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H Vetter

Publications and source records attributed to H Vetter.

At least 73 records · Page 4Linked to original sources
PubMed2000

[Silent myocardial ischemia in hypertensive patients].

Silent myocardial ischemia occurs in hypertensive individuals with a prevalence of approximately 35%. ST-alterations are triggered by a) hypertensive peaks and b) heart rate increase. Like in patients with coronary heart disease most ischemic events occur without angina. They are clinically silent. In daily practice silent myocardial ischemia may be detected by ECG under physical load or with 24 h Holter ECG-monitoring. The latter can detect ischemic events missed by ECG-monitored exercise tolerance. In hypertensive patients the simultaneous, ST-triggered recording of ECG and blood pressure data is more meaningful. Patients with silent ischemia are at higher risk than individuals without. Angor is not as strong a determinant of risk as silent ischemia. Hypertensive patients without coronary artery disease (CAD) who have silent ischemia may even have a worse prognosis than those with known CAD. It is therefore important to substantiate the objective extent of silent ischemia by ST-analysis. If detected it has to be included into therapeutic considerations with the goal to prevent such episodes by antihypertensive treatment.

Adult↗
PubMed2000

Green tea compounds inhibit tyrosine phosphorylation of PDGF beta-receptor and transformation of A172 human glioblastoma.

The effect of the green tea compounds 2-(3,4-dihydroxyphenyl)-3, 4-dihydro-2H-1-benzopyran-3,5,7-triol (catechin), epicathechin (EC), epigallocathechin-3 gallate (EGCG), epicathechin-3 gallate (ECG) and catechin-3 gallate (CG) on the tyrosine phosphorylation of PDGF beta-receptor (PDGF-Rbeta) and on the anchorage-independent growth of A172 glioblastoma cells in semisolid agar has been investigated. Treatment of A172 glioblastoma with 50 microM CG, ECG, EGCG and 25 microM Tyrphostin 1296 resulted in an 82+/-17%, 77+/-21%, 75+/-8% and 55+/-11%, respectively (mean+/-S.D., n=3) inhibition of the PDGF-BB-induced tyrosine phosphorylation of PDGF-Rbeta. The PDGF-Rbeta downstream intracellular transduction pathway including tyrosine phosphorylation of phospholipase C-gamma1 (PLC-gamma1) and phosphatidylinositol 3'-kinase (PI 3'-K) was also inhibited. Spheroid formation was completely inhibited by 50 microM ECG, CG, EGCG and by 25 microM Tyrphostin 1296. We conclude that catechins of the green tea possessing the gallate group in their chemical structure act as anticancer agents probably partly via their ability to suppress the tyrosine kinase activity of the PDGF-Rbeta.

Catechin↗
PubMed2000

Identification of syntenin and other TNF-inducible genes in human umbilical arterial endothelial cells by suppression subtractive hybridization.

Endothelial cells play an important regulatory role in inflammatory responses by upregulating various proinflammatory gene products including cytokines and adhesion molecules. A highly potent mediator of this process is tumor necrosis factor-alpha (TNF). In the present study, the suppression subtractive hybridization (SSH) method was employed to identify rarely transcribed TNF-inducible genes in human umbilical arterial endothelial cells. Following mRNA isolation of non-stimulated and TNF-stimulated cells, cDNAs of both populations were prepared and subtracted by suppression PCR. Sequencing of the enriched cDNAs identified 12 genes differentially expressed including vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, interleukin-8 and IkappaBalpha, an inhibitor of the transcription factor nuclear factor-kappaB. Interestingly, also syntenin, a PDZ motif-containing protein which binds to the cytoplasmic domain of syndecans, was identified by SSH. Time course studies using RT-PCR analysis confirmed that all genes were differentially expressed and rapidly induced by TNF. Our data reveal that SSH is a powerful technique of high sensitivity for the detection of differential gene expression in primary arterial endothelial cells.

Carrier Proteins↗
PubMed2000

[Prevalence of diagnoses in ambulatory and hospitalized patients].

