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Biomedical subjects

Y Ouchi

Publications and source records attributed to Y Ouchi.

At least 307 records · Page 17Linked to original sources
PubMed1990

The role of calcium antagonists in the treatment of atherosclerosis and hypertension.

Results of animal studies suggest that calcium antagonists can inhibit the development of experimentally induced atherosclerosis. Although the biological process underlying this phenomenon has not been fully elucidated, several mechanisms have been proposed. Notably, calcium antagonists may suppress free radical-induced damage of the vascular endothelial cells with the consequent transport of low-density lipoproteins across the vascular endothelium and the accumulation of the lipids in the intima. Studies have shown that calcium antagonists can inhibit the stimulatory effects of epidermal growth factor on intracellular calcium concentrations and DNA synthesis in cultured rat aortic smooth muscle cells, but not those of platelet-derived growth factor or somatomedin C. Further experimental studies have demonstrated that calcium antagonists stimulate prostacyclin production and inhibit 12-hydroxyeicosatetraenoic acid-induced vascular smooth muscle cell migration, therefore preventing platelet aggregation and intimal thickening, respectively. Despite the encouraging results in animals, comparatively few clinical studies have been undertaken to establish the efficacy of calcium antagonists in the prevention of cardiovascular disease in hypertensive patients. This, in part, is due to the technical difficulties associated with measuring coronary artery stenosis, but the recent development of a technique for the video-densitometric analysis of coronary angiograms has enabled stenotic regions to be quantified. Using this approach, a retrospective study has been undertaken of the efficacy of long-term treatment with a calcium antagonist on the progression of coronary atherosclerosis. Results are encouraging and a prospective long-term, multicenter trial is proposed.

Animals↗
PubMed1989

Role of brain acetylcholine in vasopressin release during osmotic stimulation and hemorrhage.

There is considerable evidence to suggest that there is a cholinergic link in the neural control of vasopressin release, but the precise role for this link has not been adequately demonstrated in the intact animal. We have, therefore, examined in conscious unrestrained rats the effects of central cholinergic blockade on the stimulation of vasopressin release by increased plasma osmotality (iv infusion of 2.5 M NaCl at 0.1 mg/kg body weight.min for 30 min) and by decreased blood volume (2 successive hemorrhages of 10% of blood volume each). The vasopressin responses to these stimuli were unaffected by either intracerebroventricular (icv) atropine (10 micrograms; muscarinic blockade) or icv hexamethonium (10 micrograms; nicotinic blockade) in doses which block the vasopressin responses to icv cholinergic agonists. The implications of these findings are discussed.

Acetylcholine↗
PubMed1989

Central effect of endothelin on blood pressure in conscious rats.

This study was conducted to investigate the effect of intracerebroventricular administration of endothelin (EDT), a novel potent vasoconstricting peptide, on blood pressure in conscious rats. The lateral cerebral ventricle of male Wistar rats was cannulated, and the femoral artery was also cannulated to measure the mean arterial blood pressure (MABP) and heart rate (HR). EDT dissolved in 10 microliters of artificial cerebrospinal fluid (ACSF) (8.25-66 pmol icv) provoked a dose-dependent increase in MABP. EDT also increased HR, although the effect of 66 pmol was variable. Intracerebroventricular ACSF did not provoke any effects on MABP and HR. Intracerebroventricular EDT also provoked contralateral rotational behavior. Pretreatment with 2 mg/kg iv phenoxybenzamine significantly suppressed the 16.5 pmol icv EDT-induced increase in MABP. Moreover, 16.5 pmol icv EDT markedly increased plasma epinephrine and norepinephrine concentration. These results indicate that EDT has a central pressor action, and the action might be mediated, at least in part, by catecholamine release to the periphery. EDT might play a role in the central control of blood pressure, although the physiological implications have not yet been determined.

Animals↗
PubMed1989

Clinical significance of cerebral aneurysm in renovascular hypertension due to fibromuscular dysplasia: two cases in siblings.

