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Biomedical subjects

M Daimon

Publications and source records attributed to M Daimon.

At least 19 recordsLinked to original sources
PubMed2001

Neonatal-onset hereditary coproporphyria with male pseudohermaphrodism.

The appearance of hereditary coproporphyria (HCP) before puberty is very rare, and all reported cases of early-onset HCP have been in the homozygous or the compound heterozygous state. Some have been identified as harderoporphyria, which is a rare erythropoietic variant form of HCP. These conditions can be differentiated by molecular analysis because the gene abnormality responsible for harderoporphyria seems to be unique (K404E). Early-onset HCP, not harderoporphyria, is reported with a gene mutation in the heterozygous state and male pseudohermaphrodism. It was shown that adrenal gland hypofunction resulted in male pseudohermaphrodism. This case demonstrates the possibility that abnormalities of steroid metabolism influence porphyria.

Adrenal Insufficiency↗
PubMed2001

Candesartan inhibits carotid intimal thickening and ameliorates insulin resistance in balloon-injured diabetic rats.

This study investigates the effects of candesartan, an angiotensin II type 1 receptor blockade, on carotid arterial intimal thickening and glucose tolerance in balloon-injured male Wistar fatty rats and their littermates (Wistar lean rats). Candesartan was orally administered to 12-week-old rats for 21 days, and age-matched rats without the agent were used as the respective controls. Balloon catheterization in the left common carotid artery was performed on day 7, and the artery was removed on day 14 for histological analysis. Compared with the area ratios of the neointima/media in fatty rats without treatment, the ratios in fatty rats treated with candesartan at 1 mg. kg(-1). d(-1) and lean rats without treatment were significantly decreased to 65%; on the other hand, the ratios of fatty rats treated with candesartan at 10 mg. kg(-1). d(-1) and lean rats treated with 1 mg. kg(-1). d(-1) were reduced to 35%, and those of lean rats treated with 10 mg. kg(-1). d(-1) were reduced to 28%. The administration of candesartan also decreased the level of plasma glucose time- and dose-dependently in fatty rats. In an intragastric glucose load, the levels of both glucose and insulin at 30 and 60 minutes were significantly decreased when fatty rats were treated with candesartan at 10 mg. kg(-1). d(-1). In cultured vascular smooth muscle cells from fatty rats, insulin-stimulated Akt (New England Biolabs) phosphorylation and 2-deoxy-D-glucose uptake were inhibited to 59% and 68%, respectively, by angiotensin II, but the effects were ameliorated by the addition of 10(-7) mol/L candesartan. We conclude that candesartan could be effective for the suppression of vascular smooth muscle cell growth dose-dependently in Wistar fatty and lean rats. Furthermore, the agent could improve insulin resistance in Wistar fatty rats.

Angiotensin Receptor Antagonists↗
PubMed2001

Galectin-1 is a component of neurofilamentous lesions in sporadic and familial amyotrophic lateral sclerosis.

In amyotrophic lateral sclerosis (ALS), abnormal accumulation of neurofilaments induces pathological changes such as axonal spheroids, cord-like neurite swellings, and perikaryal conglomerate inclusions in degenerating motor neurons of the spinal cord, and the accumulation seems to cause motor neuron degeneration in this disease. Such ALS lesions were intensely labeled with HepSS-1, a monoclonal antibody to heparan sulfate. Since the identification of HepSS-1-immunoreactive substance seems to be an important step for understanding the molecular pathology of ALS, we purified the substance from human spinal cord tissue to homogeneity. Amino acid sequence of the protein was consistent with that of galectin-1. Immunohistochemistry using antibodies against recombinant human galectin-1 showed that galectin-1 was accumulated in these lesions in ALS. Although HepSS-1 was believed to be specific for heparan sulfate, it reacted with recombinant human galectin-1 which has no heparan sulfate moiety. The results show that galectin-1 is a component of the neurofilamentous lesions in ALS. Since galectin-1 has axonal regeneration-enhancing activity, the abnormal accumulation of galectin-1 to the lesions seems to be related to the pathological process of ALS.

Aged↗
PubMed2001

Physiologic assessment of coronary artery stenosis by coronary flow reserve measurements with transthoracic Doppler echocardiography: comparison with exercise thallium-201 single piston emission computed tomography.

