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Biomedical subjects

Koji Fujii

Publications and source records attributed to Koji Fujii.

At least 37 records · Page 2Linked to original sources
PubMed2004

Association of QT interval with blood pressure in 80-year-old subjects.

Few data are available on the association between the prolonged heart rate-adjusted QT (QTc) interval and high blood pressure in elderly individuals, particularly in subjects over 80 years old. The aim of the present study was to determine the association between the QTc interval and blood pressure in 80-year-old subjects. This study was part of the 8020 Data Bank Survey, which was designed to collect the baseline data of systemic and dental health conditions in 80-year-old subjects. We studied the cross-sectional association of the QTc interval with blood pressure in 642 Japanese (257 men and 385 women), all 80 years old. Mean systolic blood pressure (SBP) rose from 146.0 mmHg in the first quartile of QTc interval to 149.1 mmHg in the second, 154.6 mmHg in the third, and 152.3 mmHg in the fourth quartile (test for trend, p=0.008). Mean diastolic blood pressure (DBP) also rose from 76.9 mmHg in the first quartile of QTc interval to 77.7 mmHg in the second, 81.8 mmHg in the third, and 79.0 mmHg in the fourth quartile (test for trend, p=0.003). We performed multiple regression analysis, controlling for factors known to influence the QTc intervals-e.g., SBP, heart rate, sex, and left ventricular hypertrophy assessed by the voltage amplitudes recorded in the precordial leads of the electrocardiogram. The association between the QTc interval and SBP was highly statistically significant in all analyses. These results show that SBP by itself may influence the QTc interval in very old subjects.

Aged↗
PubMed2004

Alleles responsible for ABO phenotype-genotype discrepancy and alleles in individuals with a weak expression of A or B antigens.

ABO types obtained from evidentiary samples have been used effectively to obtain the initial information leading to the apprehension of culprits in Japanese criminal investigations. A simple ABO genotyping method using multiplex sequence-specific PCR and capillary electrophoresis was developed as a supplement to serological ABO typing. Limitations in predicting a phenotype based on genotype were evaluated using 1134 randomly selected Japanese peripheral blood samples. A concordance rate of 99.82% (1132/1134 samples) was found between genotypes and phenotypes defined as Groups A, B, AB, and O. Sequencing analysis revealed that one discrepant sample contained an O allele having a previously unreported point mutation at the primer binding site in exon 6, and another discrepant sample contained an O allele lacking the guanine deletion at nt 261 (the O301 allele). Therefore, the existence of such alleles must be given some consideration when predicting phenotype based on genotype.

ABO Blood-Group System↗
PubMed2004

[C4b-binding protein].

Explore the source record for details and available documents.

Complement Inactivator Proteins↗
PubMed2003

Neural regulation of blood pressure by leptin and the related peptides.

Recent biological advances make it possible to discover new peptides associated with obesity. Leptin, neuropeptide Y, corticotrophin-releasing factor (CRF), alpha-melanocyte stimulating hormone (alpha-MSH), and cocaine- and amphetamine-regulated transcript (CART) peptides are known to participate in appetite and feeding behavior. Various lines of evidence suggest that these peptides participate not only in feeding behavior but also in cardiovascular and sympathetic regulations. Both leptin and ghrelin are secreted from the peripheral tissue; then they reach the brain to modulate sympathetic activity. These two peptides seem to play important roles to transmit peripheral metabolic information to the brain, and to convert it to cardiovascular and sympathetic information. Leptin activates neurons containing alpha-melanocyte stimulating hormone and cocaine- and amphetamine-regulated transcript peptides, resulting in increases in sympathetic activity and blood pressure. Cardiovascular action of alpha-melanocyte stimulating hormone is mediated through melanocortin-4 receptor, and agouti-related protein (AGRP) plays a role as an endogenous melanocortin-4 receptor antagonist. In contrast, ghrelin and neuropeptide Y in the brain suppress sympathetic activity and decrease blood pressure. Depressor and sympathoinhibitory effects of central neuropeptide Y are inhibited by leptin. Furthermore, central ghrelin modulates baroreflex control of renal sympathetic nerve activity and heart rate. Thus, leptin and the related peptides, which participate in appetite and feeding behavior, seem to function together to regulate cardiovascular system and sympathetic nerve activity, and may play a key role in the association between obesity and hypertension.

