Biomedical subjects

H Nishimura

Publications and source records attributed to H Nishimura.

At least 145 records · Page 8Linked to original sources

PubMed1999

IL-15 is elevated in the patients of postoperative enterocolitis.

Serum interleukin 15 (IL-15) levels were measured in 77 patients who were consecutively admitted to our intensive care unit. Postoperative enterocolitis occurred in four patients and Methicillin-resistant Staphylococcus aureus (MRSA), but not Clostridium difficile, was identified in the faecal specimens from these patients. The IL-15 levels in the patients with MRSA enterocolitis were significantly elevated compared with those of other MRSA infections without enterocolitis including pneumonia (n=6) and cholangitis (n=1), and other MRSA non-colonized patients (n=66) (21.2+/-5.2 pg/ml vs 4.3+/-0.2, 4.3+/-0.5). Notably, an increase in serum IL-15 was observed just before clinical manifestation of severe diarrhoea. Our findings suggest that IL-15 may be associated in the pathogenesis of postoperative enterocolitis and its serum level may be a severity indicator of the disease.

Adult↗

PubMed1999

Vascular angiotensin II receptor and calcium signaling in toadfish.

The renin-angiotensin system evolved during the early evolution of vertebrates and regulates blood pressure/blood volume homeostasis in nonmammalian and mammalian vertebrates. Properties of vascular angiotensin (ANG) receptors and signal pathways in primitive animals are, however, not well understood. We aimed to determine whether vascular ANG II receptors in the toadfish, Opsanus tau, an aglomerular teleost, pharmacologically resemble either the ANG subtype 1 receptor (AT1) or the subtype 2 receptor (AT2) by examining (i) the effects of selective ANG receptor antagonists on ANG II-induced vasopressor action and binding and (ii) ANG II's effect on cytosolic Ca2+ signaling. [Asn1, Val5]ANG II (native teleost ANG II) dose-dependently increased the mean arterial pressure of conscious toadfish. ANG II-induced pressor responses (100-500 ng/kg) were inhibited substantially (79-83%) by [Sar1, Ile8]ANG II (5 microg x kg-1 + 5 microg x kg-1 x min-1) and moderately (34-53%) by losartan (AT1 antagonist, 10 mg/kg + 20 mg x kg-1 x h-1) and by PD 123319 (AT2 antagonist, 10 mg/kg + 20 mg x kg-1 x h-1) (36-60%). Likewise, the [Asp1, Val5, His9]ANG I-induced pressor effect was completely eliminated by an ANG I-converting enzyme inhibitor, SQ 14,225. Specific 125I-ANG II binding to vascular smooth muscle (VSM) membrane fractions was displaced completely by [Asn1, Val5]ANG II and [Sar1, Ile8]ANG II. Losartan, but not PD 123319, partly displaced ANG II binding at 10(-10)-10(-6) M. Furthermore, ANG II (10(-7) or 10(-8) M) caused a rapid, transient increase in the cytosolic Ca2+ signal (fluorescence ratio (FR) of 340/380 nm) of isolated VSM tissues measured by fura-2 and a dual wavelength fluorospectrometer, whereas extracellular K+ induced sustained, dose-dependent (P < 0.01) increases in FR. The results indicate that toadfish VSM tissues possess a rather nonselective ANG receptor; partial inhibition of ANG II binding by losartan and stimulation of cytosolic Ca2+ signaling by ANG II suggest that the receptor has some resemblance to AT1 homologous receptors.

1-Sarcosine-8-Isoleucine Angiotensin II↗

PubMed1999

Isolation of Biopterin-alpha-glucoside from Spirulina (Arthrospira) platensis and Its Physiologic Function.

: A fluorescent substance was isolated from the cyanobacterium with a yield of 4.5 mg per 10 g of dried Spirulina (Arthrospira) platensis cells by gentle extraction and ethanol fractionation followed by column chromatography. The fluorescent substance, which has absorption maxima at 256 nm and 362 nm (pH 8.4), was identified as biopterin-alpha-glucoside by spectrophotometry and nuclear magnetic resonance spectroscopy. Biopterin-alpha-glucoside prevented decolorization of the photosynthetic pigments, chlorophyll a, phycocyanin, and carotenoids in photosynthetic vesicles of Spirulina platensis cells, by ultraviolet irradiation.

