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Biomedical subjects

G Yasuda

Publications and source records attributed to G Yasuda.

At least 19 recordsLinked to original sources
PubMed1998

Cough-challenge trial with a new angiotensin-converting enzyme inhibitor, imidapril.

This study was conducted to examine whether imidaprilat, an active diacid of the angiotensin-converting enzyme (ACE) inhibitor imidapril, preferentially inhibits angiotensin I degradation rather than bradykinin degradation, and whether imidapril is less active than other ACE inhibitors in inducing cough in patients with hypertension. The effect of imidaprilat on the inhibition of pressor response to angiotensin I and augmentation of depressor response to bradykinin was compared with that of enalaprilat and captopril in anesthetized rats. To determine the incidence of cough associated with imidapril, patients with a history of ACE inhibitor-induced dry cough were enrolled in a randomized, open-labeled, crossover trial with two 6-week periods to be treated with imidapril or amlodipine, a calcium-channel blocker. The recurrence of cough was assessed during both treatments. In the animal study, there were no significant differences in the ratio of inhibition of pressor response to angiotensin I and the augmentation of depressor response to bradykinin among the ACE inhibitors. In the cough-challenge trial, a total of 60 patients with hypertension were enrolled in the study. Cough and cough related symptoms recurred in 98.3% of the patients (59/ 60) during imidapril therapy. In contrast, only two patients reported cough during treatment with amlodipine. These results indicate that imidapril has no selectivity in inhibiting angiotensin I- and bradykinin-degradation in rats, and that clinically it is not different from other ACE inhibitors in inducing cough in patients with hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Regulation of cAMP production in initial and terminal inner medullary collecting ducts.

BACKGROUND: The inner medullary collecting duct (IMCD) is composed of at least two functionally and morphologically distinct segments, the initial (IMCDi) and the terminal (IMCDt) portions. However, most studies of receptor signaling have been performed on cells obtained from the entire inner medulla. The purpose of this study was to determine whether the patterns of receptor-activated cAMP accumulation were different between these segments. METHODS: We measured cAMP accumulation stimulated by vasopressin and isoproterenol, and the effect of epinephrine in freshly dissected IMCDi and IMCDt segments cultured and IMCDi and IMCDt cells in primary culture. RESULTS: The maximum response to vasopressin was twofold higher in fresh IMCDt verus IMCDi (P < 0.05), however, it increased in cultured IMCDi by 40% verus fresh cells with no change in the response in fresh verus cultured IMCDt. The maximum response to isoproterenol was small in fresh cells but increased by five- and sixfold, respectively, in cultured IMCDi and IMCDt cells. alpha 2-Adrenoceptor stimulation almost completely inhibited both vasopressin and isoproterenol-stimulated cAMP accumulations in fresh IMCDi and IMCDt cells, but only partially inhibited either accumulation by 34 to 49% in cultured cells. CONCLUSIONS: (1) IMCDi and IMCDt cells are both subject to vasopressin and alpha 2- and beta-adrenergic regulation of adenylyl cyclase activity; (2) the relative influence of beta-adrenergic, alpha 2-adrenergic and V2 receptors to affect cAMP accumulation is altered in primary culture versus freshly dissected IMCD segments, suggesting that caution must be exercised in the extrapolation of data from cultured IMCD cells to in vivo models.

Adrenergic alpha-Agonists↗
PubMed1998

Intravascular ultrasound imaging of atherosclerotic renal arteries: comparison between in vitro and in vivo studies.