Prevalence and distribution of different clinical presentations were analyzed in 6000 hospitalized and ambulatory patients. One medical University clinic and three further hospital units, two university outpatient clinics and four practitioners participated. 6000 main diagnoses and 2560 additional diagnoses had been recorded. The mean age was 64 for the hospitalized patients, 50 years for the outpatient clinic and 47 years at the doctors' office. Cardiovascular diseases were most common. This group of diagnoses was twice as common in hospitalized patients (40.9%) than in the ambulatory group: 19.5% (outpatient clinic) and 15.2% (private practice). In contrast, psychiatric diagnoses were 5 times more frequent in the practice than in the hospital (11.6% vs. 2.4%) and musculoskeletal diseases were even 7 times more common in the practice (13.3% vs. 1.9). 93% of the hospitalized patients had one of the 25 most prevalent diagnoses. This percentage was substantially lower in patients of the outpatient clinic (73%) and of private practice (64%). An additional diagnosis was posed for every other patient in the hospital or at the outpatient clinic, in the practitioners office only for every fourth patient. The analysis shows that hospitalized patients often have a different set of diagnoses than ambulatory ones. To guarantee a broad internistic training outpatient clinics are of great importance. A part of internistic education, however, can also be obtained by cooperation with practitioners.

Adult↗
PubMed2000

Differential gene expression in synovium of rheumatoid arthritis and osteoarthritis.

Rheumatoid arthritis (RA) and osteoarthritis (OA) are the major types of arthritis. Although both diseases are characterized by joint destruction, their etiologies are different. To get insights into pathophysiological pathways, we used the suppression subtractive hybridization (SSH) method to identify differentially expressed genes in RA. DNA sequencing identified 12 gene products including cytoskeletal gamma-actin and extracellular matrix components such as fibronectin, collagen III alpha(1), and superficial zone protein. Interferon gamma-inducible genes such as a novel thiol reductase, two genes of unknown function (HSIFNIN4, RING3), and annexin II were also found. Two genes encoded proteins involved in proliferation such as elongation factor 1 alpha and the granulin precursor. Furthermore, the protease cathepsin B and synovial phospholipase A2 group IIA were detected by SSH. To confirm the differential expression of the genes, we performed RT-PCR analyses of RA and OA synovial tissues. Compared to OA patients, 9 of the 12 genes were overexpressed in RA, suggesting that SSH is a powerful tool for the detection of differential gene expression in synovial tissues. Further characterization of the gene products may help to identify pathophysiological mechanisms in arthritic diseases.

Adult↗
PubMed2000

Rapid analysis of alpha1-antitrypsin PiZ genotype by a real-time PCR approach.

alpha1-Antitrypsin (AAT) deficiency is a common inherited cause of emphysema and cirrhotic liver disease. Current laboratory diagnosis of Pi (proteinase inhibitor) status by protein analysis depends on the availability of blood samples and has a limited accuracy. Single-strand conformational polymorphism (SSCP) analysis and direct DNA sequencing can be performed from blood cells or from tissue samples, but it is a time-consuming procedure not suitable for screening purposes. We used a Light-Cycler assisted PCR approach to identify the PiZ mutation and to determine hetero- and homozygous carrier status from whole blood and from paraffin-embedded archival tissue specimens. The results were compared to those obtained by standard PCR amplification followed by SSCP and direct DNA sequencing. Light-Cycler assisted PCR identified heterozygous PiZ mutations in 16 samples, a homozygous PiZ status in three cases, and wild-type PiM in five control samples. In all cases the results were confirmed by SSCP and direct DNA sequencing. Light-Cycler assisted PCR has a high detection rate for the PiZ mutation. It can be performed from blood or from fixed archival tissues, requires only small amounts of DNA, and allows a rapid diagnosis on a high output level.

DNA↗
PubMed2000

The effect of C1-esterase inhibitor in definite and suspected streptococcal toxic shock syndrome. Report of seven patients.

OBJECTIVE: To evaluate the effect of adjunctive C1-esterase inhibitor substitution therapy on clinical characteristics and outcome of patients with streptococcal toxic shock syndrome (TSS). DESIGN: Observational. SETTING: Medizinische Poliklinik, University of Bonn, Germany. PATIENTS: Seven patients with direct or indirect evidence of streptococcal TSS. INTERVENTION: In addition to conventional and supportive therapy, all patients received 2-3 single doses of C1-esterase inhibitor totaling 6,000-10,000 U within the first 24 h after admission. MEASUREMENTS AND RESULTS: All patients developed fulminant septic shock, multiorgan failure and/or capillary leak syndrome and necrotizing fasciitis within 10-72 h following the onset of first symptoms. Between 1 and 4 days following administration of C1-esterase inhibitor, a marked shift of fluid from extravascular to intravascular compartments took place in all but one patient, accompanied by a transient intra-alveolar lung edema and rapidly decreasing need for adrenergic agents. Six of seven patients survived. CONCLUSIONS: These clinical observations in a small series of patients and the favorable outcome point towards a positive effect of early and high-dose administration of C1-esterase inhibitor as adjunctive therapy in streptococcal TSS. The possible mechanism involved may be the attenuation of capillary leak syndrome (CLS) via early inactivation of complement and contact systems. Controlled studies are needed to establish an improvement of the survival rates of patients with streptococcal TSS following administration of C1-esterase inhibitor.