Agouti-Related Protein↗
PubMed2003

Risk factors for the progression of early carotid atherosclerosis in a male working population.

Increased intima-media thickness (IMT) of the carotid artery may represent early atherosclerosis. Although several studies have evaluated risk factors for carotid IMT, only limited information is available concerning risk factors for the progression of carotid IMT. The present study was designed to determine risk factors for the progression of carotid IMT in a male working population. Male employees of a regional transport company (n = 220, 50.9 +/- 4.4 years) underwent baseline physical and laboratory examinations, and ultrasonographic assessment of the maximum common carotid IMT between 1992 and 1994, and they were reexamined 5 years later. In a multivariate analysis at baseline, carotid IMT was positively associated with age, diastolic blood pressure and total cholesterol, and negatively with high density lipoprotein (HDL) cholesterol. During the follow-up period, carotid IMT increased from 0.669 +/- 0.135 mm to 0.784 +/- 0.229 mm, or at a rate of 0.023 +/- 0.039 mm/year. In a multivariate regression analysis using baseline values of carotid IMT, age, body mass index, diastolic blood pressure, total cholesterol, HDL cholesterol and HbA1c as independent variables, the progression of carotid IMT was associated only with baseline total cholesterol. These findings suggest that in middle-aged men, although age, blood pressure, and total cholesterol were associated with baseline carotid IMT, total cholesterol level appeared to be the strongest determinant of the progression of carotid IMT, a result which underscores the importance of maintaining lower cholesterol levels to prevent early atherosclerosis.

Adult↗
PubMed2003

Central cardiovascular action of urotensin II in spontaneously hypertensive rats.

We have previously reported that urotensin II acts on the central nervous system to increase blood pressure in normotensive rats. In the present study, we have determined the central cardiovascular action of urotensin II in spontaneously hypertensive rats (SHR). Intracerebroventricular (ICV) injection of urotensin II elicited a dose-dependent increase in blood pressure in both SHR and normotensive Wistar-Kyoto rats (WKY). The changes in mean arterial pressure induced by ICV urotensin II at doses of 1 and 10 nmol in the WKY were 8 +/- 2 and 23 +/- 3 mmHg, respectively. ICV administration of urotensin II caused significantly greater increases in blood pressure in SHR (16 +/- 3 mmHg at 1 nmol and 35 +/- 3 mmHg at 10 nmol, respectively) compared with those in WKY. Urotensin II (10 nmol) elicited significant and comparable increases in heart rate in SHR (107 +/- 10 bpm) and WKY (101 +/- 21 bpm). Plasma epinephrine concentrations after ICV administration of 10 nmol urotensin II were 203 +/- 58 pmol/ml in SHR and 227 +/- 47 pmol/ml in WKY, which tended to be higher than those in artificial cerebrospinal fluid-injected rats (73+/- 7 and 87 +/- 28 pmol/ml, respectively, p < 0.1). The immunoreactivity of urotensin II receptor GPR 14 was expressed extensively in the glial cells within the brainstem, hypothalamus, and thalamus. These results suggest that central urotensin II may play a role in the pathogenesis of hypertension in SHR. Since GPR 14 was expressed in the glial cells of the brain, urotensin II may act as a neuromodulator to regulate blood pressure.

Animals↗
PubMed2002

Critical role of gap junctions in endothelium-dependent hyperpolarization in rat mesenteric arteries.