Two cases, in siblings, of renovascular hypertension caused by fibromuscular dysplasia (FMD) of the renal artery associated with cerebral aneurysms are reported. Both of the cases were found to have cerebral aneurysm, as well as multiple stenotic or occluded lesions in arteries such as renal, mesenteric, celiac, and internal carotid arteries. One case died of subarachnoid hemorrhage and the other case was successfully operated on for the aneurysm. This report suggests that FMD should be considered to be a systemic angiopathy including the cerebral artery, as well as the renal artery. Thus, cerebral angiography is recommended to detect the association with cerebral aneurysm, at least, in cases with multiple lesions of FMD. Occurrence of FMD in siblings also indicates that a genetic factor might be involved in the pathogenesis of FMD.

Adult↗
PubMed1989

Effects of growth factors on cytosolic free calcium concentration and DNA synthesis in cultured rat aortic smooth muscle cells.

Proliferation of vascular smooth muscle cells (SMCs) has been considered to be an important process in the development of atherosclerosis. This study was conducted to investigate the role of cytosolic free calcium in DNA synthesis of SMCs stimulated by growth factors. Platelet-derived growth factor (PDGF), epidermal growth factor (EGF) and somatomedin-C (Sm-C) increased [3H]thymidine incorporation, an index of DNA synthesis, and cell number of rat aortic SMCs after 36 hr of incubation. Cytosolic free calcium concentration [( Ca++]i) in quiescent SMCs, measured by using quin 2, was 178 +/- 18 nM (n = 15). Both PDGF and EGF provoked a rapid and transient rise in [Ca++]i, while Sm-C did not alter [Ca++]i. Nifedipine (3 X 10(-6) M) suppressed the rise in [Ca++]i provoked by PDGF and EGF. On the other hand, nifedipine suppressed the enhancement of DNA synthesis provoked by EGF, but did not suppress those by PDGF and Sm-C. These results suggest that the transient rise in [Ca++]i plays an important role in the proliferation of SMCs stimulated by EGF, while the rise in [Ca++]i is not involved in the mechanism of proliferation of SMCs provoked by Sm-C. The role of cytosolic free calcium in the proliferation of SMCs provoked by Sm-C. The role of cytosolic free calcium in the proliferation of SMCs provoked by PDGF was not definitive.

Animals↗
PubMed1989

[Calcium and magnesium metabolism in the aged].

Although serum calcium concentration remains constant during ageing, the plasma concentration of calcium regulating hormones has been known to show dramatic change with ageing. The plasma concentration of parathyroid hormone increases with ageing, whereas plasma concentrations of calcitonin and active vitamin D metabolite decrease with ageing. The age-related change in plasma concentrations of calcium regulating hormones might be a major cause of the age-related bone loss by stimulating bone resorption and thereby releasing calcium from bone. On the other hand, the incidence of soft tissue calcification is known to increase with ageing. In order to further study the relationship between these age-related phenomena, we studied the relationship between radial bone mineral density (BMC) and aortic pulse wave velocity (PWV) which is considered to be a clinical index for the magnitude of aortic calcification. Multi-variate analysis showed the significant relationship (p less than 0.05) between BMC and PWV, suggesting that the decrease in bone mass might be an independent risk factor for the development of aortic calcification. Low calcium intake is an important factor for the development of age-related bone loss. The recommended dietary allowance (RDA) of calcium intake for the Japanese is considered to be 600 mg/day. In order to reevaluate RDA of calcium for the elderly Japanese women, a calcium balance study was performed in 13 subjects; six with osteoporosis (age: 75 +/- 2) and seven without osteoporosis (age: 72 +/- 2). Calcium balance in the individual subject was evaluated by measuring the intake of calcium (food) and output (feces and urine) every 2 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Inhibitory effect of transforming growth factor-beta on epidermal growth factor-induced proliferation of cultured rat aortic smooth muscle cells.

This study was conducted to investigate the effect of transforming growth factor-beta (TGF-beta) on the proliferation of cultured rat aortic smooth muscle cells (SMCs). DNA synthesis, measured by the incorporation of [3H] thymidine, and the cell number of monolayered SMCs were measured after incubation with TGF-beta (1-100 ng/ml) in the presence or absence of epidermal growth factor (EGF; 100 ng/ml). TGF-beta alone did not affect DNA synthesis of SMCs. EGF significantly increased both DNA synthesis and cell number, while TGF-beta inhibited the increase in both in a dose-dependent manner without accompanying the significant cellular damage. These results indicate that TGF-beta exerts an inhibitory effect on the proliferation of cultured SMCs provoked by EGF.

