Tsuneo Ogawa

Immunoreactive endothelin in rat kidney inner medulla: marked decrease in spontaneously hypertensive rats

Using a specific and sensitive radioimmunoassay for endothelin, the regional distribution and molecular form of endothelin was investigated in rat tissue. The highest concentration was observed in the inner medulla of the kidney (8.7 +/- 2.2 pg/mg wet weight). On two kinds of reverse phase high performance liquid chromatography, immunoreactive endothelin in the inner medulla of the kidney was separated into two peaks at positions where authentic porcine/human and putative rat/human endothelin eluted. Furthermore, the concentration of immunoreactive endothelin in the inner medulla of the kidney was remarkably decreased in spontaneously hypertensive rats (SHR) compared with normotensive control Wistar Kyoto rats (WKY) but no difference was observed in lung immunoreactive endothelin.

Reciprocal Contribution of Pentraxin 3 and C-Reactive Protein to Obesity and Metabolic Syndrome

Pentraxin 3 (PTX3) is an acute‐phase protein that shares structural homology with C‐reactive protein (CRP). PTX3 is produced in macrophages, endothelial cells, and adipocytes in response to inflammatory stimuli, whereas hepatocytes are the main source of CRP. Because obesity and metabolic syndrome (MetS) are considered chronic inflammatory states, PTX3 might be involved in the pathogenesis of obesity and MetS as well as CRP. Levels of CRP correlated positively with body weight, BMI, waist circumference (WC), fasting plasma glucose and interleukin (IL)‐6, and negatively with high‐density lipoprotein cholesterol and adiponectin in healthy males. In contrast, PTX3 correlated positively with adiponectin, and negatively with body weight, BMI, WC, and triglyceride. Plasma CRP significantly increased, whereas plasma PTX3 significantly decreased with increasing BMI. Plasma CRP and PTX3 levels were significantly higher and lower, respectively, in individuals who had more than one MetS component compared with those who had none. In conclusion, PTX3 and CRP antagonistically participate in the development of obesity or MetS.

Increased immunoreactive neuropeptide Y in platelets of spontaneously hypertensive rats (SHR)

A high concentration of immunoreactive neuropeptide Y was observed in rat platelets using a specific and sensitive radioimmunoassay for neuropeptide Y. Three kinds of high performance liquid chromatography combined with radioimmunoassay for neuropeptide Y showed that immunoreactive neuropeptide Y in rat platelets is identical to rat authentic neuropeptide Y. To investigate the pathological role of platelet neuropeptide Y in genetic hypertensive rats, the platelet content and plasma concentration of neuropeptide Y were measured by a sensitive radioimmunoassay for rat neuropeptide Y in 5-, 10- and 15-wk old spontaneously hypertensive rat and age-matched Wistar Kyoto rat. Platelet content of immunoreactive neuropeptide Y in 5-, 10- and 15-wk old spontaneously hypertensive rat was higher than that in Wistar Kyoto rat at each age. No difference was observed in plasma concentration of immunoreactive neuropeptide Y between spontaneously hypertensive rat and Wistar Kyoto rat at each age.

Platelet neuropeptide Y in spontaneously hypertensive rats

Objective To investigate the pathological role of platelet neuropeptide Y (NPY) in genetically hypertensive rats, we measured the platelet content and plasma concentration of immunoreactive (ir)-NPY in hypertensive and normotensive rats and examined the aggregating ability of rat platelets and the NPY releasing reaction in each of these rat types. In addition, we purified platelet NPY and determined its amino acid sequence. Design and methods To characterize immunoreactive NPY in rat platelets, rat platelet NPY was purified to homogeneity and the purified peptide was analysed by gas-phase sequencer. Platelet content and plasma concentration of NPY was measured by a sensitive radioimmunoassay for NPY. Aggregating ability was examined by a turbidimetric method; aggregation was recorded for 5 min and the maximum aggregation was read. Results Rat platelet NPY was purified and the amino acid sequence was determined to be YPSKPDNPGEDAPAEDMARYYSALRHYINUTRQRY. The platelet content of ir-NPY in 5-, 10-, and 15-week-old spontaneously hypertensive rats (SHR) was higher than that in Wistar-Kyoto (WKY) rats of the same age. The platelet content of ir-NPY in 10-week-old stroke prone-SHR was also higher than that in 10-week-old WKY rats. No differences were observed between any of the pairs in any WKY rats, SHR or stroke-prone SHR group with regard to the plasma concentration of ir-NPY. Ir-NPY was not released from rat platelets when adenosine diphosphate was used for aggregation. However, NPY was released from the platelets when they were aggregated by collagen and, furthermore, in this case the amount of NPY released from platelets was greater in SHR than in WKY rats. Conclusion That the platelet content of NPY in SHR (and stroke-prone SHR) was higher than that in WKY rats seems to be an important genetic characteristic of SHR. As NPY is a potent vasoconstrictor, it may be involved in the progression of vascular lesions.