Journal Article↗

PubMed1999

Down regulation of peroxisome proliferator-activated receptorgamma expression by inflammatory cytokines and its reversal by thiazolidinediones.

AIMS/HYPOTHESIS: Previous studies show that inflammatory cytokines play a part in the development of insulin resistance. Thiazolidinediones were developed as insulin-sensitizing drugs and are ligands for the peroxisome proliferator-activated receptory (PPARgamma). We hypothesized that the anti-diabetic mechanism of thiazolidinediones depends on the quantity of PPARgamma in the insulin resistant state in which inflammatory cytokines play a part. METHODS: We isolated rat PPARgamma1 and gamma2 cDNAs and examined effects of various cytokines and thiazolidinediones on PPARgamma mRNA expression in rat mature adipocytes. RESULTS: Various inflammatory cytokines, such as tumour necrosis factor-alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), IL-1beta, IL-6 and leukaemia inhibitory factor decreased PPARgamma mRNA expression. In addition, hydrogen peroxide, lysophosphatidylcholine or phorbol 12-myristate 13-acetate also decreased the expression of PPARgamma. The suppression of PPARgamma mRNA expression caused by 10 nmol/l of TNF-alpha was reversed 60% and 55% by treatment with 10(-4) mol/l of troglitazone and 10(-4) mol/l of pioglitazone, respectively. The suppression of glucose transporter 4 mRNA expression caused by TNF-alpha was also reversed by thiazolidinediones. Associated with the change of PPARgamma mRNA expression, troglitazone improved glucose uptake suppressed by TNF-alpha. CONCLUSION/INTERPRETATION: Our study suggests that inflammatory cytokines could be factors that regulate PPARgamma expression for possible modulation of insulin resistance. In addition, we speculate that the regulation of PPARgamma mRNA expression may contribute to the anti-diabetic mechanism of thiazolidinediones.

Adipocytes↗

PubMed1999

Cerebral blood-flow responses to induced hypotension and to CO2 inhalation in patients with major cerebral artery occlusive disease: a positron-emission tomography study.

Our aim was to study the relationship between cerebral blood flow (CBF) responses to induced hypotension and to CO2 inhalation in patients with occlusive disease of the carotid or middle cerebral arteries. In 13 patients (8 men, 5 women) aged 31-73 years (mean +/- 1 SD = 63.2 +/- 10.6), regional CBF values during the resting state (CBFrest), 7% CO2 inhalation (CBFhypercapnia), and hypotension induced by 10-20 microg/kg/min intravenous trimethaphan (CBFhypotension) were measured using positron-emission tomography (PET) with H2(15)O. The % CBF change during induced hypotension (% CBFhypotension) was defined as (CBFhypotension - CBFrest)/CBFrest multiplied by 100. The % CBF change during CO2 inhalation (% CBFhypercapnia) was defined as (CBFhypercapnia - CBFrest)/CBFrest/mm Hg arterial partial pressure of CO2 x 100. We defined symptomatic hemispheres as those with a stenotic or occlusive lesion with neurological symptoms or signs and asymptomatic hemispheres as those which had a similar lesion and/or were influenced by the collateral flow pattern without neurological symptoms. In the territory of the occlusive lesion, % CBFhypotension correlated significantly with % CBFhypercapnia (r = 0.793, P < 0.002) in the symptomatic hemispheres. In the brain regions in which trimethaphan did not induce a reduction in CBF. % CBFhypercapnia was 6.13 +/- 1.79. In those in which % CBFhypotension ranged from 0 to -5, from -5 to -10, and more than -10%, % CBFhypercapnia was 4.05 +/- 1.99, 3.21 +/- 1.17, and 1.73 +/- 1.61, respectively, with significant differences between each pair of groups. In the asymptomatic hemispheres, % CBFhypotension also correlated with % CBFhypercapnia (r = 0.979, P < 0.0001). Failure to maintain CBF during induced hypotension was associated with diminished cerebrovascular vasoreactivity to hypercapnia in patients with arterial disease. This may indicate that failure of autoregulation can be assessed by the CBF response to both induced hypotension and CO2 inhalation. From the technical point of view, estimation of the CO2 response may be useful for assessing failure of autoregulation.

Administration, Inhalation↗

PubMed1999

Thyrotropin decreases leptin production in rat adipocytes.

