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Biomedical subjects

I Abe

Publications and source records attributed to I Abe.

At least 91 records · Page 5Linked to original sources
PubMed1998

Photoaffinity labeling of oxidosqualene cyclase and squalene cyclase by a benzophenone-containing inhibitor.

A new orally active oxidosqualene:lanosterol cyclase (OSLC) inhibitor (Ro48-8071; Morand, O. H. et al. (1997) J. Lipid Res. 38, 373-390) showed potent noncompetitive inhibition of bacterial squalene:hopene cyclase (SHC) from Alicyclobacillus acidocaldarius (IC50 = 9.0 nM, KI = 6.6 nM) and OSLC (IC50 = 40 nM, KI = 22 nM for homogeneous rat liver OSLC). A tritium-labeled isotopomer (18.8 Ci/mmol) of this nonterpenoid inhibitor, which possesses a benzophenone (BP) photophore, was chemically synthesized as a photoaffinity label. Specific, efficient covalent modification of both OSLC and SHC enzymes was observed after UV irradiation at 360 nm. Labeling of both OSLC and SHC by [3H]Ro48-8071 was competitively displaced by coincubation with a 1000-fold molar excess of 18-thia-2, 3-oxidosqualene or the nonterpenoid inhibitor BIBX79. Displacement of labeling of OSLC was also achieved with the suicide substrate (3S)-29-methylidene-2,3-oxidosqualene. Thus, the nonsubstrate Ro48-8071 and both terpenoid and nonterpenoid inhibitors of these enzymes appear to share a common binding site.

Animals↗
PubMed1998

Troglitazone, an insulin sensitizer, increases forearm blood flow in humans.

To test whether troglitazone, a thiazolidinedione insulin sensitizer, increases the peripheral blood flow, the changes in forearm blood flow (FBF) were evaluated by venous occlusion plethysmography in 11 lean healthy male volunteers (age range, 24 to 39 years) after a single oral dose of 200 mg of troglitazone. Forearm vascular resistance (FVR) was calculated from FBF and blood pressure. Two hours after the dose, FBF increased from 3.66+/-0.31 to 4.81+/-0.57 mL/100 mL/min (P < .01), and FVR decreased from 24.7+/-2.2 to 20.2+/-2.2 units (P < .01), whereas both these values did not change during the control recordings obtained without troglitazone. Blood pressure, blood glucose levels, and serum immunoreactive insulin levels did not change significantly during the observation period. Serum concentrations of nitrate ions decreased from 27.0+/-3.5 mmol/L to 23.1+/-2.7 mmol/L (P < .01) after the administration. These results suggest that troglitazone increases muscular blood flow through vasodilation induced by a mechanism other than the correction of hyperinsulinemia or the increase in nitric oxide. The present study provides the first evidence that troglitazone dilates the vasculature in humans.

Adult↗
PubMed1998

Changes in blood pressure and heart rate variability during dental surgery.

The objective of the present study was to determine the changes in blood pressure, pulse rate, and heart rate variability during dental surgery. The study included 40 patients, 19 to 74 years of age (mean age: 42.7+/-3.0 years), who underwent tooth extraction at our hospital. Holter electrocardiographic monitoring was used to determine the power spectrum of R-R variability before and during dental surgery. The low frequency (LF: 0.041 to 0.140 Hz), high frequency (HF: 0.140 to 0.500 Hz), and total spectral powers (TF; 0.000 to 4.000 Hz) were calculated, and the ratio of LF to HF and percentage of HF relative to TF (%HF: HF/TF x 100) were used as indices of sympathetic and parasympathetic activities, respectively. The baseline blood pressure and pulse rate were 121+/-3/70+/-2 mm Hg and 70+/-1 beats/min, respectively. After the administration of local anesthetic (2% lidocaine) containing 1:80,000 epinephrine, both the blood pressure and pulse rate increased. During dental surgery, blood pressure increased further to 132+/-3/73+/-2 mm Hg. The increase in blood pressure was greater in middle-aged and older patients (> or =40 years old). In young patients (<40 years old), the %HF decreased and the LF/HF increased during local anesthesia. In contrast, in middle-aged and older patients, the LF/HF decreased during local anesthesia. These results suggest 1) that middle-aged and older patients have a greater increase in blood pressure during dental surgery than younger patients, and 2) that the regulation of the autonomic nervous system during dental surgery differs between younger and older patients.