OBJECTIVES: We evaluated the value of coronary flow reserve (CFR), as determined by transthoracic Doppler echocardiography (TTDE), for physiologic assessment of coronary artery stenosis severity, and we compared TTDE measurements with those obtained by exercise thallium-201 (Tl-201) single-photon emission computed tomography (SPECT). BACKGROUND: Coronary flow reserve measurements by TTDE have been reported to be useful for assessing angiographic left anterior descending coronary artery (LAD) stenosis. However, discrepancies exist between angiographic and physiologic estimates of coronary lesion severity. METHODS: We studied 36 patients suspected of having coronary artery disease. The flow velocity in the distal LAD was measured by TTDE both at rest and during intravenous infusion of adenosine. Coronary flow reserve was calculated as the ratio of hyperemic to basal peak (peak CFR) and mean (mean CFR) diastolic flow velocities. The CFR measurements by TTDE were compared with the results of Tl-201-SPECT. RESULTS: Complete TTDE data were acquired for 33 of 36 study patients. Of these 33 patients, Tl-201-SPECT confirmed reversible perfusion defects in the LAD territories in 12 patients (group A). Twenty-one patients had normal perfusion in the LAD territories (group B). Peak CFR and mean CFR (mean value +/- SD) were 1.5 +/- 0.6 and 1.5 +/- 0.7 in group A and 2.8 +/- 0.8 and 2.7 +/- 0.7 in group B, respectively. Both peak and mean CFR < or = 2.0 predicted reversible perfusion defects, with a sensitivity and specificity of 92% and 90%, respectively. CONCLUSIONS: Noninvasive measurement of CFR by TTDE provides data equivalent to those obtained by Tl-201-SPECT for physiologic estimation of the severity of LAD stenosis.

Aged↗
PubMed2001

Characterization of platelet-derived growth factor-induced p38 mitogen-activated protein kinase activation in vascular smooth muscle cells.

BACKGROUND: The mitogen-activated protein (MAP) kinase super-family plays a crucial role in cell growth and differentiation and even in programmed cell death in response to diverse extracellular stimuli. The platelet-derived growth factor (PDGF)-BB is well known to promote the proliferation of vascular smooth muscle cells (VSMC) via extracellular-regulated protein kinases (ERKs), leading to the development of cardiovascular diseases. However, it has not yet been clarified whether PDGFs that include other isoforms can activate the other parallel signal transduction pathways, c-jun NH2-terminal protein kinase (JNK) and p38 MAP kinase (p38), in VSMC. In this study, we investigated the effect of PDGFs on p38 activation in cultured rat VSMC. MATERIALS AND METHODS: After stimulation by PDGFs with SB-203580 or PD-98059, the cells were solubilized, and the expressions of MAP kinases, MAP kinase kinases (MKKs), phosphorylated DNA-binding proteins, and cyclooxigenases (COXs) were examined by immunoblot analysis. RESULTS: PDGFs activated p38 phosphorylation dose-dependently, and the phosphorylations were specifically inhibited by SB-203580 but not by PD-98059. PDGFs also activated the phosphorylation of MKK 3/MKK 6 but not that of either stress-activated protein kinase/ERK kinase or JNK. PDGFs affected the activation of a cyclic AMP response-element binding protein, which was inhibited by SB-203580. However, the activating transcription factor-2 was not activated by PDGFs. Interestingly, the stimulation of PDGFs for 72 h enhanced the level of COX-2, and these levels were decreased by SB-203580. CONCLUSION: These results have clarified that PDGFs activate the p38 cascade via an MKK 3/6 pathway, independently of the ERK cascade, and subsequently regulate the level of COX-2 in rat VSMC, providing that PDGFs influence the inflammatory process in the vascular wall.

Activating Transcription Factor 2↗
PubMed2001

Characterization of an inhibitory effect of pioglitazone on balloon-injured vascular smooth muscle cell growth.

This study investigates whether pioglitazone could suppress an atherogenic process such as balloon-injured carotid intimal thickening and the proliferation of vascular smooth muscle cells (VSMC). We first examined the effect of pioglitazone to determine whether it could suppress intimal thickening induced by balloon catheterization in Sprague-Dawley rats. After 14 days postcatheterization in the left common carotid artery, the neointimal layers were completely occupied by proliferated VSMC, and the area ratio of neointima to media treated with 10 mg/kg/d of pioglitazone was significantly decreased to 57%. Next, we evaluated the effect of pioglitazone on the proliferation of rat cultured VSMC. Piogliotazone dose-dependently decreased the values of DNA synthesis, total cellular protein content, phosphorylations of extracellular signal-regulated protein kinase 1/2 and mitogen-activated protein kinase kinase 1/2, and proliferative cell nuclear antigen in VSMC. Pioglitazone also inhibited the phosphorylation of Pyk2. We conclude that pioglitazone itself could be effective for suppressing the growth of VSMC and consequent carotid intimal thickening.