Animals↗
PubMed1988

Effect of superoxide and lipid peroxide on cytosolic free calcium concentration in cultured pig aortic endothelial cells.

The effect of reactive oxygen on cytosolic free calcium concentration [( Ca++]i) in pig aortic endothelial cells (ECs) was studied. Linoleate hydroperoxide (LHO) and superoxide radicals generated from xanthine with xanthine oxidase (X-XO) were used as sources of reactive oxygen. [Ca++]i in ECs was measured with quin 2 and the value for quiescent ECs was 112 +/- 11 nM. Both LHO and X-XO increased [Ca++]i in a dose-dependent manner without accompanying the significant cellular damage. Nifedipine suppressed the increase in [Ca++]i provoked by LHO and X-XO. Thus, the biological effects of reactive oxygen might be mediated, at least in part, by the activation of voltage-dependent calcium channels in ECs.

Animals↗
PubMed1988

Alpha-blocker, bunazosinhydrochloride decreases cytosolic Ca++ of cultured rat aortic smooth muscle cells.

Effect of alpha-blocker, bunazosinhydrochloride on cytosolic Ca++ concentration of rat aortic smooth muscle cells (SMC) was studied. Marked and sustained decrease in cytosolic Ca++ concentration of SMC was observed following the addition of 10(-7) M bunazosinhydrochloride. Furthermore, 10(-7) M bunazosinhydrochloride completely blocked the phenylephrine induced increase in cytosolic Ca++ of rat aortic SMC. It is of interest that a decrease in cytosolic Ca++ of vascular SMC was caused by alpha-blocker.

Adrenergic alpha-Antagonists↗
PubMed1988

Vasopressin: sexual dimorphism in secretion, cardiovascular actions and hypertension.

We have investigated the issue of sexual dimorphism in the secretion of vasopressin, its pressor action, and the development of deoxycorticosterone (DOC)-salt hypertension. In normal human subjects on controlled salt intake, the basal secretion of vasopressin, indicated by plasma vasopressin levels and urinary excretion of vasopressin, was higher in men than in women and in blacks than in whites. Basal vasopressin secretion also was higher in male than in female rats. This effect was not associated with a difference in the metabolic clearance of the hormone. The sex-related difference in vasopressin release in rats was abolished by gonadectomy and restored by treatment of males with testosterone and females with ovarian hormones. The pressor responsiveness to vasopressin was higher in male than in randomly cycling female rats. Finally, DOC-salt hypertension, which is dependent on vasopressin, developed more rapidly in male than in female rats. Although there was no sex-related difference in the extent to which plasma vasopressin levels were elevated, pressor responsiveness to vasopressin was greater and baroreflex sensitivity was attenuated to a lesser extent in hypertensive males than in hypertensive females. Thus, it seems likely that gonadal hormones play a significant role in cardiovascular regulation.

Animals↗
PubMed1988

Pressor response to vasopressin and norepinephrine in DOC-salt hypertensive and prehypertensive rats.

Pressor responses to arginine-vasopressin (AVP) and norepinephrine (NE) were studied in deoxycorticosterone (DOC)-salt hypertensive and prehypertensive rats. DOC-salt rats received weekly subcutaneous injection of DOC acetate (30 mg/kg) and given 1% saline for drinking. Salt and control rats received injections of sesame oil and given 1% saline or tap water, respectively. On the 5th day (prehypertensive stage) and at 6th week (hypertensive stage) after treatment had started, pressor responses were studied by measuring changes in mean arterial pressure recorded from the iliac artery in response to i.v. injections of AVP or NE under urethane anesthesia. Pressor response to AVP was enhanced both in DOC-salt hypertensive and prehypertensive rats compared with that in salt and control rats. Pressor response to NE tended to be enhanced in DOC-salt hypertensive rats, however, the enhancement was not observed in the rats in prehypertensive stage. Enhanced pressor response to AVP in DOC-salt prehypertensive rats was not due to the structural change of vascular beds, because peripheral resistance in isolated hindlimb preparations was similar in the three groups. Thus, pressor response to AVP was enhanced even in the prehypertensive stage in DOC-salt rats and the enhancement might be involved in the pathogenesis of hypertension in DOC-salt rats.