Adult↗
PubMed1998

Inhibitory action of insulin-sensitizing agents on calcium channels in smooth muscle cells from resistance arteries of guinea-pig.

1. The actions of troglitazone, pioglitazone, metformin and bezafibrate, agents that improve insulin-resistance, on voltage-dependent Ca2+ channels in arterial smooth muscle cells were examined by use of the conventional and nystatin-perforated whole-cell clamp methods. Single cells were freshly isolated from resistance mesenteric arteries of guinea-pigs. The actions of these agents on 77 mM K+-induced contraction of the isolated arteries were also examined with the use of isometric tension recording. 2. The thiazolidinedione derivatives, troglitazone and pioglitazone, inhibited whole-cell Ca2+ currents in a dose-dependent manner with dissociation constants of 3.0 microM and 44.9 microM and Hill coefficients of 0.61 and 0.68, respectively. These two agents inhibited the 77 mM K+-induced contraction with similar potencies as those inhibiting the Ca2+ currents. Metformin and bezafibrate had no apparent effects on the Ca2+ current or high K+-induced contraction. 3. The inhibitory action of troglitazone on Ca2+ currents was not affected by the command potential, the holding potential, or the stimulation frequency, suggesting that its mode of the action differs from that of known organic Ca2+ channel antagonists. 4. The inhibitory action of troglitazone on Ca2+ currents was not affected by the addition of insulin to, or the removal of glucose from, the solutions. 5. In conclusion, the thiazolidinedione derivatives directly inhibited the voltage-dependent Ca2+ channels in a different manner from that of organic Ca2+ channel antagonists. This inhibitory action on Ca2+ channels was not a common feature of insulin-sensitizing agents.

Animals↗
PubMed1998

Central nitric oxide attenuates the baroreceptor reflex in conscious rabbits.

We examined the role of central nitric oxide (NO) in the baroreceptor reflex in conscious rabbits. Intracerebroventricular infusion of 20 mumol of N omega-nitro-L-arginine methyl ester (L-NAME) to block central NO resulted in increases in arterial pressure, renal sympathetic nerve activity (RSNA), and plasma catecholamine levels, and the pressor response was suppressed by pretreatment with pentolinium (5 mg/kg i.v.). On the other hand, a subpressor dose of intracerebroventricular L-NAME (10 mumol/h) caused significant increases in baroreflex sensitivities assessed by RSNA and heart rate compared with vehicle infusion [maximum gain: -18.2 +/- 0.9 vs. -9.6 +/- 0.9%/mmHg (P < 0.001) and -14.3 +/- 2.3 vs. -5.7 +/- 0.4 beats.min-1.mmHg-1 (P < 0.05), respectively]. Conversely, an intracerebroventricular infusion of Et2N[N(O)NO]Na, an NO donor (1 mumol/h) significantly attenuated the baroreflex sensitivities. However, intracerebroventricular infusion of N omega-nitro-D-arginine methyl ester (10 mumol/h), an enantiomer of L-NAME, failed to alter the baroreflex sensitivities. These results suggest that 1) the pressor response induced by inhibition of central NO synthesis is mainly mediated by the enhanced sympathetic outflow and 2) central NO attenuates the baroreflex control of RSNA and heart rate in conscious rabbits.

Animals↗
PubMed1998

Stretch-activated channels in arterial smooth muscle of genetic hypertensive rats.

Electrical and contractile responses of small arteries to mechanical stress are reportedly enhanced in spontaneously hypertensive rats (SHR), compared with those in Wistar Kyoto rats (WKY). We have previously shown that stretch-activated cation channels exist in arterial smooth muscle membrane, of which opening causes Na+ and Ca2+ influx and membrane depolarization. We thus hypothesize that activation of stretch-activated channels is enhanced in arterial smooth muscle of SHR compared with WKY. To test this hypothesis, stretch-activated currents were recorded in single smooth muscle cells of resistance mesenteric arteries from SHR and WKY (16 to 24 weeks of age). In the whole-cell recording, membrane stretch was applied by inflating the cell with positive pressure to the recording pipette. Cell-inflation evoked Gd3+-sensitive cation currents. This current appeared with less stretch stimulation and its amplitude was larger in SHR cells compared with WKY cells. In the cell-attached recording, suction to the recording pipette evoked single stretch-activated channel currents (conductance of 32 pS with 150 mmol/L Na+), which were blocked by Gd3+. Channels were activated with less negative pressure and their availability was greater in SHR cells than in WKY cells. Results suggest that the activation of stretch-activated channels is enhanced in smooth muscle of resistance arteries from SHR compared with WKY, which may contribute to the enhanced vascular responses to mechanical stress in SHR.

