2 h of reperfusion, ACP increased 4.5-fold, and gastrocnemius muscle taurine content was reduced by 33%. In taurine-treated animals, at 2h reperfusion, the mean arterial blood pressure and heart rate were increased, by 6% and 10%. ACP decreased by 39%, muscle edema decreased by 16%, TTC reduction increased by 150%, and lactate dehydrogenase decreased by 36% compared to control group. Plasma and muscle taurine content increased by 70% and 88%, respectively. In the taurine-treated group, at 2 h reperfusion, plasma malondialdehyde and conjugated diene content were decreased by 38% and 23%, respectively, and muscle malondialdehyde and conjugated diene content decreased by 22% and 30%, respectively compared to the control group. At 2 h reperfusion, myeloperoxidase activity was increased 3.5-fold in control animals. In the in vitro study, taurine decreased malondialdehyde content in muscle slices incubated with hypochlorous acid in a dose-dependent manner, but there was no change when incubated with hydrogen peroxide and xanthine oxidase. CONCLUSION: Treatment with taurine inhibited I/R-induced compartment syndrome by at least in part attenuating oxidative stress injury induced by I/R, suggesting clinical application of taurine might be a new strategy for the prevention and treatment of compartment syndrome.

Animals↗
PubMed2005

Endogenous hydrogen sulfide in patients with COPD.

OBJECTIVES: COPD is characterized by progressive airway obstruction. Recent studies showed that besides nitric oxide (NO) and carbon monoxide (CO), endogenous hydrogen sulfide (H(2)S) might be the third signaling gasotransmitter. To clarify the role of endogenous H(2)S in the pathogenesis of COPD, we investigated the relation of serum H(2)S level to severity of COPD as defined by lung function and airway inflammation. METHODS: Levels of serum H(2)S and NO, lung function, and cell differential counts in induced sputum were studied in 27 patients with acute exacerbation of COPD (AECOPD), 37 patients with stable COPD, and 13 healthy subjects. Patients with AECOPD had arterial blood gas levels measured and underwent Doppler echocardiography. In addition, in order to clarify the effects of age and smoking status on serum H(2)S level, we recruited three groups who were age matched to the study group but had no airflow limitation (59 subjects). RESULTS: Serum H(2)S level (34.0 +/- 0.9 to 36.4 +/- 1.1 micromol/L [+/- SEM]) did not differ among healthy control subjects with different ages (56.6 to 75.0 years, respectively). Serum H(2)S level was significantly higher in patients with stable COPD than in patients with AECOPD and age-matched control subjects (p < 0.01) and correlated positively with NO level in all healthy control subjects and all patients with COPD (r = 0.352, p = 0.000). Serum H(2)S level was significantly lower in smokers than nonsmokers, both with AECOPD (p < 0.05) and healthy control subjects (p < 0.01). It was significantly lower in smokers with AECOPD than healthy smokers and smokers with stable COPD (p < 0.01). Serum H(2)S level differed and was decreased (p < 0.05) among stable COPD patients by stage of airway obstruction (p < 0.05), and it was lower in patients with stage III than stage I obstruction (p < 0.05). Serum H(2)S level in all patients with COPD and healthy control subjects correlated positively with the percentage of predicted FEV(1) value (r = 0.300, p = 0.009). It was lower in patients with AECOPD and systolic pulmonary artery pressure (PASP) > or = 35 mm Hg than those with PASP within the normal range (< 35 mm Hg) [p < 0.05] and was negatively correlated with PASP (r = - 0.561, p = 0.011). Serum H(2)S level was negatively correlated with proportion of neutrophils in sputum (r = - 0.422, p = 0.001) and positively correlated with proportion of lymphocytes (r = 0.286, p = 0.028) and macrophages (r = 0.334, p = 0.01) in all patients with COPD. CONCLUSIONS: Endogenous H(2)S is involved in the pathogenesis of airway obstruction in COPD, and its alteration in level may be connected with disease activity and severity.

Aged↗
PubMed2005

[Emphasize the role of bioactive small molecules in the homeostasis regulation of cardiovascular system].

Bioactive small molecules play a crucial role in maintaining structural and functional homeostasis of cardiovascular system. However, systemic research pattern is rare because of the multiple forms, diverse effects and complicated interaction of these molecules. Therefore firstly, they can be classified into different single 'families' according to their internal relationships. Secondly, studies may be focused on the network of members within each 'family' as well as network among different 'families', especially the physiological and pathological significance of each member in the cardiovascular diseases. Lastly, efforts should be made to establish a primary and simple regulation network as the strategy of researches on biology of cardiovascular systems, and to promote the transition to a network covering more complicated multiplex 'families', even the whole body.