Leptin, which is secreted from adipocytes, has a role in the regulation of appetite and energy expenditure. The thyrotropin receptor (TSH-R) was recently found in adipocytes. We examined the effects of TSH on leptin production and lipolysis in rat epididymal adipocytes. TSH decreased the concentration of leptin in the medium time (approximately 24 hours)- and dose (approximately 10(-7) mol/L)-dependently (half-maximal inhibition [IC50] approximately 10(-9) mol/L). TSH also decreased the ob mRNA level approximately 55% in adipocytes. We confirmed the presence of TSH-R mRNA in the adipocytes by reverse transcription-polymerase chain reaction (RT-PCR). TSH stimulated glycerol release dose-dependently (IC50 approximately 10(-8) mol/L) in adipocytes. This TSH-induced glycerol release was further enhanced by adenosine deaminase (ADA). In summary, TSH reduced leptin production and stimulated lipolysis in rat epididymal adipocytes. Although the pathophysiological relevance of the regulation of leptin production and lipolysis by TSH is unknown, we speculate that TSH may affect the regulation of appetite and energy expenditure in pathophysiological states.

Adipocytes↗

PubMed1999

Characterization of mutated protein encoded by partially duplicated fibrillin-1 gene in tight skin (TSK) mice.

Fibrillin-1 (Fbn-1) is a ubiquitous protein present in the extracellular matrix of various organs and it is a major component of microfibrils embedded in the core of elastic fibers. In humans, mutations or deletions of the Fbn-1 gene are associated with several genetic diseases. In addition, several microsatellite alleles near Fbn-1 gene were found associated with diffuse scleroderma. In TSK/+ mice, which develop a scleroderma-like syndrome, the Fbn-1 gene exhibits an inframe duplication of exons 17-40. In this study, we report that the synthesis and secretion of wild-type Fbn-1 in TSK/+ is higher than that of the mutated Fbn-1 protein excluding the possibility that TSK genetic defect is due to a loss of the wild allele. We also demonstrate for the first time that TGF-beta, which plays a crucial role in skin fibrosis, binds to both wild-type and mutated Fbn-1. The amount of bound TGF-beta was higher in mutated than wild-type Fbn-1 and appears related to the number of TGF-beta binding motifs.

Animals↗

PubMed1999

Minimum structure of peptidoglycan required for induction of antibacterial protein synthesis in the silkworm, Bombyx mori.

Various peptidoglycan fragments, different in mode of cross-linking and molecular size, were isolated, and the elicitor activity was tested for induction of antibacterial protein synthesis in larvae of Bombyx mori. Linear uncross-linked peptidoglycans from Bacillus licheniformis and Micrococcus luteus were effective elicitors, similar to the directly cross-linked peptidoglycan from B. licheniformis cell wall. The fragments of uncross-linked peptidoglycan with a sugar chain length of four or more were active elicitors, but the disaccharide unit had no elicitor activity. The minimum structure of peptidoglycan required for induction of antibacterial protein synthesis was determined to be two repeating N-acetylglucosamine-N-acetylmuramic acid units with peptide side chains.

Animals↗

PubMed1999

Longterm effects of pulmonary resection on cardiopulmonary function.

BACKGROUND: Major lung resection decreases ventilatory capacity and reduces exercise tolerance, impairing postoperative quality of life. But we have often seen respiratory symptoms improve during several years of postoperative followup. In the current study, we evaluated postoperative changes in cardiopulmonary function on exertion of patients with lung cancer surviving for more than three years, and the corresponding changes of their respiratory symptoms. METHODS: The effects of pulmonary resection on cardiopulmonary function were evaluated in eight patients with lung cancer. Pulmonary function tests and hemodynamic study at rest and during exercise were performed before, in the early (4 to 6 months) and late (42 to 48 months) postoperative phases after major lung resection. RESULTS: None of the eight patients had any remarkable symptoms before lung resection. In the early postoperative study, the general condition of five patients deteriorated compared with their preoperative status. In the late postoperative study, four patients showed an improvement of their daily activities from the early postoperative phase. Pulmonary function in the late postoperative phase did not show major changes except for airway resistance and percentage of carbon monoxide diffusing capacity as compared with the early phase, which showed deterioration as compared with the preoperative period. Cardiac index and stroke volume index were significantly decreased during exercise on maximal effort in the late postoperative phase compared with other phases. These results suggest that the peak blood flow per unit of remaining lung during exercise becomes lower with time after lung resection, indicating deterioration of the condition of the pulmonary vascular bed. The deterioration was also revealed from the pressure-flow curve. CONCLUSIONS: The condition of the pulmonary vascular bed after major lung resection does not improve, even in the late postoperative phase, although clinical symptoms were sometimes improved compared with the early postoperative period.