Animals↗
PubMed1998

Antihypertensive treatment and the responsiveness to glutamate in ventrolateral medulla.

We have recently reported that the cardiovascular responses to excitatory amino acids are augmented in the rostral ventrolateral medulla of spontaneously hypertensive rats (SHR). In the present study, we investigated whether the responsiveness to excitatory amino acids would be normalized by antihypertensive treatment. Thus we treated 4-week-old SHR and age-matched Wistar-Kyoto (WKY) rats with either enalapril (25 mg/kg per day in drinking water) or vehicle for 8 weeks. At 12 weeks of age, systolic blood pressure in the untreated SHR (248+/-9 mm Hg) was significantly (P<.01) higher than that in the enalapril-treated SHR (140+/-4 mm Hg), untreated WKY rats (148+/-4 mm Hg), and enalapril-treated WKY rats (117+/-1 mm Hg). The pressor responses to L-glutamate (2 nmol) microinjected into the rostral ventrolateral medulla were similar in enalapril-treated and untreated SHR (40+/-5 and 47+/-3 mm Hg, respectively, NS), and these responses were significantly greater than that seen in the untreated WKY rats (24+/-2 mm Hg, P<.01). On the other hand, the pressor response to either N-methyl-D-aspartate, an ionotropic glutamate receptor agonist, or (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid, a metabotropic glutamate receptor agonist, in the enalapril-treated SHR was slightly but significantly smaller than that in the untreated SHR but was still markedly greater than those in untreated and enalapril-treated WKY rats. These results suggest that the augmented responsiveness to excitatory amino acids in the rostral ventrolateral medulla of SHR may be at least partly genetically determined and cannot be normalized by the treatment with enalapril.

Animals↗
PubMed1998

Enhanced depressor response to nitric oxide in the rostral ventrolateral medulla of spontaneously hypertensive rats.

Possible impairment of the L-arginine-nitric oxide (NO) pathway in the rostral ventrolateral medulla of adult spontaneously hypertensive rats (SHR) was investigated by microinjecting N(G)-nitro-L-arginine methyl ester (L-NAME), NOC 18 (an NO donor), or L-arginine. Unilateral injection of L-NAME (10 nmol/50 nL) into the rostral ventrolateral medulla significantly increased mean arterial pressure (MAP) in both SHR and Wistar-Kyoto rats (WKY). The increases in MAP did not differ significantly between the two strains (15+/-3 versus 10+/-2 mm Hg, respectively; n=8). In contrast, microinjection of L-arginine elicited significant (P<.05) dose-dependent decreases in MAP in both strains, and these depressor responses were significantly greater in SHR than in WKY (in 10 nmol of L-arginine: -29+/-2 versus -15+/-2 mm Hg, respectively; n=8, P<.01). Similarly, microinjection of NOC 18 (10 nmol/50 nL) reduced MAP in both strains, and the depressor response was also significantly greater in SHR than in WKY (-38+/-7 versus -22+/-3 mm Hg, respectively; n=8, P<.05). These results suggest that the L-arginine-NO pathway in the rostral ventrolateral medulla is impaired in SHR and that this impairment may contribute to the increase in arterial pressure in this animal model of genetic hypertension.

Animals↗
PubMed1998

Single L-type calcium channels in smooth muscle cells from resistance arteries of spontaneously hypertensive rats.

The amplitude of the whole-cell L-type Ca2+ channel current recorded from vascular smooth muscle cells is reportedly greater in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto rats (WKY). However, no study has examined properties of single Ca2+ channels in arterial cells from these strains. To further test the hypothesis that activation of L-type Ca2+ channels in arterial smooth muscle cells would be enhanced in SHR, we recorded single Ca2+ channel currents in resistance mesenteric artery cells from SHR and WKY (8 to 9 weeks of age) using a cell-attached patch clamp technique. With 50 mmol/L Ba2+ in the recording pipette, the depolarizing pulse from a holding potential of -40 mV evoked the single L-type Ca2+ channel current. Opening of the single channels was more frequent in cells from SHR than from WKY. Single-channel conductance (20 pS) and open time (1 ms at 0 mV) did not differ in the two strains. The results suggest that an increased amplitude of the whole-cell current can be attributed to the enhanced opening of single Ca2+ channels in the arterial smooth muscle cells from SHR compared with WKY.