BACKGROUND: Intravascular ultrasound (IVUS) imaging, a new modality, may be feasible and useful for the assessment of atherosclerotic renal arteries. However, comparison between in vivo and in vitro studies to confirm pathological changes corresponding with IVUS findings obtained from renal arteries was not fully evaluated. METHODS: We evaluated ultrasound images of 18 post-mortem human renal arteries and cross-sectional IVUS images of main renal arteries in five patients with renal artery stenosis (RAS) or essential hypertension. RESULTS: In vitro studies have shown that renal-artery images had three layers when the arteries had fibrous intimal thickening and medial hypertrophy. Renal arteries, in which the fibrous intima was not well developed, showed circumferentially homogeneous bright echoes. In patients with atherosclerotic RAS and essential hypertension, IVUS images showed hyperechoic areas in the renal arterial walls, probably due to atherosclerosis. Typical three-layered ultrasound appearance was not easily seen during in vivo studies. CONCLUSION: Our findings suggest that hyperechoic images can be a diagnostic clue of atherosclerosis However, in vitro results do not always correspond exactly to in vivo findings, and caution is needed when findings from in vitro IVUS imaging studies are applied to in vivo studies.

Adolescent↗
PubMed1998

Effective dose in diagnostic radiology as a function of x-ray beam filtration for a constant exit dose and constant film density.

Individual organ absorbed dose and total effective dose for nine common radiographic projections were investigated as a function of half-value-layer, HVL, and total equivalent filtration for the following cases: (1) with the patient exit dose held constant and (2) with the film density held constant. As expected, the absorbed dose to organs proximal to the x-ray beam entry point tracked with skin dose as a function of HVL, whereas organ dose distal to the x-ray beam entry point was almost independent of HVL. Dose to organs near mid-line showed an intermediate HVL dependence. For the nine radiographic projections, increasing the total filtration from 1.5 to 4.0 mm Al while holding the kVp fixed resulted in mean decreases in the effective dose of 17% for the case of a constant exit dose, and 25% for a constant film density with a "400 speed" rare-earth screen-film system. The decreases in the mean skin entrance doses were 38% and 45%, respectively. With the screen-film system, the average effective dose decreased at 16% per mm of added Al between 1.5 and 2.5 mm Al total filtration, and at 7% per mm between 2.5 and 4.0 mm. These results partially support the NCRP Report No. 102 recommendation that the minimum filtration be 2.5 mm Al for general diagnostic x-ray tubes. They also suggest, using the linear no-threshold radiation risk model, that further significant reductions in stochastic risk to the U.S. population can be achieved by raising the minimum beyond 2.5 mm. Experience over a 12 year period in our tertiary care teaching hospital indicates that adding 1-1.5 mm Al filtration beyond the 2.5 mm minimum does not pose a problem in terms of additional tube loading or reduction in image quality. However, these issues need to be more formally addressed.

Abdomen↗
PubMed1998

Long-term therapy with an ACE inhibitor, temocapril, reduces microalbuminuria in essential hypertension.

The present study was conducted to prospectively evaluate whether a new ACE inhibitor, temocapril, could modify urinary microalbumin excretion rate (UAE) in a group of hypertensive outpatients who had no evidence of renal impairment. Sixty-three outpatients (32 men and 31 women; mean age, 59.9 +/- 1.5 yr) with essential hypertension entered the study, all having been treated for at least 6 mo with dihydropyridine calcium-channel blockers (CCBs: nitrendipine, nisoldipine, or amlodipine). Their blood pressures (BPs) had been controlled to adequate levels with the CCBs. None had overt proteinuria (determined by Albustix) or abnormal serum creatinine levels. After 3 mo of baseline observation under the previous treatment, the subjects were randomly divided into two groups. In group A (n = 31), the previously used CCBs were switched to temocapril, 2 to 4 mg once daily for 12 mo, and BP was controlled at a level equivalent to that during CCB treatment. In group B (n = 32), the subjects were maintained on their previous treatment for a further 12 mo. The effect of temocapril on BP appeared to be clinically similar to that of the previously used CCBs, but it significantly decreased UAE as compared with the previous therapy. In group A, UAE decreased significantly (p < 0.01) from the baseline value of 38.9 +/- 5.1 mg/g creatinine (Cr) to 22.2 +/- 4.2 and 25.3 +/- 5.6 mg/g Cr at the 6th and 12th months of temocapril therapy, respectively. In contrast, in group B UAE was unchanged (baseline 39.8 +/- 6.6 mg/g Cr; 6 mo, 44.6 +/- 6.8; 12 mo, 45.9 +/- 7.7). In group A, 17 of 31 patients (54.8%) had abnormal UAE levels (> or = 29.5 mg/g Cr) during previous therapy with CCBs, but 6 mo after switching to temocapril 25 of these patients (80.6%) had normal UAE (< 29.5 mg/g Cr). In group B, 15 of 32 patients (46.9%) had abnormal UAE levels during the observation period, and these abnormal UAE levels remained unchanged; 17 of the 32 patients (53.1%) had abnormal UAE levels after a further 6 mo of continued CCBs therapy. We conclude that long-term therapy with temocapril may provide renal protection by reducing UAE even in hypertensive patients with no evidence of renal impairment.

