Biomedical subjects

Hiroyuki Sumino

Publications and source records attributed to Hiroyuki Sumino.

9 recordsLinked to original sources

PubMed2003

Hormone replacement therapy causes a decrease in hepatocyte growth factor in hypertensive women.

OBJECTIVE: Serum hepatocyte growth factor (HGF) is associated with blood pressure. We investigated whether the serum HGF level differs between hypertensive and normotensive postmenopausal women (PMW) and whether hormone replacement therapy (HRT) alters the serum HGF level and blood pressure in hypertensive and normotensive PMW. DESIGN: Prospective observational study. METHODS: A total of 33 PMW with mild to moderate essential hypertension controlled by antihypertensive treatment (mean age, 57 +/- 6 years) and 23 normotensive PMW (mean age, 57 +/- 7 years) received continuous HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) once a day orally for 12 months, and we measured serum HGF levels and blood pressure before and 12 months after the start of HRT. RESULTS: The baseline serum HGF level was significantly higher in hypertensive PMW than in normotensive PMW. HRT significantly decreased the serum HGF level in hypertensive subjects, from 2.85 +/- 0.64 pmol/l to 2.49 +/- 0.65 pmol/l (P < 0.001), but not in normotensive subjects. HRT did not change blood pressure in either group. CONCLUSIONS: Serum HGF level before the start of HRT was higher in the hypertensive PMW than in the normotensive PMW. Furthermore, HRT decreases serum HGF without decreasing blood pressure in hypertensive PMW. The HRT-induced decrease in serum HGF was greater in hypertensive PMW than in normotensive PMW, and the decrease was independent of blood pressure changes.

Aged↗

PubMed2003

Hormone replacement therapy decreases insulin resistance and lipid metabolism in Japanese postmenopausal women with impaired and normal glucose tolerance.

OBJECTS: To investigate the effect of combined estrogen and progesterone therapy on insulin resistance (IR) and carbohydrate and lipid metabolism in postmenopausal women (PMW) with impaired (IGT) and normal glucose tolerance (NGT). METHODS: Sixteen Japanese PMW with IGT and 33 with NGT received daily oral hormone replacement therapy (HRT; 0.625 mg of conjugated equine estrogen plus 2.5 mg of medroxyprogesterone acetate) for 12 months. As controls, 13 Japanese PMW with IGT and 31 with NGT were enrolled and not treated by HRT. Fasting plasma glucose (FPG), fasting immunoreactive insulin (IRI), and IR were measured in each subject at study initiation and 12 months later. We used homeostasis model assessment (HOMA) to determine IR. RESULTS: FPG and HOMA IR were decreased in both HRT groups, and fasting IRI was reduced in the HRT-NGT group. In controls, FPG, fasting IRI, and HOMA IR were unaltered. Total and low-density lipoprotein cholesterol were decreased and high-density lipoprotein cholesterol was increased in both HRT groups, but triglyceride was unchanged. In controls, lipid metabolism was unaltered. CONCLUSION: HRT decreased IR and improved carbohydrate and lipid metabolism in Japanese PMW with IGT and NGT. These beneficial effects argue for the use of HRT in PMW with IGT as well as NGT.

Asian People↗

PubMed2003

Effects of hormone replacement therapy on office and ambulatory blood pressure in Japanese hypertensive postmenopausal women.

No study has demonstrated that hormone replacement therapy (HRT) affects blood pressure (BP) measured by 24-h ambulatory blood pressure monitoring (ABPM) in Japanese postmenopausal women (PMW) with normotension or mild-to-moderate essential hypertension. In the present study, we examined the effects of HRT on office BP and 24-h ambulatory blood pressure (ABP) in Japanese hypertensive or normotensive PMW. Thirty-one hypertensive (HT-HRT group) and 17 normotensive PMW (NT-HRT group) received HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) orally for 12 months, and 30 hypertensive (HT-Control group) and 19 normotensive PMW (NT-Control group) did not receive HRT. In all of the hypertensive PMW, BP was controlled by a variety of antihypertensive drugs before starting HRT. The hypertensive PMW were divided into two groups according to the results of ABP before HRT: nondippers (those without a diurnal change in BP) and dippers (those with a diurnal change in BP). In all patients, office BP measurements and 24-h ABPM were performed before and 12 months after the start of HRT. HRT did not change either the office or the 24-h ambulatory systolic, diastolic, or mean BP in any of the groups. Therefore, HRT did not significantly alter the proportion of nondippers. We conclude that with respect to BP, HRT might not be harmful in hypertensive PMW whose BP has been well-controlled prior to the initiation of HRT, as well as in normotensive PMW.