Animals↗
PubMed2001

Insulin inhibits glucagon-induced glycogenolysis in perivenous hepatocytes specifically.

Hepatocytes form the hepatic acinus as the unit of microcirculation. Following the bloodstream, at least 2 different zones can be discerned: the periportal and perivenous zones. Two types of hepatocytes, periportal hepatocytes (PPHs) and perivenous hepatocytes (PVHs), have been thought to be functionally heterogeneous, with PPHs being predominantly gluconeogenic and PVHs being glycolytic. We therefore investigated the region-specific functional effects of insulin on glycogen synthesis, glycolysis, glycogenolysis, and gluconeogenesis in isolated PPHs and PVHs prepared by using the digitonin-collagenase method. Glycogen synthesis from 5 to 20 mmol/L glucose did not differ between the PPHs and PVHs of fed rats during 60 minutes of incubation. Lactate release induced by 5 to 20 mmol/L glucose was 3 times greater from PVHs than from PPHs (P <.01). The addition of insulin did not accelerate either glycogen synthesis or lactate release during 60 minutes of incubation. Insulin did not inhibit glucose release from gluconeogenic substrates with or without 0.2 nmol/L glucagon in either the PPHs or the PVHs of fasting rats. Insulin antagonized the 0.1 nmol/L glucagon-induced increase in glucose release from the PVHs of fed rats during 30 minutes of incubation (to 56.1% +/- 7.2%, P <.01) but not that from the PPHs (to 81.8% +/- 7.3%, P =.10). Thus the antagonizing effect was greater in PVHs than in PPHs (P <.01). Insulin binding did not differ between the PPHs and PVHs of fed rats. It was confirmed that PVHs are actually glycolytic. An acute metabolic effect of insulin was observed only in antagonizing glucagon-induced glycogenolysis in PVHs specifically. The specific effect of insulin on PVHs might depend on the differences in intracellular characteristics between PPHs and PVHs rather than hormone binding.

Animals↗
PubMed2001

Platelet-derived growth factor BB-induced p38 mitogen-activated protein kinase activation causes cell growth, but not apoptosis, in vascular smooth muscle cells.

The aim of this experiment was to examine the regulation of p38 mitogen-activated protein (MAP) kinase by platelet-derived growth factor (PDGF)-BB and its biological effects on rat cultured vascular smooth muscle cells (VSMCs). VSMCs were obtained from aortae of male Wistar rats by the media explant technique. After being stimulated by PDGF-BB with or without the p38 MAP kinase-specific inhibitor, SB-203580, the cells were solubilized, and the levels of phosphorylated p38 MAP kinase were examined by immunoblot analysis. The amounts of DNA synthesis and content were measured by using [3H]-thymidine and Hoechst-33258 dye, respectively. The detection of apoptotic cells was evaluated by the TUNEL method. PDGF-BB could phosphorylate p38 MAP kinase dose-dependently, and the phosphorylation was specifically inhibited by SB-203580 in a dose-dependent manner. However, PDGF-BB did not affect the protein level of p38 MAP kinase. Both [3H]-thymidine incorporation and total cellular DNA content were increased by PDGF-BB, and these elevations were prevented by SB-203580. In contrast, PDGF-BB-stimulated VSMCs did not show apoptotic change in spite of the presence or absence of SB-203580. These results established that PDGF-BB activated p38 MAP kinase and subsequently regulated cell growth in VSMCs, providing a molecular mechanism by which p38 MAP kinase can cause the development of cardiovascular diseases, including atherosclerosis.

Animals↗
PubMed2001

Genotype Arg/Arg, but not Trp/Arg, of the Trp64Arg polymorphism of the beta(3)-adrenergic receptor is associated with type 2 diabetes and obesity in a large Japanese sample.