Albuminuria↗
PubMed1997

Characterization of bunazosin-sensitive alpha1-adrenoceptors in human renal medulla.

We studied the characteristics of bunazosin-sensitive alpha1-adrenoceptors in human renal medullae by using renal-clearance studies and radioligand-binding assay. In 12 patients with hypertension, renal-clearance studies demonstrated that bunazosin significantly increased renal blood flow from 683 +/- 82 (SD) to 829 +/- 103 ml/min (p < 0.05) and decreased renal vascular resistance from 0.18 +/- 0.02 to 0.14 +/- 0.02 mm Hg/(ml/min) (p < 0.05), but that prazosin had little effect on renal function. In a radioligand-binding assay, specific, saturable, and stereoselective [3H]bunazosin binding, with a single class of binding sites (Kd = 2.7 +/- 1.4 nM; Bmax = 44 +/- 16 fmol/mg protein; n = 11) was detected in membrane preparations of human renal medullae. The rank order of potency of antagonists that inhibited [3H]bunazosin-binding was bunazosin (Ki in nM = 49) > prazosin (57) > yohimbine (3,900) > propranolol (29,000), and that of agonists, l-norepinephrine (7,400) > l-epinephrine (19,000) > d-norepinephrine (71,000). The competition curves fit a one-site model. These findings suggest that bunazosin-sensitive alpha1-adrenoceptors exist in human renal medullae and participate in the regulation of renal hemodynamics.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1997

Effect of epinephrine on cAMP accumulation in cultured rat inner medullary collecting duct cells.

In a previous study we have reported the existence of alpha2- and beta-adrenoceptors in cultured rat inner medullary collecting duct (IMCD) cells. In this report, we examined the effect of epinephrine on intracellular adenosine 3',5'-cyclic monophosphate (cAMP) accumulation and evaluated whether alpha2-adrenoceptors interact with beta-receptors, vasopressin receptors, and prostaglandin (PG) E2 receptors by measuring cAMP generation. Epinephrine stimulated cAMP accumulation in a dose-dependent manner [half-maximal effective concentration (EC50) = 300 nM]. Rauwolscine (10 microM) enhanced epinephrine effects, shifting the dose-response curve for epinephrine to the left (EC50 = 120 nM); however, beta-antagonists inhibited epinephrine-induced cAMP accumulation. Epinephrine (10 microM) inhibited cAMP accumulation maximally induced by isoproterenol (10 microM); this effect was reversed by rauwolscine (10 microM). Epinephrine inhibited vasopressin (100 nM)-induced cAMP accumulation but failed to inhibit PGE2 (10 microM)-induced cAMP accumulation. We conclude that epinephrine acts as an alpha2- and beta-adrenoceptor agonist and that alpha2-adrenoceptors interact with beta-adrenoceptors and vasopressin receptors but not with PGE2 receptors on cAMP accumulation. This suggests that alpha2-adrenoceptors play a physiological role via interaction with different hormone receptors.

Adrenergic Agonists↗
PubMed1997

[Catecholamine and dopamine].