Biological Products↗
PubMed2005

[Changes of pulmonary artery structural remodeling in pulmonary hypertension induced by high pulmonary flow in rats].

UNLABELLED: To explore the changes of time-dependent pulmonary artery structural remodeling in pulmonary hypertension induced by high pulmonary flow in rats. METHODS: Eighty male SD rats were randomly divided into control group (n =40) and shunt group (n = 40). Rats in shunt group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. In the control group, rats experienced the same experimental processes except the shunting procedure. After 1 day, 3 days, 1 week, 4 weeks, and 8 weeks of experiment, systolic pulmonary artery pressure (SPAP) and mean pulmonary artery pressure (MPAP) of each rat were evaluated by using a right cardiac catheterization procedure. Heart tissues were separated as right ventricle (RV) and left ventricle plus septum (LV+SP), and the ratio of RV to LV+SP [RV/ (LV+ SP)] was calculated. The morphologic changes including micro- and ultra-structural changes of pulmonary arteries of rats were observed under optical microscope and electro-microscope, respectively. The percentages of muscularized artery (MA), partial muscularized artery (PMA) and non-muscularized artery (NMA) in small pulmonary arteries and median pulmonary arteries were calculated. The changes of relative medial thickness (RMT) and relative medial area (RMA) of pulmonary arteries were examined. RESULTS: Compared with control group, SPAP and MPAP did not change on day 1, day 3, and week 4. However, in week 1 and week 8 of experiment, SPAP and MPAP increased significantly (P < 0.01). Meanwhile, in week 8 of experiment, RV/ (LV+SP) increased significantly (P < 0.05). In contrast to control group, the percentages of MA, PMA, and NMA did not change in day 1, day 3 and week 1. But in week 4 and week 8, the percentages of MA and PMA increased significantly (P < 0.01) but that of NMA decreased significantly (P < 0.01). RMT and RMA did not change in day 1, day 3, week 1 and even week 4 in shunt group as compared with those of control group, but they increased significantly in week 8 (P < 0.05). The changes of ultra-structure of pulmonary arteries included that endothelial cells became swollen and large in size on day 3, smooth muscular cells increased in size besides the change of endothelial cells in week 1, and they changed from contractile phenotype to synthetic phenotype in week 4. Collagen deposited in pulmonary arteries markedly in week 8. CONCLUSION: Pulmonary artery structural remodeling develops in a time-dependent manner. Endothelial cells of pulmonary arteries become swollen firstly, followed by the proliferation of smooth muscular cells and finally by remodeling of extra cellular matrix.

Animals↗
PubMed2005

[Significance of gaseous signal molecule in the pathogenesis of cardiovascular diseases].

The discovery of nitric oxide (NO) initiated a novel research field, gaseous signal molecules. Other two gaseous signal molecules, carbon monoxide (CO) and hydrogen sulfide (H2S), have been approved subsequently. All of these three gaseous signal molecules are generated endogenously and exert extensive biological effects. This article reviews the significance of gaseous signal molecules in the pathogenesis of cardiovascular diseases. In the cardiovascular system, the endogenous NO, CO and H2S form three specific and relevant pathways with their corresponding enzymes including nitric oxide synthase (NOS), heme oxygenase (HO), and cystathionine-gamma-lyase (CSE). The gaseous signal molecules not only participate in the maintenance of physiological function and structure of the cardiovascular system, but also exert important pathophysiological effects in the pathogenesis of cardiovascular diseases, such as hypertension, pulmonary hypertension, septic shock and atherosclerosis. Further studies on gaseous signal molecules will remarkably promote the basic research in the cardiovascular fields, and provide a novel direction for the clinical research as well.

Animals↗
PubMed2005

[Cytochrome P450/epoxyeicosatrienoic acids system and myocardial ischemic-reperfusion injury].