Adult↗
PubMed2000

NAD(P)H quinone oxidoreductase 1 codon 609 polymorphism and its association to colorectal cancer.

The present study used a rapid and single-step method for genotyping of NAD(P)H quinone oxidoreductase (NQO1) codon 609 polymorphism using real-time polymerase chain reaction (PCR)-analysis and subsequent melting curve analysis for the analysis of allelic distribution of NQO1. The design was a case control study of 323 Caucasians with colorectal cancer and 205 healthy controls. There was no difference in the frequencies of the mutated NQO1 allele (NQO1*2): 0.190 for control individuals and 0.195 for cancer patients, respectively (P=0.947). When this allelic distribution was further compared between non-smoking and smoking colorectal cancer patients, it appeared that the frequency of the wild-type allele NQO1*1 was higher in the smoking than in the non-smoking group [Odds ratio (OR), 0.434; 95% confidence interval (CI), 0.13-1.42]. This observation may suggest a protective role of the NQO1 wild-type allele in colon cancer susceptibility of individuals exposed to NQO1-inducing chemicals.

Adenocarcinoma↗
PubMed2000

Detection of alpha-1-antitrypsin PiZ individuals by SSCP and DNA sequencing in formalin-fixed and paraffin-embedded tissue: a comparison with immunohistochemical analysis.

BACKGROUND/AIM: The role of alpha-1-antitrypsin (AAT) deficiency in the development of cirrhosis and carcinoma of the liver can be investigated from the analysis of archival biopsy specimens. Immunohistochemistry can visualize the storage of defective protease inhibitor (Pi) variant Z, but does not allow differentation between homozygous and heterozygous patients. The aim of the study was to establish a method for the detection of the PiZ mutation on the gene level. METHODS: Liver biopsy and autopsy samples in which AAT deficiency was detected immunohistochemically by a monoclonal PiZ-antibody were analyzed by single-strand conformational polymorphism (SSCP) to reliably determine hetero- and homozygote carrier state in the absence of blood samples and to confirm the histological diagnosis. The accuracy of SSCP was verified by direct DNA sequencing. RESULTS: Tissue slices (>0.8 cm2) from 29 consecutive cases with immunohistochemically detected PiZ depositions and from ten PiZ-negative control cases were provided for extraction and amplification of DNA. In comparison to wild-type sequence of AAT exon V, all 29 cases showed band shifts on SSCP analysis, with a heterozygous pattern in 28 patients and a homozygous pattern in one patient. DNA sequence analysis revealed the same single-base mutation at position 342 of AAT exon V. CONCLUSIONS: SSCP analysis proved a sensitive and specific technique for the detection of the PiZ mutation at the gene level, which allowed unequivocal differentiation between heterozygous and homozygous PiZ status from paraffin-embedded archival tissue specimens. Besides a use in diagnostic pathology, this technique could be valuable for prenatal diagnosis and population screening purposes.

Base Sequence↗
PubMed2000

Normal values of blood pressure self-measurement in view of the 1999 World Health Organization-International Society of Hypertension guidelines.

New guidelines for the management of hypertension have been published in 1999 by the World Health Organization (WHO) and the International Society of Hypertension (ISH). The WHO/ISH Committee has adopted in principle the definition and classification of hypertension provided by the JNC VI (1997). The new classification defines a blood pressure of 120/80 mm Hg as optimal and of 130/85 mm Hg as the limit between normal and high-normal blood pressure. It is unclear which self-measured home blood pressure values correspond to these office blood pressure limits. In this study we reevaluated data from our Dübendorf study to determine self-measured blood pressure values corresponding to optimal and normal office blood pressure using the percentiles of the (office and home) blood pressure distributions of 503 individuals (age, 20 to 90 years; mean age, 46.5 years; 265 men, 238 women). Self-measured blood pressure values corresponding to office values of 130/85 mm Hg and 120/80 mm Hg were 124.1/79.9 mm Hg and 114.3/75.1 mm Hg. Thus, we propose 125/80 mm Hg as a home blood pressure corresponding to an office blood pressure of 130/85 mm Hg (WHO 1999: normal) and 115/75 mm Hg corresponding to 120/80 mm Hg (optimal).