Aged↗

PubMed1999

Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor.

PD-1, a 55 kDa transmembrane protein containing an immunoreceptor tyrosine-based inhibitory motif, is induced in lymphocytes and monocytic cells following activation. Aged C57BL/6(B6)-PD-1(-/-) congenic mice spontaneously developed characteristic lupus-like proliferative arthritis and glomerulonephritis with predominant IgG3 deposition, which were markedly accelerated by introduction of a Fas mutation (lpr). Introduction of a PD-1 null mutation into the 2C-TCR (anti-H-2Ld) transgenic mice of the H-2(b/d) background resulted in the chronic and systemic graft-versus-host-like disease. Furthermore, CD8+ 2C-TCR+ PD-1(-/-) T cells exhibited markedly augmented proliferation in vitro in response to H-2d allogenic cells. Collectively, it is suggested that PD-1 is involved in the maintenance of peripheral self-tolerance by serving as a negative regulator of immune responses.

Animals↗

PubMed1999

Role of the angiotensin type 2 receptor gene in congenital anomalies of the kidney and urinary tract, CAKUT, of mice and men.

Angiotensin type 2 receptor gene null mutant mice display congenital anomalies of the kidney and urinary tract (CAKUT). Various features of mouse CAKUT impressively mimic human CAKUT. Studies of the human type 2 receptor (AGTR2) gene in two independent cohorts found that a significant association exists between CAKUT and a nucleotide transition within the lariat branchpoint motif of intron 1, which perturbs AGTR2 mRNA splicing efficiency. AGTR2, therefore, has a significant ontogenic role for the kidney and urinary tract system. Studies revealed that the establishment of CAKUT is preceded by delayed apoptosis of undifferentiated mesenchymal cells surrounding the urinary tract during key ontogenic events, from the ureteral budding to the expansive growth of the kidney and ureter.

Animals↗

PubMed1999

Inhibition of Df-protease associated with allergic diseases by polyphenol.

It was reported that Df-protease from house dust mite (Dermatophagoides farinae) catalyzes the activation of the kallikrein-kinin system in human plasma and is closely associated with mite-induced allergy. Therefore, to prevent the release of kinin by Df-protease, the inhibitory activity of polyphenols including catechins and flavonols was tested in vitro and in vivo. Among them, myricetin and epigallocatechin gallate (EGCg) effectively inhibited the amidase activity of Df-protease with K(i) values of 1 x 10(-)(8) and 6 x 10(-)(4) M, respectively. The kinin release in human plasma was extensively inhibited by the addition of EGCg in comparison with myricetin. Enhancement of vascular permeability in guinea pigs caused by Df-protease was markedly suppressed by EGCg.

Animals↗

PubMed1999

A new quadruple therapy for Helicobacter pylori: influence of resistant strains on treatment outcome.

BACKGROUND: There have been no reports concerning the efficacy and safety of a 1-week quadruple therapy regimen of omeprazole, amoxycillin, roxithromycin and metronidazole for Helicobacter pylori infections and the impact of primary resistance on the eradication rate. METHODS: One hundred and sixty-nine consecutive patients with peptic ulcer disease as well as gastritis with biopsy-proven H. pylori infection were entered into an open study of omeprazole 20 mg o.m., amoxycillin 500 mg t.d.s., roxithromycin 150 mg b.d., and metronidazole 250 mg t.d.s. Helicobacter pylori status was determined by urease test, histology and culture. Susceptibility to amoxycillin, metronidazole and roxithromycin was determined by the E-test. RESULTS: H. pylori was eradicated in 155 out of 169 (92%; 95% CI 88-96%) by intention-to-treat analysis, and in 155 out of 163 (95%; 95% CI 92-98%) by per protocol analysis. The prevalence of primary resistance against amoxycillin, roxithromycin and metronidazole was 2 out of 166 (1%), 16 out of 166 (10%) and 27 out of 166 (16%), respectively. H. pylori was eradicated in 25 out of 27 (93%) patients with metronidazole-resistant strains compared with 130 out of 136 (96%) in patients with metronidazole-sensitive strains of H. pylori. It was eradicated in 15 out of 16 (94%) patients with roxithromycin-resistant strains while in 140 out of 147 (95%) patients with roxithromycin-sensitive strains of H. pylori, and in two out of two (100%) patients with amoxycillin-resistant stains compared with 153 out of 161 (95%) in patients with amoxycillin-sensitive strains. H. pylori was eradicated in three out of four (75%) patients with double resistance against metronidazole and roxithromycin compared with 152 out of 159 (96%) patients with sensitive strains to metronidazole and or roxithromycin. None of these differences were statistically significant. Severe side-effects were found in only one out of 169 patients-anaphylaxis due to penicillin. CONCLUSIONS: The 1-week quadruple therapy with omeprazole, amoxycillin, metronidazole and roxithromycin was found to eradicate H. pylori in over 90% of all patients. This regimen was also found to be beneficial for patients with pre-treatment resistant strains to metronidazole, roxithromycin or amoxycillin, and was observed to be safe and well-tolerated.