Interests on the effects of cytochrome P450 (CYP450) monooxygenases and epoxyeicosatrienoic acids (EETs) on myocardial ischemic-reperfusion injury has been increased in recent years. The CYP450/EET system may influence the degree of myocardial ischemic-reperfusion injury through "poly-targets", such us oxygen free radical, calcium overload, leukocytes adherence, nitric oxide, ATP-sensitive K+ channels, and mitogen activated protein kinase. The exaggeration or recovery of injury depends on the physical status. Study of factors that affects CYP450/EET, particularly identification of their involvement in cardioprotective signaling and specific roles, will elucidate the mechanisms of myocardial ischemic-reperfusion injury, and find a new way of prevention and treatment. This article will review the relationship between the changes of CYP450/EETs system and myocardial ischemic-reper-

Animals↗
PubMed2004

Changes in production and metabolism of brain natriuretic peptide in rats with myocardial necrosis.

In this study, we employed rat model of acute myocardial necrosis induced by isoproterenol (ISO) to study the possible roles of corin, the protease uniquely distributing in myocardium to convert pro-brain natriuretic peptide (proBNP) to BNP, and neutral endopeptidase (NEP), the major enzyme to degrade BNP, in changing the levels of BNP. In rats with isoproterenol alone, the myocardium necrosis occurred and the cardiac function was inhibited; the BNP contents in plasma and myocardium were upregulated, so did the myocardial corin mRNA level; the NEP activity in plasma and myocardium were downregulated. Omapatrilat (OMA) treatment relieved myocardial lesions and improved cardiac function. In the plasma and myocardium, omapatrilat treatment increased BNP contents, reduced NEP activity; in myocardium, mRNA level of proBNP and corin decreased, but NEP mRNA expression increased. Our study confirmed that omapatrilat treated myocardial necrosis effectively and suggested that increased BNP in rats with myocardial necrosis could depend on increased production and conversion as well as decreased degradation.

Animals↗
PubMed2004

Effects of adrenomedullin on aldosterone-induced cell proliferation in rat cardiac fibroblasts.

Aldosterone induces cardiac remodeling in cardiovascular diseases by stimulating the proliferation, production and secretion of collagen in fibroblasts. It also stimulates vascular smooth muscle cells to produce and secrete adrenomedullin (ADM), which has a cytoprotective effect against cardiovascular damage. We examined the effect of aldosterone on ADM production and secretion in rat cardiac fibroblasts, and the effect of ADM on aldosterone-stimulated fibroblast proliferation to observe the interaction between endogenous ADM and aldosterone. We detected ADM produced and secreted from cultured cardiac fibroblasts and the intracellular cAMP level by radioimmunoassay; evaluated cell proliferation by the level of [3H]-thymine incorporation; measured preproADM gene expression by reverse transcriptase polymerase chain reaction (RT-PCR); and monitored extracellular signal related kinase (ERK) activity by the phosphorylation of myelin basic protein in the presence of [gamma-32P] ATP. Our results showed that aldosterone-stimulated secretion of ADM and its mRNA expression were concentration-dependent, which could be inhibited by the specific antagonist of mineralocorticoid receptor, spironolactone. In contrast, ADM inhibited aldosterone-induced fibroblast proliferation and ERK activity. Treatment with ADM24-50 (a new antagonist of specific ADM receptors) and calcitonin gene-related peptide (CGRP)8-37 (the antagonist of CGRP receptor type 1), to attenuate the action of endogenous ADM, reinforced the aldosterone-induced proliferation and inhibited the intracellular cAMP production stimulated by aldosterone. Thiorphan, an inhibitor of ADM degradation, inhibited the [3H]-thymine incorporation and reinforced the intracellular cAMP level induced by aldosterone. We reach the conclusion that aldosterone stimulates rat cardiac fibroblasts to produce and secrete ADM, which in turn regulates the proliferation-induced effects of aldosterone in these cells.

Adrenomedullin↗
PubMed2004

Electrophysiological evidences for the contribution of NMDA receptors to the inhibition of clonidine on the RVLM presympathetic neurons.

The main objective of this study is to test the hypothesis that N-methyl-D-aspartate (NMDA) receptors within the rostral ventrolateral medulla (RVLM) are involved in the inhibition of clonidine on the RVLM presympathetic neurons. Totally, 22 presympathetic neurons were recorded in anesthetized and paralyzed rats. The majority of these neurons (n=16 of 22) were significantly inhibited by iontophoretic (30 nA) clonidine, the other 6 neurons were insensitive to clonidine. In seven clonidine-sensitive neurons, iontophoretic clonidine (30 nA) antagonized the neuronal excitation of iontophoretic NMDA receptor agonist NMDA (20 nA). In remaining nine clonidine-sensitive neurons, iontophoretic NMDA receptor antagonist MK801 (60 nA) significantly attenuated the neuronal inhibition of iontophoretic (30 nA) clonidine. In conclusion, these results suggest that NMDA receptors contribute to the inhibition of clonidine on the RVLM presympathetic neurons.