Antihypertensive Agents↗

PubMed2003

Effects of hormone replacement therapy on serum angiotensin-converting enzyme activity and plasma bradykinin in postmenopausal women according to angiotensin-converting enzyme-genotype.

An insertion/deletion (I/D) polymorphism in the angiotensin-converting enzyme (ACE) gene determines serum ACE levels. The D allele is associated with increased ACE activity and is linked to cardiovascular disease. Hormone replacement therapy (HRT) in postmenopausal women (PMW) decreases serum ACE activity and concomitantly increases plasma bradykinin. We investigated the effect of HRT on these parameters in PMW according to ACE-genotype. We assessed 68 PMW during 12-month oral HRT (0.625 mg conjugated estrogen +2.5 mg medroxyprogesterone acetate). ACE genotype was determined at baseline, and serum ACE activity and plasma bradykinin were measured at baseline and after 3-, 6-, and 12-month HRT. We divided the PMW into three groups according to ACE genotype: groups I/I (n = 26), I/D (n = 33), and D/D (n = 9). HRT resulted in a significant reduction in the genotype-associated increase in ACE activity in the ACE I/D and D/D groups after 6-month (p < 0.001 and p < 0.05, respectively) and 12-month HRT (p < 0.001 and p < 0.01, respectively), but not in the I/I group. While the reduction of ACE activity was expected to increase bradykinin in the ACE I/D and D/D groups, HRT significantly increased the bradykinin levels not only in these two groups but also in the ACE I/I group at both 6 months (p < 0.01, p < 0.05, and p < 0.001, respectively) and 12 months after the start of HRT (p < 0.01, p < 0.01, and p < 0.01, respectively). These results suggest that the increased plasma bradykinin of PMW by HRT might not be induced solely by the reduction in serum ACE activity.

Aged↗

PubMed2003

Effects of hormone replacement therapy on circulating docosahexaenoic acid and eicosapentaenoic acid levels in postmenopausal women.

Hormone replacement therapy (HRT) has antiatherosclerotic effects of which the mechanism remains unclear. The ingestion of fish oil or other sources of n-3 polyunsaturated fatty acids has been included in comprehensive strategies to prevent atherosclerosis. Many epidemiologic studies have shown that the dietary intake of docosahexaenoic acid and eicosapentaenoic acid has antiatherosclerotic effects. We investigated the effect of HRT on plasma docosahexaenoic acid and eicosapentaenoic acid concentrations in postmenopausal women. Fifty-nine postmenopausal women, who received conjugated estrogens (0.625 mg/day) and medroxyprogesterone (2.5 mg/day) for 12 months, and 45 control postmenopausal women, who did not receive HRT, volunteered to participate in this study. Plasma docosahexaenoic acid and eicosapentaenoic acid concentrations were measured at baseline and at 6 and 12 months after the start of HRT. HRT significantly increased the plasma docosahexaenoic acid and eicosapentaenoic acid concentrations from 134 +/- 5 microg/ml and 69 +/- 4 microg/ml at baseline to 156 +/- 7 microg/ml and 85 +/- 7 microg/ml after 12 months (both p<0.01). However, the control group showed no significant change in their plasma docosahexaenoic acid and eicosapentaenoic acid levels during the study. HRT increased plasma docosahexaenoic acid and eicosapentaenoic acid levels in postmenopausal women. We propose that the increase in docosahexaenoic acid and eicosapentaenoic acid may be partially responsible for the beneficial mechanisms by which HRT induces an antiatherosclerotic effect in postmenopausal women.

Adult↗

PubMed2003

[Study on blood rheology measured by MC-FAN].

We investigated the effects of various factors on blood rheology, which was evaluated by the passage time of heparinized whole blood using MC-FAN (Micro Channel array Flow ANalyzer). The time for 100 microliters of whole blood to pass through a microchannel array (Bloody 6-7) was determined. Each passage time was corrected by the saline passage time determined just before the measurement of sample blood. Our results suggest that blood rheology measured by MC-FAN is related to aging, body weight, body mass index and serum lipid parameters (total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglyceride). These results suggest that MC-FAN is useful to analyze blood rheology in pathophysiological conditions.