Almost all the genes of the enzymes which synthesize and metabolize the catecholamines (dopamine, norepinephrine, epinephrine) have been cloned and the gene targeting technology have been applied to introduce the gene knockout mouse such as thyrosine hydroxylase and dopamine beta hydroxylase. At least nine adrenergic receptors and five dopamine receptors have been cloned, which include alpha 1A-, alpha 1 B-, alpha 1 D-, alpha 2 A-, alpha 2B-, alpha 2C-, beta 1-, beta 2-, beta 3-adrenergic receptors and D1-, D2-, D3-, D4-, D5-dopamine receptors. Transgenic mouse as well as gene knockout mouse of these genes have been also produced. Furthermore, intracellular signal transduction systems of the catecholamines have been clarified using molecular techniques, including nine subtypes of adenylyl cyclase. Using these cloned genes and transgenic and gene knockout mouse, more detailed features of the catecholamine systems and those receptors and intracellular signal transduction systems will be clarified in near future.

Adenylyl Cyclases↗
PubMed1996

The beta 1- and beta 2-adrenoceptor subtypes in cultured rat inner medullary collecting duct cells.

We investigated beta-adrenoceptor subtype(s) expressed in cultured rat inner medullary collecting duct (IMCD) cells. In radioligand binding assay, [125I]iodocyanopindolol bound to IMCD cell membranes, representing a single class of binding sites (dissociation constant = 96.1 pM, maximum binding capacity = 18.2 fmol/mg protein, n = 8). In competition studies, ICI-89406 (beta 1-antagonist) and ICI-118551 (beta 2-antagonist) bound with high affinity, fitting a two-site model. Isoproterenol increased intracellular adenosine 3',5'-cyclic monophosphate (cAMP) accumulation (half-maximal effective concentration = 200 nM). Propranolol completely inhibited isoproterenol-induced cAMP accumulation [half-maximal inhibitory concentration (IC50) = 270 nM]. ICI-89406 and ICI-118551 inhibited cAMP accumulation by 50% (IC50 = 1.5 microM and 1.7 microM, respectively). The combined addition of ICI-89406 and ICI-118551 resulted in a curve indistinguishable from that of propranolol. The beta 1- and beta 2-adrenoceptor mRNAs have been demonstrated using reverse transcription-polymerase chain reaction. In initial and terminal IMCD cells, propranolol (3 microM) inhibited isoproterenol-stimulated cAMP accumulation by 80%, whereas ICI-89406 (3 microM) and ICI-118551 (3 microM) resulted in only partial inhibition (50%). We conclude that both beta 1- and beta 2-adrenoceptors are expressed in initial and terminal IMCD cells in primary culture.

Adrenergic beta-Agonists↗
PubMed1995

[A new protein titrator tape for self-assessment by outpatients with proteinuria].

ł- have invented a new dipstick (protein titrator tape) for measuring the volume of protein excreted in the 24-hour urine. The principle of the method is based on the protein error of indicators with the modification of a conventional dipstick test. The dipstick consists of two thick filter papers, containing differently adjusted pH indicators of tetrabromphenol blue, making it possible to detect a wide range of protein concentrations in the urine using a standard color chart that includes twenty color blocks. Two hundred and ninety outpatients had their urine samples assessed with this method as well as with the pyrogallol red test as a comparative study for quantitative measurement of protein concentrations. The new-type dipstick method exhibited good correlation with the results of the pyrogallol red test, especially in the range of protein concentrations from 50 mg/dl to 400 mg/dl, showing the linear equation of "y (Pyrogallol red) = 10.5 + 0.99 x (Dipstick) (r = 0.91, P < 0.01)". Although there was good correlation with the pyrogallol red test at higher concentrations from 400 mg/dl to 1,000 mg/dl, the dipstick method tended to exhibit lower concentrations than those indicated by the counterpart method. The rate of consistency between observers was quite high. This new-type dipstick method will offer a reliable method for patients or their family to assess their protein excretion in the urine every 24 hours at home using a portable urine sampling device.

Adult↗
PubMed1994

Ammonium urate nephrolithiasis in a variant of Bartter's syndrome with intact renal tubular function.