Animals↗
PubMed1998

Asymptomatic moyamoya disease associated with coronary and renal artery stenoses--a case report.

Moyamoya disease is an occlusive intracranial arteriopathy with abnormal cerebral vascular collateral networks. Although this disease is known to be associated with stenosis of extracranial arteries, such as the renal artery, a case associated with stenoses of the coronary and renal arteries has not been reported. We described here a 23-year-old man who had effort angina, renovascular hypertension, and asymptomatic moyamoya disease. Arterioangiography revealed bilateral occlusion of the intracranial carotid arteries and stenoses in the left coronary artery and the left renal artery.

Adult↗
PubMed1998

Interaction of opioids and vasopressin in central action of angiotensin II in conscious rabbits.

It has been demonstrated that opioids modulate the renin-angiotensin and sympathetic nervous system. To clarify the interaction of central angiotensin II (Ang II) and endogenous opioids, we studied the effects of naloxone, an opioid antagonist, on cardiovascular and sympathetic responses to intracerebroventricular (i.c.v.) Ang II in conscious rabbits. I.c.v. Ang II (20 ng/min) significantly increased mean arterial pressure (MAP), plasma epinephrine, and arginine vasopressin (AVP) levels, with no significant change in renal sympathetic nerve activity (RSNA) or heart rate. Pretreatment with intravenous naloxone (0.1 mg/kg) failed to alter the cardiovascular and neurohormonal responses to i.c.v. Ang II. To eliminate the effect of AVP on cardiovascular and sympathetic responses, [d(CH2)5Thy(Me)]AVP, a vasopressin V1-receptor antagonist, was given intravenously. Pretreatment with intravenous injection of the V1-receptor antagonist (30 micrograms/kg) augmented the maximum increase in RSNA caused by i.c.v. Ang II (8.9 +/- 2.2 vs. 16.2 +/- 0.7%, p < 0.05). Combined pretreatment with naloxone and V1-receptor antagonist further increased MAP and RSNA in response to ICV Ang II (20 +/- 1 vs. 16 +/- 2 mmHg, p < 0.05, and 30.9 +/- 3.7 vs. 16.2 +/- 0.7%, p < 0.01, respectively). These results suggest that opioids and AVP synergistically modulate sympathetic outflow so as to suppress the central pressor action of Ang II in conscious rabbits.

Angiotensin II↗
PubMed1998

Comparative efficacies of a calcium antagonist and an alpha1 blocker in elderly hypertensive patients with stroke.

We compared the effects of nilvadipine, a calcium antagonist, and terazosin. an alpha1 blocker, on the hemodynamics and quality of life (QOL) in 12 elderly hypertensive patients with stroke. Following a washout period of 2 weeks. nilvadipine or terazosin was administered for 2 weeks in a randomized crossover manner. At the end of control and treatment periods, we measured the 24-hour-ambulatory blood pressure (BP) and postural change of BP, and interviewed QOL. Terazosin treatment did not show consistent decrease of casual BP, but was associated with a transient decrease of systolic BP and an increase of pulse rate after standing, and enhanced postprandial decrease in BP. Nilvadipine decreased casual BP in a dose-dependent manner, but showed neither postural nor postprandial change of BP. There was no difference in QOL scores with either treatment. Results suggest that nilvadipine is preferable to terazosin for the treatment of elderly hypertensive patients with stroke.

Adrenergic alpha-Antagonists↗
PubMed1998

Mechanism-based inhibitors and other active-site targeted inhibitors of oxidosqualene cyclase and squalene cyclase.

Enzymatic cyclizations of squalene and oxidosqualene lead to sterols and other triterpenoids in bacteria, fungi, plants, and animals. The cyclases for these reactions catalyze formation and stabilization of polycyclic carbocations and direct the enzyme-specific, templated formation of new carbon-carbon bonds in regio- and stereochemically defined contexts. The development of mechanism-based irreversible inhibitors, photoactivatable inhibitors, and numerous substrate analogs have helped to unravel the stepwise events occurring in the catalytic sites of these enzymes by covalent modification of specific amino acid residues.