Adult↗

PubMed2002

Reciprocal expression of vascular endothelial growth factor and nitric oxide synthase by coronary arterial wall cells during chronic inhibition of nitric oxide synthesis in rats.

Chronic inhibition of nitric oxide (NO) synthesis by oral administration of N(G)-nitro-L-arginine methyl ester (L-NAME) causes hypertension and produces arteriosclerosis in rats. Balloon injury induces upregulation of vascular endothelial growth factor (VEGF) in medial smooth muscle cells of the rat arterial wall, and NO secreted by a restored endothelium acts as the negative feedback mechanism that downregulates VEGF expression to basal levels. In this study, we tested the hypothesis that a reciprocal relation between VEGF and NO would be established in a rat model of chronic NO blockade. Male Wister rats received plain drinking water (n = 10) or L-NAME (0.5 mg/ml) in the drinking water (n = 11) for 6 weeks. After 6 weeks, the wall-to-lumen ratios and perivascular fibrosis in the coronary arteries were greater in the L-NAME group than in the control group. NO synthase-positive cells in the intima were abundantly observed in the control group, whereas no such cells were seen in the L-NAME group. In contrast, the number of VEGF-positive smooth muscle cells in the media was greater in the L-NAME group than in the control group. These findings strongly suggest a reciprocal relation between VEGF and NO even in a rat model of chronic NO blockade.

Animals↗

PubMed2002

Production of nitric oxide, but not prostacyclin, is reduced in klotho mice.

A novel murine model of aging (kl/kl mice) has been developed by in vivo mutagenesis. We analyzed endothelial function in this strain. Ring preparations of the thoracic aorta were obtained from 6- to 9-week old wild-type (+/+) and heterozygous (kl/+) klotho mice. The aortas of kl/+ mice showed an exaggerated contractile response to norepinephrine and attenuated vasodilator responses to acetylcholine and lecithinized superoxide dismutase (SOD) compared to +/+ mice. The response to sodium nitroprusside was unaltered in kl/+ mice. The contraction in response to norepinephrine was augmented by treatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-5) M) to a greater extent in +/+ mice than in kl/+ mice. Treatment with L-NAME abolished the vasodilator responses to both acetylcholine and lecithinized SOD. NO metabolites (NO2- and NO3-) and cGMP concentrations in the urine were significantly reduced in kl/+ mice compared to +/+ mice. However, the urinary excretion of 6-keto-prostaglandin F1alpha was unaltered. There was little immunostaining for NO synthase and vascular endothelial growth factor (VEGF) in the aorta of kl/+ mice. No immunostaining for NO synthase was noted in the aorta of kl/kl mice. The expression of the klotho gene product may have a role in the regulation of VEGF expression and is tightly linked to endothelial release of NO.

Animals↗

PubMed2002

Effects of hormone replacement therapy on left ventricular hypertrophy and growth-promoting factors in hypertensive postmenopausal women.

We investigated the effects of hormone replacement therapy (HRT) on left ventricular hypertrophy (LVH) and growth-promoting factors in hypertensive postmenopausal women (PMW) with LVH. Twenty-one Japanese hypertensive PMW (age 55.3+/-0.8 years) with LVH who had never received HRT volunteered to participate in this study. Eleven subjects received a daily dose of HRT (0.625 mg conjugated equine estrogen, 2.5 mg medroxyprogesterone acetate) orally for 12 months. Ten PMW who refused HRT were enrolled as controls. Blood pressure and serum angiotensin-converting enzyme (ACE) activity, plasma aldosterone, and insulin resistance were measured. M-mode echocardiography and blood pressure measurements were performed in all patients. Data obtained before and after 12 months of HRT were compared. No significant differences in blood pressure were observed between the two groups after 12 months of HRT. In the HRT group, the LV mass index (p<0.01), serum ACE activity (p<0.01), and plasma aldosterone (p<0.01) levels were reduced after 12 months of treatment. The changes in serum ACE activity and plasma aldosterone were not correlated with the change in LV mass index in the HRT group. No significant changes in blood pressure, LV mass index, serum ACE activity, plasma aldosterone, or insulin resistance were observed in the control group. HRT contributed to the reduction of LV mass in hypertensive PMW. However, the effect of HRT on LVH did not appear to be associated with changes in growth-promoting factors, such as blood pressure, serum ACE activity, plasma aldosterone, and insulin resistance.

Aldosterone↗