OBJECTIVE: Despite a large number of studies, no association of the Trp64Arg polymorphism of the beta(3)-adrenergic receptor gene with obesity and type 2 diabetes has yet to be clearly elucidated. We examined the associations in a large population-based sample. RESEARCH DESIGN AND METHODS: A total of 1,685 subjects (935 women and 750 men, aged 58.7 +/- 12.4 years) from a cohort population (n = 3,706) of the Funagata Diabetes Study were divided into three groups according to genotypes: Trp/Trp (n = 1,155), Trp/Arg (n = 486), and Arg/Arg (n = 44). Glucose tolerance was diagnosed according to the 1985 World Health Organization criteria. Subjects who had a BMI > or =30 kg/m(2) were considered obese. Associations with the traits related to obesity, diabetes, hypertension, and dyslipidemia were also examined. The chi(2) test and analysis of variance were used for the association studies and to assess the differences in the traits' values, respectively. RESULTS: More subjects with genotype Arg/Arg were obese and had diabetes (13.6% for each) than those with genotype Trp/Trp (3.29%, P < 0.001; and 4.16%, P = 0.007, respectively) or genotype Trp/Arg (2.06%, P < 0.001; and 5.97%, P = 0.051, respectively). No significant differences in the frequencies of occurrence of these conditions were observed between genotypes Trp/Arg and Trp/Trp. Traits related to obesity, such as percent body fat (28.82 +/- 7.95 vs. 25.93 +/- 7.21, P = 0.038) and BMI (25.07 +/- 3.84 vs. 23.63 +/- 3.18, P = 0.018), were higher in the genotype Arg/Arg than in the genotype Trp/Trp groups. CONCLUSIONS: Genotype Arg/Arg, but not Trp/Arg, of the beta(3)-adrenergic receptor was associated with both obesity and type 2 diabetes in a large Japanese sample.

Aged↗
PubMed2001

[Evaluation of value of coronary artery bypass grafting without cardiopulmonary bypass for emergency or subemergency case].

From August 1999 through September 2000, emergency (operation within 24 hours after hospitalization) or subemergency (within 48 hours) coronary artery bypass grafting without cardiopulmonary bypass (OPCAB) was performed in 16 patients (EM group) with a mean age 71.9 years old (range: 47-85). The patients were divided into 3 groups of which were acute myocardial infarction (AMI) group, chronic heart failure (CHF) group and unstable angina (u-AP) group, and compared preoperative hemodynamics, the number of graft, target arteries, bypass patency and hospitalization period after surgery with 26 patients performed the elective OPCAB in the same duration (EL group). All patients in EM group were used intra-aortic balloon pumping (IABP) assist before operation. In EL group, 16 patients (61.5%) were required IABP (p < 0.05). Ejection fraction and cardiac index in CHF group were significantly lower than those of EL group (47.8 +/- 1.1 vs. 63.3 +/- 2.4, 2.8 +/- 0.2 vs. 1.9 +/- 0.2: p < 0.05). Pulmonary capillary wedge pressure in AMI group and CHF group was significantly higher than that of EL group (16.7 +/- 5.9, 20.8 +/- 5.4 vs. 7.2 +/- 0.8: p < 0.01). There was a significant difference in the mean number of bypass in EM group compared with that of EL group (1.8 +/- 0.2 vs. 2.7 +/- 0.2: p < 0.05). In AMI group and CHF group, the grafting rate to the major vessel in the anterior wall was occupied in more than 70% of all bypasses per patient, however that was less than 50% in EL group. The arterial graft was actively used for revascularization. The hospitalization period in AMI group and CHF group was longer than that in u-AP group and EL group (28.5 +/- 9.8, 38.8 +/- 7.4 vs. 15.7 +/- 1.5, 13.0 +/- 0.7: p < 0.01). There was no difference in bypass patency between EM group and EL group (96.6 vs. 97.2). During the follow-up period, any death and complications were not recognized in both groups. These results suggested that OPCAB would be one of the valuable procedures in the emergent coronary artery bypass grafting.

Adult↗
PubMed2001

[Optimal setting of focus points for myocardial contrast echocardiography with intravenous Optison (FS-69): an experimental study].