1. Acetylcholine (ACh) evokes endothelium-dependent hyperpolarization in arterial cells, presumably through endothelium-derived hyperpolarizing factor (EDHF). The identity of EDHF is still elusive; however, several recent studies suggest the possible involvement of myoendothelial gap junctions in the EDHF response. 2. To elucidate the role of gap junctions in endothelium-dependent hyperpolarization, we examined the effects of the gap junction inhibitors 18 alpha-glycyrrhetinic acid (18 alpha-GA; 10(-4) mol/L) and carbenoxolone (3 x 10(-4) mol/L), a water-soluble form of 18 beta-GA, on hyperpolarization and relaxation to ACh in rat proximal and distal mesenteric arteries. Experiments were performed in the presence of indomethacin (10(-5) mol/L) and N(G)-nitro-L-arginine (10(-4) mol/L). 3. In both proximal and distal mesenteric arteries, ACh-induced hyperpolarization and relaxation were partially inhibited by 18 alpha-GA and abolished by carbenoxolone. 4. Endothelium-independent hyperpolarization to levcromakalim, an ATP-sensitive K+ channel opener, were unaffected by 18 alpha-GA or carbenoxolone in both arteries. 5. Relaxations to levcromakalim were unaffected by 18 alpha-GA, but were inhibited somewhat by carbenoxolone in proximal mesenteric arteries. 6. These findings suggest that myoendothelial gap junctions play a critical role in EDHF-mediated responses in both proximal and distal mesenteric arteries of the rat.

Acetylcholine↗
PubMed2002

Angiotensin II receptor antagonist improves age-related endothelial dysfunction.

BACKGROUND: We previously demonstrated that the angiotensin converting enzyme (ACE) inhibitor, enalapril, prevents the age-related impairment of endothelium-dependent hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF). OBJECTIVE: To test whether angiotensin II type 1 (AT1) receptor antagonists would also improve age-related endothelial dysfunction. METHODS: Normotensive Wistar-Kyoto (WKY) rats were treated for 3 months with either the AT1 receptor antagonist, candesartan cilexetil (3.5 mg/kg per day; candesartan group), or the ACE inhibitor, enalapril (20 mg/kg per day; enalapril group), from 9 to 12 months of age. Untreated 12-month-old WKY rats (old group) served as controls (n = 7-12). RESULTS: The two treatments decreased systolic blood pressure comparably. EDHF-mediated hyperpolarization in response to acetylcholine (ACh; 10(-5) mol/l) in the presence of norepinephrine in mesenteric arteries was improved in both the candesartan and enalapril groups to a similar extent compared with the old group (candesartan group, -24 +/- 3 mV; enalapril group, -21 +/- 2 mV; old group, -13 +/- 2 mV). EDHF-mediated relaxation was similarly improved in the candesartan and enalapril groups (maximum relaxation: candesartan group, 70 +/- 7%; enalapril group, 63 +/- 8%; old group, 33 +/- 9%). Hyperpolarization and relaxation responses to levcromakalim, an ATP-sensitive K+-channel opener, were similar in all groups. CONCLUSIONS: These findings suggest that the AT1 receptor antagonist is as effective as the ACE inhibitor in improving the age-related decline in EDHF-mediated hyperpolarization and relaxation in normotensive rats. Thus AT1 receptor antagonists might serve as novel tools with which to prevent endothelial dysfunction associated with aging.

Acetylcholine↗
PubMed2002

Central ghrelin modulates sympathetic activity in conscious rabbits.

Ghrelin is an orexigenic peptide originally isolated from the stomach. Intravenous administration of ghrelin has been shown to elicit a decrease in arterial pressure without a significant change in heart rate (HR), suggesting that ghrelin may act on the central nervous system to modulate sympathetic activity. The aim of the present study was to determine the central effects of ghrelin on cardiovascular and sympathetic responses in conscious rabbits. Intravenous injection of ghrelin elicited dose-related decreases in arterial pressure and HR, without a significant change in renal sympathetic nerve activity. On the other hand, intracerebroventricular injection of 1 nmol of ghrelin decreased arterial pressure, HR, and renal sympathetic nerve activity. Peak depressor or sympathoinhibitory responses of mean arterial pressure and renal sympathetic nerve activity (-19.0+/-1.5 mm Hg and -43.3+/-5.4%) were observed at 50 and 40 minutes, respectively, after intracerebroventricular injection of 1 nmol of ghrelin. Furthermore, a subdepressor dose of intracerebroventricular infusion of ghrelin (0.3 nmol/150 micro L per hour) significantly augmented the baroreflex sensitivities assessed by renal sympathetic nerve activity and HR compared with those of vehicle infusion (G(max); -17.8+/-3.1 versus -9.4+/-1.6%/mm Hg, P<0.05; -12.5+/-1.8 versus -6.6+/-1.2 bpm/mm Hg, P<0.05; respectively). These results suggest that intravenous injection of ghrelin acts, at least in part, on the central nervous system to decrease arterial pressure and renal sympathetic nerve activity, and that central ghrelin participates in the regulations of the sympathetic nerve activity to the kidney and the baroreceptor reflex in conscious rabbits.

