No abstract available.
Angiotensin II* ; Angiotensins*

BACKGROUND AND OBJECTIVES: The purpose of this study was to analyze the patterns of coronary artery flow, using transthoracic Doppler echocardiography(TE), in subjects with chest pains and normal coronary angiograms. SUBJECTS AND METHODS: 93 patients(M:F=34:59, mean age:57+/-11 years) ith chest pains and normal coronary angiograms were included in this study. After obtaining baseline clinical data, an exercise treadmill test(TT) as performed, according to the Bruce protocol. The peak diastolic coronary artery flow velocity(DV), at rest, and the coronary flow reserve(FR), in the distal left anterior descending coronary artery(AD), were estimated, using dipyridamole, with TTE. After the administration of angiotensin II receptor(AT II) lockers to 12 patients with a CFR <2.1. The ETT and CFR were followed up. RESULTS: Of the 93 subjects 63(7.7%) ere female, and 53(6.9%) ad a history of hypertension and 61(5.5%) howed ST or T abnormality on their resting ECG. Five subjects(30.3%) ad metabolic or hematologic problems, such as hyperthyroidism or anemia. Twenty-seven(0.3%) of the 89 subjects showed a reduced CFR value less than 2.1. The subjects with horizontal or down-sloping ST depression on their ETT showed a decreased CFR, compared with those with no ST shifting or an up-sloping ST depression(<0.05, respectively). Twenty-six(7.9%) f the 93 subjects showed a slow coronary flow velocity <14 cm/sec, and 15(3.3%) f 18 subjects who estimated CFR had CFR > or =2.1. In 7(8.3%) of 12 subjects with a CFR <2.1, their CFR increased, with an improvement of the ETT results, following the administration of the AT II blocker, after an average 19+/-9 months. CONCLUSION: The patients with chest pains and normal coronary angiograms have a heterogeneous clinical spectrum, such as hypertensin, slow flow, reduced CFR, and so on. These subjects need treatment according to the etiology and pathogenesis of their condition, which can be followed up by coronary flow measurements, using TTE.
Anemia ; Angiotensin Amide ; Angiotensin II ; Blood Flow Velocity ; Chest Pain* ; Coronary Vessels* ; Depression ; Dipyridamole ; Echocardiography, Doppler* ; Electrocardiography ; Female ; Humans ; Hypertension ; Hyperthyroidism ; Thorax*

BACKGROUND AND OBJECTIVES: The octapeptide hormone of the renin-angiotensin system, angiotensin ii, regulates a wide variety of physiological responses including salt and water balance, blood pressure, and vascular tone. Contradictory results have been reported regarding the effects of angiotensin ii on vascular smooth mu-scle cell (VSMC) proliferation. The aim of the present study was to investigate the direct effect of angiotensin ii on the growth of VSMC. MATERIALS AND METHOD: Rat aortic smooth muscle cells were obtained by the combined collagenase and elastase methods. Cells between the 4th and 8th passages were used for the experiments. Cultures were treated daily for 3 days with either angiotensin ii alone or angiotensin ii with equimolar concentrations of saralasin. Incorporated radioactivity of [3H]thymidine and [14C]phenylalanine was measured by liquid scintillation spectrometry. RESULTS: Angiotensin ii increased [14C]phenyalanine incor-poration about 20-30%, and saralasin completely blocked the stimulation by angiotensin ii. However, there was no significant increase in [3H]thymidine incorporation by angiotensin ii stimulation in this study. CONCLUSION: These results suggest that angiotensin ii alone induces cellular hypertrophy but has no detectable mitogenic activity in cultured rat aortic VSMC.
Angiotensin II* ; Angiotensins* ; Animals ; Blood Pressure ; Collagenases ; Hypertrophy ; Muscle, Smooth, Vascular* ; Myocytes, Smooth Muscle ; Pancreatic Elastase ; Radioactivity ; Rats ; Renin-Angiotensin System ; Saralasin ; Spectrum Analysis