In two patients with Bartter's syndrome proximal tubular function and distal chloride reabsorption were intact on admission; however, chloride reabsorption and distal tubular acidifying capacity decreased in one patient over a period of 10 years. Renal prostaglandin E excretion and urinary and plasma uric acid were in the normal range, but urinary ammonium was significantly elevated during controlled diet. One patient developed ammonium urate nephrolithiasis. In both patients renal biopsy demonstrated lymphocytic infiltration of the interstitial tissue and hypercellularity of the macula densa. Indomethacin treatment improved serum potassium concentration and decreased plasma renin activity, plasma aldosterone concentration, and urinary prostaglandin E but had to be discontinued because of side effects. It is likely that our patients represent a variant form of the syndrome originally described by Bartter.

Adult↗
PubMed1994

Association analysis of restriction fragment length polymorphism for alpha 2-adrenergic receptor genes in essential hypertension in Japan.

Recently, restriction fragment length polymorphism (RFLP) of alpha 2-adrenergic receptor gene (alpha 2-C10) digested with Bsu36I restriction enzyme has been reported in US populations. Therefore, we examined the association of this RFLP with essential hypertension by comparing the frequency of specific alleles for this gene in Japanese populations. The distribution of this RFLP was compared with that in US populations. Subjects were hypertensive patients with a family history of essential hypertension (n = 56) and normotensive subjects whose parents had no history of essential hypertension (n = 46). DNA was prepared from leukocytes. RFLP was determined by use of Southern blot analysis with an alpha 2-C10 probe and Bsu36I. The frequencies of the major (12-kb) and minor (5.8-kb) alleles were 0.30 and 0.70 in hypertensive patients and 0.38 and 0.62 in normotensive subjects, respectively. The difference between observed alleles in all subjects in each group was not significant (chi 2 = 1.33, P > .1). The difference between the overall allelic frequency in Japan and that reported in US populations was significant. This study found no evidence for an association between alpha 2-adrenergic receptor gene/Bsu36I RFLP and essential hypertension in Japan. However, the findings showed that the allele frequency in Japan differed from that reported in US populations.

Adult↗
PubMed1994

Exaggerated blood pressure response to angiotensin II in patients with Cushing's syndrome due to adrenocortical adenoma.

We studied the roles played by the renin-angiotensin system in inducing hypertension in nine patients with Cushing's syndrome (CS) resulting from adrenocortical adenoma, and compared them with those in patients with primary aldosteronism (PA), renovascular hypertension (RVH) and essential hypertension (EH). In the CS group, each parameter, including serum potassium, plasma renin activity, plasma aldosterone, deoxycorticosterone and corticosterone concentrations, is within the normal range. However, plasma renin activity in the CS group was lower than that in the RVH group but higher than that in the PA group, and plasma aldosterone concentration was lower than that in each RVH or PA group. These findings indicated that the CS group had a different type of hypertension from that in either RVH or PA, in which the renin angiotensin system or mineralocorticoids play an important role in hypertension. Meanwhile, captopril (50 mg) administration either with or without indomethacin pretreatment decreased the mean blood pressure in the CS group, although captopril failed to change it in the PA group or in normal subjects. Furthermore, the pressor response to exogenous angiotensin II in the CS group was higher than that in the RVH or EH group, but was not different from that in the PA group. Thus, the hypertension in patients with CS due to adrenocortical adenoma appears to be mediated through a change in the renin-angiotensin system in the form of exaggerated pressor responses to angiotensin II.

Adenoma↗
PubMed1994

The impaired control of plasma renin activity in hypertensive patients with end-stage renal disease due to chronic glomerulonephritis.

In twelve hypertensive patients with end-stage renal disease (ESRD) due to chronic glomerulonephritis (CGN), the mechanisms of renin and aldosterone regulation were studied by exogenously infused angiotensin II, captopril, and upright posture. The results were compared to those obtained in ten patients with unilateral renovascular hypertension (RVH), eleven patients with essential hypertension (EH), and in eleven normal subjects (NS). Exogenously infused angiotensin II (5.0 ng/kg/min) failed to decrease the plasma renin activity (PRA) in the ESRD group but significantly decreased the PRA in the RVH, EH, and NS groups. The plasma aldosterone concentration (PAC) in the ESRD group and in the other control groups significantly increased after the addition of exogenous angiotensin II. An oral dose of 50 mg of captopril failed to increase the PRA in the ESRD group. However, it significantly raised the PRA in the RVH, EH, and NS groups. The plasma aldosterone concentration was significantly reduced by captopril in the ESRD group, and similar results were obtained in the other three groups. The ratio between the PRA before and after being in an upright posture for 4 hours in the ESRD group was lower than that in the three other groups. Meanwhile, there was no difference in the PAC ratio between the ESRD group and the control groups. Thus, we conclude that, in hypertensive patients with ESRD due to CGN, PRA regulation is different from that in the other three groups, although there were no differences in the regulation of the PAC among the four groups, suggesting that renin production in the ESRD group is somewhat autonomous.