Animals↗
PubMed2002

Bradykinin enhances sympathetic neurotransmission in rat blood vessels.

Bradykinin evokes endothelium-dependent relaxation in some vascular beds; on the other hand, the possibility has been demonstrated that in certain organs, such as the adrenal medulla or atria, bradykinin may enhance transmitter release from the sympathetic nerves. We hypothesized that bradykinin may also enhance postganglionic sympathetic neurotransmission in blood vessels. To test this hypothesis, we recorded excitatory junction potentials (EJPs), a measure of sympathetic purinergic neurotransmission, in rat mesenteric resistance arteries with a conventional microelectrode technique. EJPs were elicited by repetitive perivascular nerve stimulation (1 Hz, 20 to 50 V, 30 to 60 micros, 11 pulses). In this preparation, bradykinin (10(-7) or 10(-6) mol/L) significantly enhanced the amplitude of EJPs without altering the resting membrane potential. This effect of bradykinin was blocked by Hoe 140, a bradykinin B2 receptor antagonist, but not by des-Arg(9),[Leu(8)]-bradykinin, a bradykinin B1 receptor antagonist. The cyclooxygenase inhibitor indomethacin or NO synthase inhibitor N(G)-nitro-L-arginine did not alter the effect of bradykinin. Captopril, an ACE inhibitor, but not candesartan, an angiotensin II type 1 receptor antagonist, enhanced the action of a low concentration (10(-8) mol/L) of bradykinin on EJPs. These findings suggest that in rat mesenteric resistance arteries, bradykinin enhances sympathetic purinergic neurotransmission, presumably through presynaptic bradykinin B2 receptors. The clinical relevance of the present findings remains unclear; however, the fact that the ACE inhibitor, but not the angiotensin II type 1 receptor antagonist, enhanced the action of bradykinin on sympathetic neurotransmission may warrant further investigation.

Adenosine Triphosphate↗
PubMed2002

Fractures of the distal end of radius in elderly patients: a comparative study of anatomical and functional results.

The functional and anatomical results of distal end of radius fractures with severe displacement in 22 elderly patients are reviewed in this retrospective study. The mean age of the patients was 69.4 years (range, 60-88 years) and the mean follow-up period was 24 months (range, 12-53 months). According to the sum of demerit points (Saito, 1983), the latest follow-up functional end results were excellent in 64% of fractures and good in 36%. As for the anatomical results at follow-up, the average radial tilt was 20.7 degrees, ulnar variance was 4.0 mm, and palmar tilt was -2.7 degrees respectively. Though most of the patients had satisfactory outcome and the functional results did not correlate with the radiographic evidence of minor deformities, the functional results of the patients with radial shortening of 6 mm or over were poor. Furthermore, the grip power was the most significant factor related to subjective evaluation and did not improve significantly in patients with the non-dominant hand injured.

Aged↗
PubMed2002

Clinical evaluation of aged patients who underwent surgery for femoral neck fractures -- comparative study of clinical results according to age.

The objective was to assess mortality and ambulatory ability for elderly patients over 90 years of age with femoral neck fractures treated surgically. From January 1998 to March 1999, 60 patients aged over 80 years were chosen for the study. The patients had a mean age of 87.1 years. The mean follow-up period was 12.9 months. The patients were classified into three groups according to age: group A (80-84 years old), group B (85-89 years old) and group C (over 90 years old). The rates of recovered postoperative walking ability were 72.2% (13/18) of group A, 65.2% (15/23) of group B and 84.2% (16/19) of group C. These patients were followed up until death or for at least one year. The overall mortality rates were 11.1% (2/18) of group A, 17.4% (4/23) of group B and 10.5% (2/19) of group C.

