Search Results
You are looking at 1 - 3 of 3 items for
- Author: T Imamura x
- Refine by access: All content x
Search for other papers by N Hirayama in
Google Scholar
PubMed
Search for other papers by K Kitamura in
Google Scholar
PubMed
Search for other papers by T Imamura in
Google Scholar
PubMed
Search for other papers by J Kato in
Google Scholar
PubMed
Search for other papers by Y Koiwaya in
Google Scholar
PubMed
Search for other papers by T Tsuji in
Google Scholar
PubMed
Search for other papers by K Kangawa in
Google Scholar
PubMed
Search for other papers by T Eto in
Google Scholar
PubMed
In the biosynthesis of adrenomedullin (AM), an intermediate form, AM(1-52)-glycine-COOH (iAM), is cleaved from proAM and subsequently processed to a biologically active mature form, AM(1-52)-NH2 (mAM), by enzymatic amidation. We recently reported that immunoreactive AM in human plasma consists of mAM and iAM. To clarify the pathophysiological roles of mAM and iAM in heart failure, we established an assay method to specifically detect mAM, and we determined the plasma concentrations of mAM and iAM in 68 patients with congestive heart failure (CHF). The plasma mAM concentrations of the CHF patients classified as being class I or II of New York Heart Association (NYHA) functional classification were significantly greater than those of the 28 healthy controls, and a further increase was noted in the class III or IV patients. Similar increases in plasma iAM were also observed in these patients compared with controls. The increased plasma mAM and iAM in 12 patients with exacerbated CHF were significantly reduced by treatment of their CHF for 7 days. In addition, the plasma concentrations of both mAM and iAM were significantly correlated with pulmonary capillary wedge pressure, pulmonary artery pressure, right atrial pressure, cardiothoracic ratio, heart rate, and the plasma concentrations of atrial and brain natriuretic peptides in the CHF patients. Thus the plasma concentrations of both mAM and iAM were increased progressively in proportion to the severity of CHF. These results suggest that, though the role of iAM remains to be clarified, mAM acts against the further deterioration of heart failure in patients with CHF.
Search for other papers by Y Itoh in
Google Scholar
PubMed
Search for other papers by S Imamura in
Google Scholar
PubMed
Search for other papers by K Yamamoto in
Google Scholar
PubMed
Search for other papers by Y Ono in
Google Scholar
PubMed
Search for other papers by M Nagata in
Google Scholar
PubMed
Search for other papers by T Kobayashi in
Google Scholar
PubMed
Search for other papers by T Kato in
Google Scholar
PubMed
Search for other papers by M Tomita in
Google Scholar
PubMed
Search for other papers by A Nakai in
Google Scholar
PubMed
Search for other papers by M Itoh in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Endothelin-1 (ET-1) concentrations are increased in patients with diabetes mellitus, particularly those with diabetic retinopathy, or essential hypertension. We hypothesized that ET-1 might participate in the development and progression of diabetic microangiopathy. In this study, the effects of the angiotensin converting enzyme (ACE) inhibitor, enalapril maleate, on diabetic angiopathy were examined in streptozotocin (STZ)-induced diabetic (STZ-DM) rats by monitoring variations in renal function and ET-1 concentrations in blood and organ tissues. Significant increases in kidney weight and in concentrations of urinary albumin, N-acetyl-fl-d-glucosamidase (NAG) and serum ET-1 were observed in the STZ-DM rats as compared with the non-diabetic rats, and the concentration of ET-1 in the kidneys tended to be increased. Microscopic and electron microscopic analyses showed increased mesangial cell proliferation, matrix expansion and enlarged mesangial area in the kidney of the diabetic rats. After administration of the ACE inhibitor, increased concentrations of urinary albumin and NAG in the STZ-DM rats were reduced to the control values with a slight improvement in the electron microscopic changes. These data suggest that ET-1 may be involved in the development and progression of diabetic nephropathy and may explain, in part, why diabetes is liable to complicate hypertension. ACE inhibitor may help to restore diabetic nephropathy in the STZ-induced diabetic rats.
Search for other papers by M Makino in
Google Scholar
PubMed
Search for other papers by N Oda in
Google Scholar
PubMed
Search for other papers by N Miura in
Google Scholar
PubMed
Search for other papers by S Imamura in
Google Scholar
PubMed
Search for other papers by K Yamamoto in
Google Scholar
PubMed
Search for other papers by T Kato in
Google Scholar
PubMed
Search for other papers by K Fujiwara in
Google Scholar
PubMed
Search for other papers by Y Sawai in
Google Scholar
PubMed
Search for other papers by K Iwase in
Google Scholar
PubMed
Search for other papers by A Nagasaka in
Google Scholar
PubMed
Search for other papers by M Itoh in
Google Scholar
PubMed
Thyroid hormones affect reactions in almost all pathways of lipid metabolism. It has been reported that plasma free fatty acid (FFA) concentration in hypothyroidism is generally within the normal range. In this study, however, we show that plasma FFA concentration in some hypothyroid patients is higher than the normal range. Symptoms of thyroid dysfunction in these individuals were less severe than those of patients with lower plasma FFA concentrations. From these findings we hypothesized that the change in FFA concentration must correlate with thyroid function. Using an animal model, we then examined the effect of highly purified eicosapentaenoic acid ethyl ester (EPA-E), a n-3 polyunsaturated fatty acid derived from fish oil, on thyroid function in 1-methyl-2-imidazolethiol (MMI)-induced hypothyroid rats. Oral administration of EPA-E inhibited reduction of thyroid hormone levels and the change of thyroid follicles in MMI-induced hypothyroid rats. These findings suggest that FFA may affect thyroid functions and EPA-E may prevent MMI-induced hypothyroidism.