Pacing Failure Due to Markedly Increased Stimulation Threshold 2 Years after Implantation: Successful Management with Oral Prednisolone: A Case Report

In a 53‐year‐old male who had undergone transvenous permanent pacing, infracardiac potential reduced progressively over a 2‐year period and exit block developed, while the stimulation threshold was markedly increased. After oral prednisolone for 5 months, the stimulation threshold reduced gradually along with an increase in intracardiac potential, culminating in no recurrence of exit block for the ensuing 2 years. The clinical course suggests that progressive reduction in intracardiac potential may have presaged the late development of exit block, and that oral prednisolone may be a therapeutic approach for the restoration of ventricular capture even 2 years after implantation.

Intrahepatic Portal-Hepatic Venous Shunts Demonstrated by us, CT, and MR Imaging

Purpose: Radiological findings were investigated in 6 cases of intrahepatic portal-hepatic venous shunt (IPHVS) without chronic liver disease. Material and Methods: Six patients with IPHVS were examined using US, CT and MR imaging. US was performed in all patients and color Doppler imaging in 5 patients. CT was performed after i.v. bolus injection of contrast medium in 4 patients. MR imaging and MR angiography were performed in one patient. Results: The shunt was present in the right lobe in 4 patients and in the left lobe in 2 patients. The shunts consisted of focally dilated or tubular vessels (1 aneurysmal) in 4 patients, and multiple small vessels in 2 patients. US revealed anechoic structures with various configurations at the shunt. Color Doppler imaging could detect blood flow in various directions in the shunt vessels in 5 patients. CT and MR images showed these abnormal vascular structures in the liver. MR angiography was also useful for evaluating the relationship between the portal and the hepatic veins. Conclusion: Color Doppler imaging was the best modality for evaluation of IPHVS.

Associations of Plasma Pentraxin 3 and Monocyte Chemoattractant Protein-1 Concentrations with Cardiovascular Disease in Patients with Chronic Kidney Disease

We examined the associations of circulating levels of pentraxin 3 (PTX3), monocyte chemoattractant protein-1 (MCP-1), and some other inflammatory mediators with cardiorenal syndrome. In advanced chronic kidney disease (CKD) patients (estimated glomerular filtration rate <30 mL/min/1.73 m2), the values of area under the curve of PTX3, tumor necrosis factor α, and high-sensitivity C-reactive protein for the detection of the association of cardiovascular disease (CVD) were 0.664, 0.507, and 0.318, respectively. In contrast, serum levels of MCP-1 were significantly higher in CKD patients than in control subjects independently of association with CVD. Abstract Both pentraxin 3 (PTX3) and monocyte chemoattractant protein-1 (MCP-1) are mediators of inflammation. They also appear to play critical roles in vascular endothelial dysfunction but their associations with cardiorenal syndrome remain largely unknown. The objective of this study was to examine their associations with cardiorenal syndrome. Circulating levels of PTX3, MCP-1, and some other biomarkers were evaluated in 134 patients with chronic kidney disease (CKD) and/or cardiovascular disease (CVD) and 55 age- and gender-matched subjects without CKD or CVD. Levels of PTX3, high-sensitivity C-reactive protein (hsCRP), and tumor necrosis factor α (TNFα) were significantly higher in CKD patients with CVD than in those without CVD. In advanced CKD patients (estimated glomerular filtration rate <30 mL/min/1.73 m2), the values of area under the curve of PTX3, TNFα, and hsCRP for the detection of the association of CVD were 0.664, 0.507, and 0.318, respectively. In contrast, serum levels of MCP-1 were significantly higher in CKD patients than in control subjects independently of association with CVD. PTX3, hsCRP, and TNFα, but not MCP-1 could predict the presence of CVD as a complication associated with CKD. Additionally, PTX3 might be a more sensitive marker for the association of CVD than hsCRP and TNFα in patients with advanced CKD.