Action Potentials↗
PubMed2004

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

Lysophosphatidic acid (LPA) is a bioactive phospholipid having growth factor-like activity on fibroblasts and is involved in cardiovascular diseases such as hypertension and heart failure by inducing vascular remodeling, characterized by fibroblast proliferation and migration in adventitia. Among various bioactive factors that LPA works with, adrenomedullin (ADM) is a multiple functional peptide with an important cytoprotective effect against cardiovascular damage. We studied rat aortic adventitia to explore the possible paracrine/autocrine interaction between endogenous ADM and LPA. LPA stimulation of the adventitia to secrete ADM and express its mRNA was concentration dependent. ADM inhibited LPA-induced proliferation in adventitial cells and attenuated the activity of mitogen-activated protein kinase (MAPK) stimulated by LPA. In contrast, treatment with specific antagonists of the ADM receptor potentiated the LPA-induced proliferation in adventitial cells. We concluded that LPA stimulates the adventitia to produce and secrete ADM, which in turn regulates the vascular biological effects of LPA.

Adrenomedullin↗
PubMed2004

[Changes and significance of hydrogen sulfide/cystathionine gamma-lyase system in hypertension: an experimental study with rats].

OBJECTIVE: To explore the significance of hydrogen sulfide/cystathionine gamma-lyase (H(2)S/CSE) system in the development of hypertension and the effects of H(2)S/CSE system on the modulation of aortic remodeling process of hypertension. METHODS: Eight 4-week-old male WKY rats were used as WKY control group, and another sixteen SHR rats at the age of 4 weeks were randomly divided into SHR control group (n = 8) and SHR + NaHS (H(2)S donor) group (n = 8). The rats of SHR control and WKY control were injected with normal saline and the rats of the SHR + NaHS group were injected with NaHS each day. Five weeks later, the blood pressure and the left-to-whole heart weight ratio were determined. The transcriptional level of CSE in aorta and the H(2)S level in plasma were detected. The morphometric parameters of the thoracic aorta including the outer radius, medium area and ratio of wall thickness to lumen radius were detected too. RESULTS: At the age of 9 weeks the systolic blood pressure and the left-to-whole heart weight ratio of the SHR control rats were both higher than those of the WKY control rats [(184 +/- 12) mm Hg vs (108 +/- 23) mm Hg, 1 mm Hg = 0.133 kPa, and (0.853 +/- 0.021) vs (0.826 +/- 0.024)]. The transcriptional level of CSE in aorta and the H(2)S level in serum of the rats in the SHR control group were both lower than those of the rats in the WKY control group (9.3 +/- 0.7) x 10(-8) fmol vs (16.1 +/- 1.0) x 10(-8) fmol, and (20 +/- 9) micro mol/L vs (48 +/- 13) micro mol/L, while the morphometric parameters of the thoracic aorta including the outer radius, the medium area and ratio of lumen radius and wall thickness of the SHR control rats were all higher compared with those of the WKY control rats [outer radius: (1999 +/- 45) micro m vs (1790 +/- 96) micro m], medium area: (0.60 +/- 0.06) mm(2) vs (0.48 +/- 0.03) mm(2), and ratio of wall thickness to lumen radius: (0.066 +/- 0.006) vs (0.060 +/- 0.004). The exogenous administration of NaHS made the systolic blood pressure of rats in the SHR + NaHS group much lower than that of the rats in SHR control group [(158 +/- 13) mm Hg vs (184 +/- 12) mm Hg], however, the transcriptional level of CSE in aorta and the H(2)S level in serum of the rats in SHR + NaHS group were much higher than those of the rats in SHR control group [(12.4 +/- 1.0) x 10(-8) fmol vs (9.3 +/- 0.7) x 10(-8) fmol] vs [(96 +/- 32) micro mol/L vs (20 +/- 9) micro mol/L]. The morphometric parameters of SHR + NaHS group were lower than those of the SHR control group. CONCLUSION: Down regulation of H(2)S/CSE system is a major factor in the development of spontaneous hypertension and the accompanying structural remodeling of aorta. Exogenous administration of H(2)S may attenuate the process of hypertension.

Animals↗