No abstract available.
Angiotensin II ; Angiotensins ; Lithium ; Receptors, Angiotensin

Angiotensin II(A II) -a main effector molecule of renin-angiotensin system(RAS) has been known to increase blood pressure and glomerular capillary pressure, and filtration fraction which may be involved in the progressive renal injury process. The action of A II takes place mainly through AT1 receptor. RAS can be blocked by angiotensin converting enzyme inhibitor(ACEI) and recently developed A II AT1 receptor antagonist(AT1 RA). ACEI also activate kinin system, simultaneously. However, AT1 RA does not affect kinin system. The renoprotective mechanism of ACEI may be related with activation of kinin system. In order to evaluate the renoprotective mechanism of long-term ACEI(enalapril, 100mg/L in drinking water for 12 weeks) or AT1 RA treatment(losartan 300mg/L in drinking water for 12 weeks), and its effect on the cytokines and growth factor expressions of renal cortical tissue by compatitive RT-PCR, 46 5/6 nephrectomized(5/6 NPX) rats and 8 sham operated rats were included in this study. Five sixth NPX rats showed marked hypertensin, significant proteinuria and glomerulosclerosis(mean 30.5%) in 12 weeks after surgery. However, enelapril or losartan treated rats revealed significantly lower 24 hour urinary protein excretion(UProtV), systolic blood pressure(SBP), and glomerulosclerosis than those of control 5/6 NPX rats. Plasma renin activity and angiotensin II levels of 5/6 NPX untreated control rats were not significantly increased compared to sham operated rats in 12 week after surgery. Renal cortical renin gene expression of untreated 5/6 NPX rats was significantly suppressed compared to sham operated rats. Enalapril or losartan treated 5/6 NPX rats showed significantly increased renin gene expression compared to untreated 5/6 NPX rats. Renal cortical gene expressions of TGF-beta, TNF-alpha, MCP-1, IL-6, osteopontin, and endothelin-1 were significantly increased in 5/6 NPX untreated control rats compared to sham operated rats. Enalapril or losartan treated 5/6 NPX rats showed significantly less level of renal TGF-beta gene expression compared to 5/6 NPX control rats. The magnitude of SBP and UProtV were significantly positively correlated with the degree of glomeruloslerosis(p<0.001, p<0.001). With the above result, we speculate that because ACEI or AT1 RA showed similar renoprotective effect in 5/6 NPX rats, at least in part, local activation of RAS plays an important role in the progressive renal injury process of this model.
Angiotensin Amide ; Angiotensin II ; Angiotensins ; Animals ; Blood Pressure ; Capillaries ; Cytokines ; Drinking Water ; Enalapril ; Endothelin-1 ; Filtration ; Gene Expression ; Interleukin-6 ; Losartan ; Osteopontin ; Peptidyl-Dipeptidase A ; Plasma ; Proteinuria ; Rats ; Renin ; Renin-Angiotensin System* ; Transforming Growth Factor beta ; Tumor Necrosis Factor-alpha