Adult↗

PubMed1999

Defective immune response and severe skin damage following UVB irradiation in interleukin-6-deficient mice.

Interleukin-6 (IL-6), a multifunctional cytokine, is induced in the acute-phase reaction following ultraviolet (UV) irradiation of humans and mice. Using IL-6-deficient (IL-6-/-) mice, we investigated the role of IL-6 in immunosuppression and inflammatory responses caused by UVB (280-320 nm) radiation. The IL-6-/- mice had a defective contact hypersensitivity (CHS) in response to the sensitizers 2,4-dinitrofluorobenzene and oxazolone. The injection of recombinant IL-6 (rIL-6) into these mice resulted in a marked recovery of the CHS. Serum IL-6 was significantly elevated by UV irradiation of wild-type B6 J/129Sv (IL-6+/+) mice but was not detectable in IL-6-/- mice. Interestingly, there was no induction of serum interleukin-10 (IL-10) by UV irradiation of IL-6-/- mice, whereas UV exposure caused a significant increase in serum IL-10 levels in IL-6+/+ mice. Injection of rIL-6 into IL-6-/- mice increased IL-10 to levels similar to those of IL-6+/+ mice. Being different from IL-6+/+ mice, no epidermal proliferation was found at 48 hr in the IL-6-/- mice, but delayed cell proliferation was observed at 72 hr after UV exposure. Immunohistochemical analysis demonstrated that the epidermis was capable of synthesizing IL-6 at 72 hr after UV irradiation of IL-6+/+ mice. In addition, the IL-6-positive cells appeared to be Langerhans' cells, which were detected with dendritic cell-reactive S-100 antibody. The present study strongly suggests that IL-6 may play a crucial role in the alteration of cutaneous immune responses following UV exposure, and provides evidence that IL-6 is a potent inducer of IL-10. Furthermore, IL-6 production induced by UV radiation appears to be an important early signal for repair of UV-caused skin damage.

Animals↗

PubMed1999

Interleukin-15 production at the early stage after oral infection with Listeria monocytogenes in mice.

We previously reported that exogenous interleukin-15 (IL-15) induces proliferation and activation of intestinal intraepithelial lymphocytes (i-IEL) in naive mice. To investigate the ability of endogenous IL-15 to stimulate i-IEL in vivo, we monitored i-IEL and intestinal epithelial cells (i-EC) in mice after an oral infection with Listeria monocytogenes. Although the populations of alphabeta and gammadelta i-IEL were not significantly changed after the oral infection, the expression level of interferon-gamma (IFN-gamma) was increased both at transcriptional and protein levels, and a conversely marked decrease in interleukin-4 (IL-4) was detected in the i-IEL on day 1 after infection as compared with before infection. The T helper 1 (Th1)-biased response of i-IEL coincided with a peak response of IL-15 production in the i-EC after oral infection. These results suggested that IL-15 produced from i-EC may be at least partly involved in the stimulation of i-IEL to produce IFN-gamma after oral infection with L. monocytogenes.

Animals↗

PubMed1999

Lipopolysaccharide stimulates HepG2 human hepatoma cells in the presence of lipopolysaccharide-binding protein via CD14.