OBJECTIVES: Myocardial contrast echocardiography is useful to assess myocardil perfusion, but myocardial opacification is affected by the setup of the ultrasonic equipment. The optimal setting of focus points for adequate opacification of the myocardium was examined in myocardial contrast echocardiography. METHODS: Myocardial contrast echocardiography was performed in six dogs using triggered second harmonic technology following intravenous administration of Optison(FS-69). The short-axis view was recorded and baseline subtracted video intensity(peak intensity: PI) was calculated at three regions of the left ventricular wall, the anterior, septum, and posterior walls, to evaluate myocardial opacification. The focus point was set at near(2 cm), middle(4 cm) and far(6 cm)points. The myocardial opacification was evaluated at each focus setting. The effect of the acoustic power was also examined by changing the mechanical index to 1.6, 1.2 or 0.8. RESULTS: Myocardial opacification was recognized at all focus points, and segments near the focus points had high PI. However, the PI of the posterior wall was lowest at near focus, whereas the PI of the anterior wall was lowest at far focus. The difference of PI between the anterior and posterior walls was significant (p < 0.05, p < 0.01, respectively) at either focus point. Adequate myocardial opacification of all segments was observed when the focus was set at the middle point. The PI of the whole left ventricle increased relative to mechanical index. CONCLUSIONS: Setting up of focus points at the middle of the left ventricle provides more homogeneous myocardial opacification of the whole left ventricle in myocardial contrast echocardiography, and high acoustic power possibly improves myocardial opacification. Inadequate setting of focus points leads to inadequate estimation of myocardial perfusion by myocardial contrast echocardiography.

Albumins↗
PubMed2001

[A case report of the dissecting aneurysm of ascending aorta, which was surmised to be developed after aortic valve replacement].

Bentall operation was performed for the ascending aortic dissection in the patient of a 70-year old man, who had undergone aortic valve replacement (AVR) for aortic valve regurgitation 7 years ago. At the AVR, the diameter of the ascending aorta was 50 mm on CT. During the follow up period after AVR, the ascending aorta was gradually developed to 95 mm in diameter without any symptoms. During the reoperation, entry was recognized on the prior aortotomy reinforced with felt-strips and the intimal flap was thickened. These situations suggested that the aortic dissection might be occurred just or early after AVR, and the reinforcement of aortotomy using felt-strips and AVR could not prevent progression of aortic root enlargement and dissection. From some previous reports about ascending aortic dissection after AVR, an adequate surgical treatment for a dilated ascending aorta (40-50 min) should be required at the same time of AVR.

Aged↗
PubMed2001

[Combined off-pump CABG (OPCAB) and abdominal vascular surgery].

Two simultaneous operations for off-pump CABG (OPCAB) and abdominal vascular surgery were performed safely and effectively. [Case 1] A 52-year-old man was admitted with the right intermittent claudication and angina pectoris. Coronary angiography and aortography showed 90% stenosis of left anterior descending coronary artery (LAD) and the right external iliac artery. The patient underwent 1 CABG using left internal thoracic artery (ITA) without cardiopulmonary bypass and abdominal aorta--the right external iliac bypass simultaneously. Bleeding volume during the operation was only 150 ml. The operation time was 3 hours 50 minutes. [Case 2] A 57-year-old man was referred from the other hospital with complaints of abdominal aortic aneurysm. He had the history of 4 stroke attacks caused by idiopathic aldosteronism. Preoperative coronary angiography and aortography showed severe 3 vessels disease and abdominal aortic aneurysm. First, we harvested bilateral ITAs, the right gastroepiploic artery (GEA) and saphenous vein (SV). The complete revascularization (left ITA-LAD, right ITA-1st diagonal branch, GEA-seg. 4 posterodescending branch, SV graft-posterolateral branch) was performed on the beating heart. Then we repaired the abdominal aortic aneurysm (56 mm in diameter) using a Gelsealed Y-graft. The operative course was uneventful. The operation time was 6 hours 15 minutes. These cases suggested that OPCAB technique combined with abdominal vascular surgery reduced operation time and prevented complication in the patient with the risk of brain trouble.

Angina Pectoris↗
PubMed2000

Impaired neural regulation of insulin secretion related to the leptin receptor gene mutation in Wistar fatty rats.