Animals↗
PubMed1998

[Influence of sevoflurane on renal medullary blood flow in humans].

Proper anesthetic management is necessary to preserve renal function during anesthesia and surgery. Using ultra-sound color Doppler, we examined the influence of sevoflurane on renal medullary blood flow in 20 adult patients without renal dysfunction. After identifying an interlobar artery in the outer medulla, we measured the velocity of the arterial blood flow before induction of anesthesia, and during sevoflurane anesthesia (1 MAC, 1.5 MAC). The minimum velocity of the interlobar arterial blood flow (Vmin) during wakefulness correlated significantly with creatinine clearance measured preoperatively. We did not find any significant change in Vmin after induction of sevoflurane anesthesia, despite significant decreases in mean arterial blood pressure.

Adult↗
PubMed1998

Regression of carotid wall thickening after corticosteroid therapy in Takayasu's arteritis evaluated by B-mode ultrasonography: report of 2 cases.

We describe 2 young Japanese female patients with active Takayasu's arteritis whose diagnosis was mainly based on the characteristic ultrasonographic finding, that is, a circumferential vascular wall thickening in common carotid arteries. Following corticosteroid therapy, serial ultrasonographic examination documented the improvement of their thickened carotid walls (in Case 1 from 1.4 to 0.5 mm after 2 months of therapy, in Case 2 from 1.5 to 0.9 mm after 9 months of therapy). These cases emphasize that ultrasonography is useful for evaluation of the therapeutic effect as well as for the diagnosis of Takayasu's arteritis in its early stage.

Adrenal Cortex Hormones↗
PubMed1998

Central and peripheral mechanisms involved in hypertension induced by chronic inhibition of nitric oxide synthase in rats.

OBJECTIVE: To study the possible central and peripheral mechanisms involved in hypertension induced by chronic inhibition of nitric oxide synthase. METHODS: We evaluated neurohormonal and renal responses of Wistar rats to chronic oral administration of 20 and 100 mg/kg per day NG-nitro-L-arginine methyl ester (L-NAME). Effects of intracerebroventricular and intravenous injections of NO donors (NOC-18 and FK-409) and an angiotensin II type 1 receptor antagonist CV-11974, and intravenous injection of alpha-adrenergic receptor antagonist phentolamine after chronic treatment with 100 mg/kg per day L-NAME were also studied. RESULTS: The chronic treatment with L-NAME induced a sustained dose-dependent hypertension with a decrease in heart rate. Urinary levels of norepinephrine and epinephrine decreased with no changes in plasma catecholamine levels, renin activity, and vasopressin level. Serum nitrate/nitrite levels in the rats treated with the high dose of L-NAME decreased. The intracerebroventricular and intravenous injections of the NO donors reduced arterial pressure in L-NAME-treated rats to a significantly greater extent than they did that in control rats. The intravenous but not intracerebroventricular injection of CV-11974 produced a sustained decrease in arterial pressure of L-NAME-treated rats. The depressor responses to intravenous injection of phentolamine of L-NAME-treated and control rats were similar. CONCLUSIONS: Results indicate that L-NAME-induced hypertension is associated with a deficiency of nitric oxide, both peripherally and centrally. Circulating angiotensin II could contribute to the maintenance of hypertension via angiotensin II type 1 receptor while the sympathetic nervous system seems to be suppressed.

Acute Disease↗
PubMed1997

Adsorption Mechanisms of Pentafluoropropanol (5FP) onto Activated Carbons Produced by Tetraethoxysilane Sol-Gel Method

2,2,3,3,3-Pentafluoro-1-propanol (5FP) has been considered a viable CFC replacement compound. However, 5FP must be recovered in order to decrease the environmental impact and save energy. Activated carbons have been used for the recovery and removal of organic solvents. From the point of view of "zero emission," 5FP and activated carbon must be completely recycled. The purpose of this study is to recycle the activated carbons and to increase the recovery efficiency of 5FP using the activated carbons (ST-ACs) which were coated with tetraethoxysilane by the sol-gel method. The amount of 5FP adsorbed onto the ST-ACs and the degree of 5FP decomposition by the ST-ACs were measured in order to estimate the relationship between the ST-AC surface and 5FP. The amount of 5FP adsorbed and the degree of 5FP decomposition indicated that the recovery of 5FP is suitable for the use with the ST-ACs. Copyright 1997 Academic Press. Copyright 1997Academic Press

Journal Article↗