Animals↗
PubMed1988

Sex difference in pressor responsiveness to vasopressin and baroreflex function in DOC-salt hypertensive rats.

This study was undertaken to investigate further the possible role of vasopressin in the sexual dimorphism of deoxycorticosterone (DOC)-salt hypertension. The study was carried out 3 weeks after initiating treatment with DOC and salt in uninephrectomized male and female rats. Mean arterial pressure (MAP) was lower in female than in male DOC-salt hypertensive rats (177 +/- 7 versus 198 +/- 4 mmHg; P less than 0.01). Mean arterial pressure did not differ between male and female normotensive control rats. Increases in MAP in response to graded i.v. infusions of vasopressin were markedly attenuated in female normotensive and hypertensive rats, but there was no sex difference in pressor responses to i.v. phenylephrine. Baroreflex sensitivity was reduced in both male and female DOC-salt rats, but to a greater extent in males (P less than 0.01). Diminished pressor responsiveness to vasopressin and a smaller impairment of baroreflex sensitivity may contribute to the reduced development of DOC-salt hypertension in female rats.

Animals↗
PubMed1987

Sex difference in the development of deoxycorticosterone-salt hypertension in the rat.

To investigate a possible sex difference in the development of deoxycorticosterone (DOC)-salt hypertension in rats, systolic blood pressure was measured over 6 weeks in unilaterally nephrectomized male and female rats with or without DOC-salt treatment. Throughout the treatment, systolic blood pressure was significantly lower in female than in male DOC-salt rats (at the end of the sixth week: 190 +/- 8 vs 163 +/- 7 mm Hg, p less than 0.05). The difference in blood pressure was also confirmed by the direct measurement of mean arterial pressure at the end of the experiment. The 24-hour urinary excretion of vasopressin was significantly higher in male control rats than in female control rats; however, no difference was observed between male and female DOC-salt rats, in which the urinary excretion of vasopressin was four to five times higher than in control rats. The plasma vasopressin concentration was higher in DOC-salt rats, but there were no differences between sexes. There were no differences in the metabolic clearance rate of vasopressin among the four groups of rats. This indicates that the elevated plasma vasopressin concentration in DOC-salt hypertensive rats is due to increased release of the hormone, rather than to impaired metabolism. Thus, although vasopressin plays a pivotal role in the pathogenesis of DOC-salt hypertension, the sexual dimorphism in this form of hypertension cannot be attributed to differences in the secretion, metabolism, or plasma concentration of vasopressin.

Animals↗
PubMed1986

Central cholinergic control of vasopressin release in conscious rats.

Intracerebroventricular (icv) administration of carbachol into conscious rats evoked a substantial increase in vasopressin secretion and blood pressure in a dose-dependent manner. These effects were blocked by pretreatment with the muscarinic blocker, atropine (10 micrograms icv), but not by the nicotinic blocker, hexamethonium (10 micrograms icv). Hexamethonium did, however, block the increase in blood pressure, the decrease in heart rate, and the very small elevation in the plasma vasopressin concentration induced by nicotine (10 micrograms icv). These results indicate that stimulation of either central nicotinic or muscarinic receptors can affect the cardiovascular system and suggest that the cholinergic stimulation of vasopressin secretion may involve primarily muscarinic receptors in the conscious rat.

Animals↗
PubMed1986

Central atrial natriuretic factor reduces vasopressin secretion in the rat.

Atrial natriuretic factor (ANF, Arg 101-Tyr 126; 0.5 and 2.5 micrograms) administered into the lateral cerebral ventricle of conscious euhydrated and dehydrated rats resulted in a significant reduction in the plasma vasopressin concentration. The effect of ANF on vasopressin secretion was greater in the water-deprived animal. Central ANF was without effect on mean arterial blood pressure in both euhydrated and dehydrated rats. The data suggest that ANF occurring in the central nervous system may be important in the control of vasopressin secretion.

Animals↗
PubMed1986

A case of Takayasu's disease with ruptured carotid aneurysm.

Recently, a number of cases of Takayasu's disease having dilatative or aneurysmal lesions have been reported. Such lesions have come to be considered important manifestations of Takayasu's disease. A case, whose right common carotid artery perforated spontaneously and became a pseudoaneurysm, without any other stenotic lesion is presented with a review of the literature. Surgical treatment was performed successfully.

Adult↗