The Wistar fatty (WF) rat is a model of obese Type 2 diabetes mellitus (DM). These rats were bred by crossing Zucker fatty (ZF) and Wistar-Kyoto (WKY) rats. A homo-allelic leptin receptor gene mutation has been reported in ZF rats. We report here how these genetic factors contribute to plasma insulin regulation. The fasting plasma insulin levels were higher in WKY and Wistar lean (WL) rats than in Zucker lean (ZL) rats (p<0.05). The levels in WF and ZF rats were higher than in their respective lean littermates, WL and ZL rats (p<0.05). After intragastric glucose load, the plasma insulin increase was reduced upon pretreatment by intracerebroventricular (i. c.v.) methylatropine (an antagonist of the cholinergic receptor) injection in WL rats (p<0.05) but not in WF rats. Plasma glucagon-like peptide-1 (GLP-1) response to intragastric glucose load was not affected by methylatropine. After selective hepatic-vagotomy, plasma insulin levels increased in wild-type ZL rats (p<0.05). This increase was not observed in heterozygote ZL rats. Surprisingly, this response of plasma insulin was not shown in wild-type WL and WKY rats. ZF and WF rats did show a prominent decrease in insulin response (p<0.05). These results indicate that the genetic factor in ZF rats is associated with impaired vagal nerve-mediated control of insulin secretion. The genetic factor in WKY rats may diminish sensitivity to the vagal information of insulin release and contribute to insulin resistance. Therefore, we conclude that the presence of both genetic factors in a homo-allelic state is important to the development of DM in WF rats.

Animals↗
PubMed2000

Two deletion mutations in the hydroxymethylbilane synthase gene in two unrelated Japanese patients with acute intermittent porphyria.

Acute intermittent porphyria (AIP) is an autosomal dominant inherited disease caused by a decreased activity of hydroxymethylbilane synthase (HMBS). Regarding the abnormalities of the HMBS gene, many different mutations have been reported worldwide; however, few families from Japan have been studied. In this work, we investigated the presence of mutations in two unrelated Japanese patients with AIP. Mutational analysis was performed using the polymerase chain reaction-single strand conformation polymorphism (SSCP) method, followed by DNA sequencing. Reliable restriction enzyme cleavage assays were also established for the pedigree analyses. Unique SSCP patterns were noted in exons 12 and 15 of the HMBS gene. Sequencing revealed different mutations in each patient: a two-base deletion of CT at nucleotide 730-731 (730delCT), and also a two-base deletion of CA at position 982-983 (982delCA). Both of the deletion mutations lead to truncated proteins with an abnormal C-terminus, which would be expected to decrease the stability and/or activity of HMBS. Using the cleavage assays, we were able to definitively identify gene carriers in the family. This study adds a novel mutation to those that have been previously reported, and emphasizes that molecular analysis would be very useful not only for the identification of asymptomatic gene carriers in the family but also for the detection of ancestral founders in porphyria families.

Adult↗
PubMed2000

Nifedipine suppresses neointimal thickening by its inhibitory effect on vascular smooth muscle cell growth via a MEK-ERK pathway coupling with Pyk2.

The aim of this study was to determine whether nifedipine could suppress an atherogenic process such as balloon-injured intimal thickening in vivo and the proliferation of vascular smooth muscle cells (VSMC) in vitro. First, we examined the in vivo effect of nifedipine to determine whether it could suppress intimal thickening induced by balloon catheterization. Sprague-Dawley (SD) rats were divided into three groups (L, nifedipine 0.3 mg kg(-1) day(-1); H, nifedipine 3 mg kg(-1) day(-1); C, no nifedipine), and Alzet((R)) osmotic pumps were implanted in their backs for continuous administration. The neointimal layers were completely occupied by proliferated VSMC, and the area ratios of neointima/media treated with nifedipine significantly decreased dose-dependently compared to those of the control. Neither blood pressure nor lipid levels changed among the three groups. We next evaluated the in vitro effect of nifedipine on the proliferation of cultured rat VSMC. Nifedipine decreased the values of [(3)H]-thymidine incorporation and total cellular protein content as well as the levels of phosphorylated extracellular signal-regulated protein kinase (ERK) 1/2, mitogen-activated protein kinase kinase (MEK) 1/2, and even the phosphorylation of Pyk2, in dose-dependent fashions. In addition, nifedipine suppressed the levels of proliferative cell nuclear antigen (PCNA) dose-dependently in both VSMC and balloon-injured thoracic aortae. These results indicate that nifedipine has an inhibitory effect on intimal thickening by attenuating intimal VSMC proliferation, suggesting that nifedipine could be effective for preventing the progression of atherosclerotic plaque as in restenosis after angioplasty.

Actins↗