Lipopolysaccharide (LPS)-binding protein (LBP), an opsonin for activation of macrophages by bacterial LPS, is synthesized in hepatocytes and is known to be an acute phase protein. Recently, cytokine-induced production of LBP was reported to increase 10-fold in hepatocytes isolated from LPS-treated rats, compared with those from normal rats. However, the mechanism by which the LPS treatment enhances the effect of cytokines remains to be clarified. In the present study, we examined whether LPS alone or an LPS/LBP complex directly stimulates the hepatocytes, leading to acceleration of the cytokine-induced LBP production. HepG2 cells (a human hepatoma cell line) were shown to express CD14, a glycosylphosphatidylinositol-anchored LPS receptor, by both RT/PCR and flow cytometric analyses. An LPS/LBP complex was an effective stimulator for LBP and CD14 production in HepG2 cells, but stimulation of the cells with either LPS or LBP alone did not significantly accelerate the production of these proteins. The findings were confirmed by semiquantitative RT/PCR analysis of mRNA levels of LBP and CD14 in HepG2 cells after stimulation with LPS alone and an LPS/LBP complex. In addition, two monoclonal antibodies (mAbs) to CD14 (3C10 and MEM-18) inhibited LPS/LBP-induced cellular responses of HepG2 cells. Furthermore, prestimulation of HepG2 cells with LPS/LBP augmented cytokine-induced production and gene expression of LBP and CD14. All these findings suggest that an LPS/LBP complex, but not free LPS, stimulates HepG2 cells via CD14 leading to increased basal and cytokine-induced LBP and CD14 production.

Acute-Phase Proteins↗

PubMed1999

Effects of modified pellicles on Candida biofilm formation on acrylic surfaces.

The role of saliva or serum proteins, such as mucin, fibronectin (FN) and mannan-binding protein, on Candida biofilm formation was investigated. Supplementation of saliva with FN had no significant effect on biofilm formation. In contrast, biofilm formation on either mucin-coated or FN-coated acrylic surfaces was significantly less than that of the control. These results suggest that salivary mucin or FN alone does not facilitate biofilm formation of Candida. Supplementation of serum with FN increased biofilm formation of C. glabrata compared with the control. Pretreatment of serum with anti-FN monoclonal antibody significantly reduced biofilm formation, as did pretreatment of serum with anti-mannan-binding protein monoclonal antibody or Con-A. Therefore, Candida biofilm formation on acrylic surfaces appears to be a complex phenomenon involving a multiplicity of proteins operating intraorally.

Acrylates↗

PubMed1999

Hypertension and insulin resistance: role of peroxisome proliferator-activated receptor gamma.

1. Insulin resistance has been highlighted as a common causal factor for hypertension, hyperlipidaemia, diabetes mellitus and obesity, all of which are recognized to occur simultaneously, and a distinct clinical entity is defined as 'multiple risk factor syndrome'. 2. Recently, a new class of antidiabetic agents, thiazolidinediones (TZD) has been developed and has been shown to improve insulin resistance by binding and activating a nuclear receptor, peroxisome proliferator-activated receptor (PPAR) gamma. 3. cDNA of rat PPAR gamma 1 and gamma 2 were cloned and gene regulation of PPAR gamma in rat mature adipocytes was examined. Hydrogen peroxide, an oxygen radical, which is recognized to be the common intracellular signal for multiple risk factors, potently down-regulated PPAR gamma mRNA expression in rat mature adipocytes. 4. Tumour necrosis factor (TNF)-alpha, which is considered to play a role in obesity-induced non-insulin-dependent diabetes mellitus and to augment oxidative stress, also suppressed PPAR gamma expression. 5. Thiazolidinediones dose-dependently recovered TNF-alpha-induced down-regulation of PPAR gamma mRNA expression. 6. The modulation of PPAR gamma expression by TZD can be one mechanism for the improvement of insulin resistance by TZD. 7. Vascular tone and remodelling are controlled by several vasoactive autocrine/paracrine factors produced by endothelial cells in response to several vascular injury stimuli, including hypertension. The PPAR gamma gene transcript was detected in cultured endothelial cells. 8. The administration of TZD stimulated the endothelial secretion of type-C natriuretic peptide, which is one of the natriuretic peptide family and is demonstrated by us to act as a novel endothelium-derived relaxing peptide. 9. Concomitantly, TZD significantly suppressed the secretion of endothelin, a potent endothelium-derived vasoconstricting peptide. 10. Thiazolidinediones can affect vascular tone and growth by modulating the production of endothelium-derived vasoactive substances to influence occurrence and progression of hypertension and atherosclerosis.

Adipose Tissue↗