Aged↗
PubMed2002

Discriminating factors for recurrent hypertension in patients with primary aldosteronism after adrenalectomy.

Patients with primary aldosteronism show relatively high rates of hypertension after adrenalectomy, but the risk factors for postoperative hypertension remain unclear. Forty-six patients with primary aldosteronism (PA) who had undergone adrenalectomy between 1976 and 1998 were enrolled in this study. Follow-up information including blood pressure (BP) and cardiovascular complications was collected by means of correspondence or telephone contact. At discharge BP was normalized in 34 patients (72%); hypertension persisted in the remaining 12 patients, but BP control was significantly improved. The patients who remained hypertensive at discharge had longer durations of hypertension than did those with normalized BP. After an average follow-up period of 12.2 years, 16 of 34 BP-normalized patients (47%) had recurrent hypertension. Age at adrenalectomy, preoperative serum creatinine level and systolic blood pressure at discharge were significantly higher in patients with recurrent hypertension than in those without it. A multivariate logistic regression analysis revealed that only the level of serum creatinine was independently associated with the incidence of recurrent hypertension. Patients with serum creatinine of 0.9 mg/dl or greater had significantly higher rates of recurrent hypertension than those with lower values of serum creatinine. Cardiovascular complications occurred in 5 patients prior to the surgery and in 2 patients during the follow-up period. Although the severity of renal involvement is subclinical, renal damage may play an important role in the development of hypertension during a long period after adrenalectomy in patients with PA.

Adrenalectomy↗
PubMed2002

Decreased 4-aminopyridine sensitive K+ currents in endothelial cells from hypertensive rats.

Endothelial cell function is altered in hypertension. The present study was performed to evaluate the alterations in K+ channels in endothelial cells from hypertensive rats. Currents and membrane potentials were recorded in endothelial cells freshly dissociated from the aorta of stroke-prone spontaneously hypertensive rats (SHR-SP) and Wistar-Kyoto rats (WKY). Ca2+-dependent K+ channel blockers, charybdotoxin and apamin, a voltage-dependent K+ channel blocker, 4-aminopyridine, and a non-selective K+ channel blocker, tetrabutylammonium, were used to characterize K+ currents. Depolarizing command steps evoked delayed K+ outward currents in cells from both strains. The current density of 4-aminopyridine sensitive K+ currents was significantly smaller in SHR-SP than in WKY (1.5 +/- 0.4 vs. 4.9 +/- 0.6 pA/pF, at 36 mV, n = 13, p < 0.01), whereas that of other K+ current components did not differ between strains. The resting membrane potential of cells was significantly less negative in SHR-SP than in WKY (-25.0 +/- 1.7, n = 54 vs. -33.5 +/- 1.4 mV, n = 50, p < 0.01). Depolarization by 4-aminopyridine, but not that by charybdotoxin+apamin, abolished the difference in membrane potentials between SHR-SP and WKY (n=7-10 in each strain). Immunostaining of endothelial cells by anti-Kv1.5 antibody was decreased in SHR-SP compared to WKY. In summary, the 4-aminopyridine sensitive K+ currents in aortic endothelial cells were decreased in SHR-SP, which could contribute to the membrane depolarization. Decreased expression of Kv1.5 in SHR-SP might be associated with this alteration.

4-Aminopyridine↗
PubMed2002

[Angiotensin II receptor antagonist improves age-related impairment of EDHF-mediated hyperpolarization].