Angiotensin II(A II) -a main effector molecule of renin-angiotensin system(RAS) has been known to increase blood pressure and glomerular capillary pressure, and filtration fraction which may be involved in the progressive renal injury process. The action of A II takes place mainly through AT1 receptor. RAS can be blocked by angiotensin converting enzyme inhibitor(ACEI) and recently developed A II AT1 receptor antagonist(AT1 RA). ACEI also activate kinin system, simultaneously. However, AT1 RA does not affect kinin system. The renoprotective mechanism of ACEI may be related with activation of kinin system. In order to evaluate the renoprotective mechanism of long-term ACEI(enalapril, 100mg/L in drinking water for 12 weeks) or AT1 RA treatment(losartan 300mg/L in drinking water for 12 weeks), and its effect on the cytokines and growth factor expressions of renal cortical tissue by compatitive RT-PCR, 46 5/6 nephrectomized(5/6 NPX) rats and 8 sham operated rats were included in this study. Five sixth NPX rats showed marked hypertensin, significant proteinuria and glomerulosclerosis(mean 30.5%) in 12 weeks after surgery. However, enelapril or losartan treated rats revealed significantly lower 24 hour urinary protein excretion(UProtV), systolic blood pressure(SBP), and glomerulosclerosis than those of control 5/6 NPX rats. Plasma renin activity and angiotensin II levels of 5/6 NPX untreated control rats were not significantly increased compared to sham operated rats in 12 week after surgery. Renal cortical renin gene expression of untreated 5/6 NPX rats was significantly suppressed compared to sham operated rats. Enalapril or losartan treated 5/6 NPX rats showed significantly increased renin gene expression compared to untreated 5/6 NPX rats. Renal cortical gene expressions of TGF-beta, TNF-alpha, MCP-1, IL-6, osteopontin, and endothelin-1 were significantly increased in 5/6 NPX untreated control rats compared to sham operated rats. Enalapril or losartan treated 5/6 NPX rats showed significantly less level of renal TGF-beta gene expression compared to 5/6 NPX control rats. The magnitude of SBP and UProtV were significantly positively correlated with the degree of glomeruloslerosis(p<0.001, p<0.001). With the above result, we speculate that because ACEI or AT1 RA showed similar renoprotective effect in 5/6 NPX rats, at least in part, local activation of RAS plays an important role in the progressive renal injury process of this model.
Angiotensin Amide ; Angiotensin II ; Angiotensins ; Animals ; Blood Pressure ; Capillaries ; Cytokines ; Drinking Water ; Enalapril ; Endothelin-1 ; Filtration ; Gene Expression ; Interleukin-6 ; Losartan ; Osteopontin ; Peptidyl-Dipeptidase A ; Plasma ; Proteinuria ; Rats ; Renin ; Renin-Angiotensin System* ; Transforming Growth Factor beta ; Tumor Necrosis Factor-alpha

No abstract available.
Angiotensin II* ; Angiotensins* ; Hydrocortisone* ; Insulin*

No abstract available.
Angiotensin II ; Angiotensin Receptor Antagonists ; Angiotensins ; Hyperkalemia ; Receptors, Angiotensin

OBJECTIVE: The exact mechanism of angiotensin II to steroidogenesis is still speculative in spite of many researches especially in human and these were performed indirectly with serum or follicular fluid. Under the hypothesis that ovarian RAS increases androgen, decreases progesterone synthesis in normal human ovary, we investigated the exact action of angiotnesin II on human ovary. METHODS: After appliance of angiotensin II and saralasin to the normal human ovarian follicles, we measured sex steroids like progesterone, testosterone, DHEA and enzymes like HSD3beta2, CYP 17 to see the action of angiotensin II and its antagonist, saralasin. The results were analyzed by ANOVA test. RESULTS: Angiotensin II increased androgen synthesis but did not affect progesterone synthesis. There were no difference of HSD 3beta2 mRNA expression in angiotensin II and saralasin group compared with control group. The expression of CYP17 mRNA was increased by angiotensin II but did not reach statistically significant level. CONCLUSION: Angiotensin II could increase androgen production probably via overexpression of CYP17, but had no efffect on progesterone production.
Angiotensin II* ; Angiotensins* ; Dehydroepiandrosterone ; Female ; Follicular Fluid ; Humans* ; Ovarian Follicle* ; Ovary ; Progesterone ; RNA, Messenger ; Saralasin ; Steroid 17-alpha-Hydroxylase ; Steroids ; Testosterone

No abstract available.
Angiotensin I ; Angiotensin II* ; Angiotensins* ; Autoradiography ; Receptors, Angiotensin* ; Renin* ; Renin-Angiotensin System*