Adult↗
PubMed2000

Fibrinolytic function in diuretic-induced volume depletion.

Accumulating evidence suggests that the renin-angiotensin system (RAS) may participate in the regulation of fibrinolytic function. In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endogenous fibrinolysis. Because such an effect may depend on the degree of prestimulation of the RAS, we have studied parameters of fibrinolytic function in 15 healthy volunteer subjects during baseline (day 1) and after 10 days of treatment with 25 mg of hydrochlorothiazide (HCT)/day (day 11). On the last day of the study (day 12), a single oral dose of 50 mg of losartan was given to the volunteers in addition to HCT and fibrinolytic function was assessed at the peak effect of losartan (5 h later). Plasma renin activity (PRA) was significantly stimulated during diuretic treatment (1.35 +/- 0.21 v 0.34 +/- 0.06 ng mL(-1) x h(-1) [P < .001]) and further increased after losartan (6.39 +/- 1.16 ng mL(-1) x h(-1) [P < .001]). No effects of either the diuretic or losartan could be observed on tissue-type plasminogen activator (t-PA) antigen concentration and activity. However, 10 days of treatment with HCT significantly increased plasminogen activator inhibitor-1 (PAI-1) antigen (26.8 +/- 5.8 v 21.1 +/- 3.4 ng/mL [p = .037]). In addition, PAI-1 activity was also tentatively raised by HCT treatment (5.48 +/- 1.82 v 3.88 +/- 0.79 IU/mL [P = .067]). In spite of the marked further rise in PRA after losartan, the stimulation of PAI-1 antigen and activity was blunted by losartan (24.4 +/- 3.6 ng/mL and 4.55 +/- 0.99 IU/mL, respectively). Our results demonstrate that volume depletion induced by HCT treatment is associated with a rise in PAI-1. Acute administration of losartan is capable of blunting this effect, suggesting that the angiotensin II type 1 receptor may participate in this effect of angiotensin II.

Adult↗
PubMed2000

Cholera toxin treatment of vascular smooth muscle cells decreases smooth muscle alpha-actin content and abolishes the platelet-derived growth factor-BB-stimulated DNA synthesis.

The second messenger cyclic AMP regulates diverse biological processes such as cell morphology and cell growth. We examined the role of the second messenger cyclic AMP on rat aortic vascular smooth muscle cell (VSMC) morphology and the intracellular transduction pathway mediated by platelet-derived growth factor beta-receptor (PDGF-Rbeta). The effect of PDGF-BB on VSMCs growth was assessed by [(3)H]-thymidine incorporation. Tyrosine phosphorylation of PDGF-Rbeta, PLC-gamma1, ERK1 and ERK2, p125(FAK) and paxillin as well as Sm alpha-actin was examined by the chemiluminescence Western blotting method. Actin mRNA level was quantitated by Northern blotting. Visualization of Sm alpha-actin filaments, paxillin and PDGF-Rbeta was performed by immunfluorescence microscopy. Cholera toxin (CTX; 10 nM) treatment lead to a large and sustained increase in the cyclic AMP concentration after 2 h which correlated with change of VSMC morphology including complete disruption of the Sm alpha-actin filament array and loss of focal adhesions. Treatment of VSMCs with CTX did not influence tyrosine phosphorylation of p125(FAK) and paxillin but decreased the content of a Sm alpha-actin protein. Maximal decrease of 70% was observed after 24 h of treatment. CTX also caused a 90% decrease of the actin mRNA level. CTX treatment completely abolished PDGF-BB stimulated DNA-synthesis although PDGF-Rbeta level and subcellular distribution and translocation was not altered. Furthermore CTX attenuated the PDGF-BB-induced tyrosine phosphorylation of the PDGF-Rbeta, PI 3'-K, PLC-gamma1 and ERK1/2 indicating an action of cyclic AMP on PDGF-beta receptor. We conclude that although cyclic AMP attenuates the PDGF-Rbeta mediated intracellular transduction pathway, an intact actin filament may be required for the PDGF-BB-induced DNA synthesis in VSMCs.