Endothelium-dependent hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor(EDHF) diminish with aging as well as by hypertension. Antihypertensive treatment improved the endothelial dysfunction associated with hypertension. We here tested whether the angiotensin II receptor antagonist candesartan or the converting enzyme inhibitor enalapril would improve the age-related impairment of the EDHF-mediated responses in normotensive rats. EDHF-mediated hyperpolarization and relaxation to acetylcholine in mesenteric arteries were improved similarly in both candesartan- and enalapril-treated aged rats, but not in rats treated with the traditional combination of hydralazine and hydrochlorothiazide. These findings suggest that the inhibitors of renin-angiotensin system might serve as novel tools to prevent the endothelial dysfunction associated with aging.

Aging↗
PubMedDate not supplied

Effects of fluvastatin on endothelium-derived hyperpolarizing factor- and nitric oxide-mediated relaxations in arteries of hypertensive rats.

Endothelial cells release endothelium-derived hyperpolarizing factor (EDHF), as well as nitric oxide (NO). It has recently been suggested that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) improve NO-mediated endothelial function, partially independently of their cholesterol-lowering effects. It is, however, unclear whether statins improve EDHF-mediated responses. Eight-month-old stroke-prone spontaneously hypertensive rats (SHRSP) were treated with fluvastatin (10 mg/kg per day) for 1 month. Age-matched, normotensive Wistar Kyoto (WKY) rats served as controls. Both EDHF- and NO-mediated relaxations were impaired in SHRSP compared with WKY rats. Fluvastatin treatment did not affect blood pressure and serum total cholesterol. The acetylcholine (ACh)-induced, EDHF-mediated hyperpolarization in mesenteric arteries did not significantly differ between fluvastatin-treated SHRSP and untreated SHRSP and the responses in both groups were significantly smaller compared with those of WKY rats. Endothelium-derived hyperpolarizing factor-mediated relaxations, as assessed by the relaxation to ACh in mesenteric arteries contracted with noradrenaline in the presence of N(G)-nitro-l-arginine and indomethacin, were virtually absent and similar in both SHRSP groups. In contrast, NO-mediated relaxation, as assessed by the relaxation in response to ACh in rings contracted with 77 mmol/L KCl, was improved in fluvastatin-treated SHRSP compared with untreated SHRSP (maximum relaxation in control and fluvastatin groups 42.0 +/- 5.2 and 61.2 +/- 3.8%, respectively; P < 0.05). Hyperpolarization and relaxation in response to levcromakalim, an ATP-sensitive K(+) channel opener, were similar between the two SHRSP groups. These findings suggest that fluvastatin improves NO-mediated relaxation, but not EDHF-mediated hyperpolarization and relaxation, in SHRSP. Thus, the beneficial effects of the statin on endothelial function may be mainly ascribed to an improvement in the NO pathway, but not EDHF.

Acetylcholine↗
PubMedDate not supplied

Prolongation of the QT interval in primary aldosteronism.

1. Only limited information is available concerning the changes in the electrocardiogram in primary aldosteronism. The aim of the present study was to determine factors influencing the QTc interval in patients with primary aldosteronism. 2. Nineteen patients with primary aldosteronism caused by a Conn's adenoma and 69 patients with essential hypertension, in whom all possible causes of secondary hypertension had been excluded, were included in the present study. Before and 10-20 days after adrenalectomy, blood and electrocardiographic examinations were conducted. 3. Systolic and diastolic blood pressures in primary aldosteronism were found to be comparable to those in essential hypertension. However, the QTc interval was significantly prolonged and serum potassium concentrations were significantly decreased in patients with primary aldosteronism compared with patients with essential hypertension (492.7+/-20.3 vs 428.5+/-3.1 msec for QTc interval, respectively (P<0.01); 3.07+/-0.12 vs 4.07+/-0.05 mEq/L for serum potassium concentrations, respectively (P<0.01)). The QTc interval was significantly correlated with serum potassium concentrations in primary aldosteronism (P=0.0011; r=-0.6902), but not in patients with essential hypertension. 4. Blood pressure significantly decreased after adrenalectomy. Furthermore, serum potassium concentrations increased significantly and did not correlate with the QTc interval after adrenalectomy (P=0.54; r=-0.1500). 5. Our results indicate that the QTc interval is prolonged in patients with primary aldosteronism, probably owing to hypokalaemia.

Adrenalectomy↗