Biomedical subjects

Minoru Takaoka

Publications and source records attributed to Minoru Takaoka.

5 recordsLinked to original sources

PubMed2006

Cardiac expression of placental growth factor predicts the improvement of chronic phase left ventricular function in patients with acute myocardial infarction.

OBJECTIVES: Our aim was to investigate cardiac expression of placental growth factor (PlGF) and its clinical significance in patients with acute myocardial infarction (AMI). BACKGROUND: Placental growth factor is known to stimulate wound healing by activating mononuclear cells and inducing angiogenesis. The clinical significance of PlGF in AMI is not yet known. METHODS: Fifty-five AMI patients and 43 control subjects participated in the study. Peripheral blood sampling was performed on days 1, 3, and 7 after AMI. Blood was also sampled from the coronary artery (CAos) and the coronary sinus (CS), before and after acute coronary recanalization. Cardiac expression of PlGF was analyzed in a mouse AMI model. RESULTS: In AMI patients, peripheral plasma PlGF levels on day 3 were significantly higher than in control subjects. Plasma PlGF levels just after recanalization were significantly higher in the CS than the CAos, which indicates cardiac production and release of PlGF. Peripheral plasma levels of PlGF on day 3 were negatively correlated with the acute phase left ventricular ejection fraction (LVEF), positively correlated with both acute phase peak peripheral monocyte counts and chronic phase changes in LVEF. Placental growth factor messenger ribonucleic acid expression was 26.6-fold greater in a mouse AMI model than in sham-operated mice, and PlGF was expressed mainly in endothelial cells within the infarct region. CONCLUSIONS: Placental growth factor is rapidly produced in infarct myocardium, especially by endothelial cells during the acute phase of myocardial infarction. Placental growth factor might be over-expressed to compensate the acute ischemic damage, and appears to then act to improve LVEF during the chronic phase.

Animals↗

PubMed2006

Inhibitory effect of efonidipine on aldosterone synthesis and secretion in human adrenocarcinoma (H295R) cells.

Targeting aldosterone synthesis and/or release represents a potentially useful approach to the prevention of cardiovascular disease. Aldosterone production is stimulated by angiotensin II (Ang II) or extracellular K+ and is mediated mainly by Ca2+ influx into adrenal glomerulosa cells through T-type calcium channels. We therefore examined the effects of efonidipine, a dual T-type/L-type Ca2+ channel blocker, on aldosterone secretion in the H295R human adrenocarcinoma cell line; 100 nmol/L Ang II and 10 mmol/L K+ respectively increased aldosterone secretion from H295R cells 12-fold and 9-fold over baseline. Efonidipine dose-dependently inhibited both Ang II- and K+-induced aldosterone secretion, and nifedipine, an L-type Ca2+ channel blocker, and mibefradil, a relatively selective T-type channel blocker, similarly inhibited Ang II- and K+-induced aldosterone secretion, but were much less potent than efonidipine. Efonidipine also lowered cortisol secretion most potently among these drugs. Notably, efonidipine and mibefradil also significantly suppressed Ang II- and K+-induced mRNA expression of 11-beta-hydroxylase and aldosterone synthase, which catalyze the final two steps in the aldosterone synthesis, whereas nifedipine reduced only K+-induced enzyme expression. These findings suggest that efonidipine acts via T-type Ca2+ channel blockade to significantly reduce aldosterone secretion, and that this effect is mediated, at least in part, by suppression of 11-beta-hydroxylase and aldosterone synthase expression.

Adrenal Gland Neoplasms↗

PubMed2004

White-coat hypertension contributes to the presence of carotid arteriosclerosis.

It remains unclear whether white-coat hypertension is associated with vascular organ damage (e.g., carotid arteriosclerosis) in the same way sustained hypertension is. We therefore compared the progression of carotid arteriosclerosis among Japanese individuals showing normal blood pressures, sustained hypertension or white-coat hypertension. A total of 30 subjects (mean age, 58 years) with white-coat hypertension, 30 (mean age, 54 years) with untreated sustained hypertension who had no plaque formation in the carotid arteries, and 30 normotensive subjects (mean age, 58 years) were enrolled in this study. The white-coat and sustained hypertensive subjects were matched with respect to their clinical blood pressures, but their ambulatory blood pressures differed. Conversely, white-coat hypertensive and normotensive subjects were matched with respect to ambulatory blood pressures, but their clinical blood pressures differed. Carotid intimal-medial thickness was measured by B-mode ultrasonography, and the cross-sectional area of the common carotid artery was calculated. The three groups were similar with respect to age, sex ratio, height, laboratory data and the incidence of smoking. Body weights and body mass indexes were significantly higher among patients with sustained hypertension than among either normotensive or white-coat hypertensive patients. Intimal-medial thicknesses and carotid cross-sectional areas were similar in patients with white-coat and sustained hypertension and significantly higher than in normotensive subjects. Collectively, these findings suggest that white-coat hypertension contributed to the presence of carotid arteriosclerosis in our subjects in a manner similar to sustained hypertension. Thus, clinical evaluation of white-coat hypertension should be conducted with the potential for target organ damage in mind.

Adult↗

PubMed2004

[NOS gene polymorphism].

Nitric oxide(NO), a potent vasodilator produced by endothelial cells, plays an important role in the regulation of blood pressure and regional blood flow, and also inhibits platelet aggregation and leukocyte adhesion to vascular endothelium and inhibits vascular smooth muscle cell proliferation. Various genetic polymorphisms of the endothelial nitric oxide synthase(eNOS) gene have been reported as susceptibility genes in a number of cardiovascular diseases. The functional significance of these polymorphisms has not yet been demonstrated, but recent study revealed that eNOS Glu298Asp variant is likely to have a functional effect on the eNOS protein. The missense Glu298Asp variant was correlated with increased coronary spasm, myocardial infarction, essential hypertension, left ventricular hypertrophy, carotid atherosclerosis, and cerebral infarction.

Cardiovascular Diseases↗

PubMed2002

Vascular remodeling of the carotid artery in patients with untreated essential hypertension increases with age.

We examined whether hypertrophy of the carotid artery in patients with untreated essential hypertension is associated with compensatory carotid artery enlargement as these patients age. Carotid ultrasonography was evaluated in 163 patients with untreated essential hypertension (74 males and 89 females) and in 76 normotensive subjects. Intima-media end-diastolic thickness (IMT) and outer vessel diameter (VD) were measured, and relative wall thickness (IMT/R, R=VD/2) and vascular mass (VM) were calculated. Determinants of vascular hypertrophy in patients with untreated essential hypertension were also investigated. VD, VM, and IMT were significantly correlated with age in both the normotensive and hypertensive groups. Additionally, IMT was significantly correlated with VD in both groups. There was no correlation between increasing age and IMT/R in either group. IMT, VD and VM were significantly higher in the hypertensive group >50 years than in age-matched normotensive controls. However, IMT/R was significantly higher in the 50-59 years hypertensive group than in normotensive controls of the same age group. In addition to age, VM was related to systolic blood pressure, pulse pressure, fasting blood sugar, IMT, VD, and IMT/R in the hypertensive group. Multivariate regression analysis in the hypertensive group indicated that IMT/R was the strongest predictor of carotid vascular mass. Age and pulse pressure were also independently related to vascular mass. These results indicate that, as patients with untreated hypertension age, carotid arteries undergo remodeling. This should add further impetus to the implementation of appropriate hypertension treatment for such patients.

Adult↗