Actins↗
PubMed2000

Angiotensin-converting enzyme (ACE) inhibition attenuates insulin-like growth factor-I (IGF-I) induced cardiac fibroblast proliferation.

The effects of angiotensin-converting enzyme (ACE) inhibition and angiotensin type 1 (AT(1)) receptor blockade on insulin-like growth factor-I (IGF-I) induced proliferation and immediate-early-gene expression of neonatal rat cardiac fibroblasts were investigated. Moreover the role of the IGF-I receptor (IGF-IR) in this process was evaluated. IGF-I (10(-9) - 10(-7) M) stimulated neonatal rat cardiac fibroblast growth in a dose-dependent fashion (maximum: 3.5+/-0.1 fold, 10(-7) M), as determined by 5-bromo-2'-deoxyuridine (BrdU) incorporation. ACE inhibition or AT(1) receptor blockade attenuated the IGF-I (10(-7) M) induced neonatal rat cardiac fibroblast growth in a concentration-dependent fashion (moexiprilat: 50+/-2%, enalaprilat: 31+/-2%, CV11974; 58+/-1%, all: 10(-7) M). IGF-I stimulated cellular growth was accompanied by an upregulation of the immediate early genes c-Fos (2.4+/-0.3 fold), Egr-1 (4.7+/-1.1 fold) and Sp1 (6.2+/-0.7 fold). IGF-I induced expression was completely inhibited by ACE inhibition or AT(1) receptor blockade. Stimulation with IGF-I or Ang II (10(-7) M) increased IGF-IR expression 5.7+/-0. 5 fold and 3.6+/-0.5 fold respectively. The IGF-I induced overexpression of the IGF-IR was reduced by ACE inhibition with moexiprilat (10(-7) M) by 79+/-7% and by AT(1) receptor blockade with CV11974 (10(-7) M) by 79+/-5%. These data demonstrate that the mitogenic action of IGF-I in neonatal rat cardiac fibroblasts is in part mediated by activation of the renin-angiotensin system (RAS) with subsequent upregulation of IGF-IR expression. This observation has important implications for the treatment of cardiac diseases with ACE inhibitors alone and their combination with IGF-I or growth hormone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Short-term stimulation of vascular smooth muscle cells with platelet-derived growth factor (PDGF)-BB and angiotensin II induces.

Growth factors such as the platelet-derived growth factor (PDGF)-BB and angiotensin II (Ang II) have been shown to induce vascular smooth muscle cell (VSMC) proliferation after long stimulation periods. Little is known though, about the effects of PDGF-BB and Ang II on VSMC proliferation after short stimulation periods. The purpose of our study was to examine whether a short term (3-60 min) stimulation of VSMC with PDGF-BB or Ang II is sufficient to induce cell proliferation. Incubation of VSMC with Ang II (100 nM) or PDGF-BB (50 ng/ml) caused a significant increase in [3H]thymidine incorporation starting after a 3-min stimulation, while the cell counts required 32 and 8 h of stimulation, respectively. Mitogen-activated protein kinase activation reached a maximum at 5-10 min of PDGF-BB or Ang II stimulation. This study demonstrates that the growth-promoting effects of PDGF-BB and Ang II are strongly dependent on the length of the stimulation period and that while prolonged stimulation periods (>8-32 h) result in VSMC proliferation, short ones (3-60 min) result only in [3H]thymidine incorporation without an increase in cell count, a fact of considerable pathophysiological significance, considering that the time kinetics of growth factors in the VSMC microenvironment have not as yet been clarified.

Angiotensin II↗
PubMed2000

Hypertension associated with multiple renal arteries may be renin-dependent.