Adult↗
PubMed1993

The genetic analysis of achiasmate segregation in Drosophila melanogaster. III. The wild-type product of the Axs gene is required for the meiotic segregation of achiasmate homologs.

The regular segregation of achiasmate chromosomes in Drosophila melanogaster females is ensured by two distinct segregational systems. The segregation of achiasmate homologs is assured by the maintenance of heterochromatic pairing; while the segregation of heterologous chromosomes is ensured by a separate mechanism that may not require physical association. AxsD (Aberrant X segregation) is a dominant mutation that specifically impairs the segregation of achiasmate homologs; heterologous achiasmate segregations are not affected. As a result, achiasmate homologs frequently participate in heterologous segregations at meiosis I. We report the isolation of two intragenic revertants of the AxsD mutation (Axsr2 and Axsr3) that exhibit a recessive meiotic phenotype identical to that observed in AxsD/AxsD females. A third revertant (Axsr1) exhibits no meiotic phenotype as a homozygote, but a meiotic defect is observed in Axsr1/Axsr2 females. Therefore mutations at the AxsD locus define a gene necessary and specific for homologous achiasmate segregation during meiosis. We also characterize the interactions of mutations at the Axs locus with two other meiotic mutations (ald and ncd). Finally, we propose a model in which Axs+ is required for the normal separation of paired achiasmate homologs. In the absence of Axs+ function, the homologs are often unable to separate from each other and behave as a single segregational unit that is free to segregate from heterologous chromosomes.

Animals↗
PubMed1993

Cushing's disease: evaluation of mineralocorticoid-induced hypertension.

A patient (32-year-old female) with Cushing's syndrome due to pituitary adenoma and hypertension with hypokalemia is reviewed. Endocrinological studies demonstrated low plasma renin activity, low plasma aldosterone concentration and high plasma deoxycorticosterone concentration. Blood pressure response to exogenous angiotensin II was enhanced. After the withdrawal of cortisol replacement following surgery, her abnormal endocrinological findings, hypertension and serum potassium level returned to normal and her blood pressure response to exogenous angiotensin II was reduced. These results suggest that in this case deoxycorticosterone might have contributed to the development and maintenance of her hypertension accompanied with hypokalemia.

Adenoma↗
PubMed1993

[Molecular biology of alpha-adrenergic receptor and essential hypertension].

The primary physiological agents for adrenergic receptors are only two, epinephrine and norepinephrine, which have been used to differentiate alpha- and beta-adrenoceptors. The pharmacological properties can distinguish subtype alpha 1-, alpha 2-, beta 1- and beta 2-receptors. Recently additional subtypes have been characterized by radioligand binding techniques and molecular biological techniques. Molecular mechanisms of regulation as well as regulatory site of gene expression of alpha-adrenergic receptors has been extensively studied. In addition, the association analysis of alpha 2-adrenergic receptor gene RFLP in essential hypertension has been performed. Eventhough we could not find any association of an alpha 2 C10-Bsu36I RFLP with essential hypertension in Japan, the finding showed significant ethnic RFLP difference at the gene locus for alpha 2 C10. The association of alpha 2 adrenergic receptor RFLP with blood pressure has been also studied using F2 generations of SHR and WKY and Dahl salt sensitive rats and resistant rats. Further studies are now in progress to clarify the role of these alpha-adrenergic receptors in cardiovascular diseases.

Amino Acid Sequence↗