OBJECTIVE: Subjects with multiple renal arteries have been shown to suffer more frequently from hypertension and to have higher blood pressures than subjects whose kidneys are supplied by single renal arteries. This study was carried out to determine whether subjects with multiple renal arteries also have higher renin activity. METHODS: We studied 62 consecutive patients who had undergone angiography for various reasons. They were divided into two groups. Group A comprised 29 patients whose kidneys were supplied by single arteries (male :female ratio 1.63, mean age 51.8 +/- 1.9 years) while Group B comprised 33 patients with multiple renal arteries (male:female ratio 2, mean age 47.3 +/- 2.3 years). RESULTS: Before stimulation with frusemide, the plasma renin in Group A was 0.79 +/- 0.13 ng angiotensin l/ml per h, while in Group B the corresponding figure was 1.73 +/- 0.38 ng angiotensin l/ml per h. This difference was statistically significant (P= 0.0127). Thirty minutes later the plasma renin level in Group A was 2.43 +/- 0.37 ng angiotensin l/ml per h versus a level of 3.86 +/- 0.53 ng angiotensin l/ml per h in Group B (P= 0.0169). Again, 30 minutes later the level was 2.59 +/- 0.4 ng angiotensin l/ ml per h in Group A, versus 3.79 +/- 0.59 ng angiotensin l/ ml per h in Group B (P= 0.0495). CONCLUSIONS: We conclude that patients with multiple renal arteries constitute a group who have high plasma renin activity and may therefore be prone to develop arterial hypertension.

Adult↗
PubMed2000

High percentage of false-positive results of cytokeratin 19 RT-PCR in blood: a model for the analysis of illegitimate gene expression.

Cytokeratin 19 (CK19) RT-PCR is widely used in order to detect circulating tumor cells in peripheral blood and bone marrow. However, increasing amounts of information support the fact that it is also associated with a high percentage of false-positive results. In our study, we not only managed to demonstrate the significant limitations of this method, but were also able to clarify the reasons behind these limitations. We developed a completely novel RT-PCR for CK19 and sequenced an intron at nucleotide (nt) 980 of the CK19 mRNA to exclude DNA contamination. Tumor dilution experiments were performed in order to analyze the specificity and sensitivity of the method. Control experiments using the blood of healthy donors were performed. Tumor cell dilution experiments gave a detection limit of one tumor cell. If tumor cells were mixed with an equal volume of pure mononuclear cells, the detection limit was 1 tumor cell in 10(5) mononuclear cells. RT-PCR of mononuclear cells from healthy blood donors gave false-positive results in 29% of the cases. We conclude that a significant decrease in the sensitivity of CK19 RT-PCR occurs if it is performed in blood cells and that the illegitimate CK19 gene expression in normal cells can lead to false-positive results. These limitations have to be taken into account if RT-PCR is to be used for the detection of tumor cells either in blood or in bone marrow in clinical practice.

Blood Donors↗
PubMed2000

Effects of the mineralocorticoid fludrocortisone on fibrinolytic function in healthy subjects.

Recent evidence suggests that the renin-angiotensin-aldosterone system (RAAS) may participate in the regulation of fibrinolytic function. Angiotensin II (Ang II) is the primary candidate to mediate this inter-relationship, since this peptide is capable of stimulating plasminogen activator inhibitor-1 (PAI-1) in vitro and in vivo. It has been suggested that aldosterone may also modulate fibrinolysis, possibly by interacting with Ang II. The present study therefore investigates the effect of short-term treatment with the synthetic mineralocorticoid fludrocortisone (F) on fibrinolytic function. Ten healthy male volunteers, aged 25 to 30 years, on a constant intake of 160-180 mmol Na(+) and 60-80 mmol K(+), were studied on a control day (C1), after two days of oral administration of F (0.1 mg b.d.), and again three days after cessation of F (C2). F was associated with a marked decrease in plasma renin activity (PRA) from 0.91 +/- 0.45 ng ml(-1) h(-1) to 0.34 +/- 0.29 ng ml(-1) h(-1) (p=0.005), which returned to the baseline range at C2 (0.65 +/- 0.45 ng ml(-1) h(-1); p=0.032). The experimental protocol was not associated with significant changes in the activity or antigen concentration of tissue plasminogen activator (t-PA). PAI-1 exhibited a circadian rhythm with highest values at 0800 hours (41.8 +/- 9.1 ng/ml), decreasing by 1230 hours (22.6 +/- 5.9 ng/ml), with a further decrease at 1630 hours (12.3 +/- 3.1 ng/ml). At all three time points, PAI-1 remained unchanged by the mineralocorticoid. Our results therefore do not support a major mineralocorticoid effect on PAI-1. However, our study does not exclude a modulatory role of F, since unchanged PAI-1 could be observed in spite of a marked suppression of the RAAS.

Adult↗