Search PubMed⌕ Search

Biomedical subjects

H Tomonari

Publications and source records attributed to H Tomonari.

47 records · Page 3Linked to original sources
PubMed1990

Lower Na(+)-H+ antiport activity in vascular smooth muscle cells of Wistar-Kyoto rats than spontaneously hypertensive and Wistar rats.

To determine whether increased Na(+)-H+ antiport activity in vascular smooth muscle cells may relate to the pathogenesis of hypertension in the spontaneously hypertensive rat (SHR), we monitored Na(+)-dependent alkalinization of acidified cells from the hypertensive strain and two normotensive controls, the Wistar-Kyoto rat (WKY) and the Wistar rat. Changes in intracellular pH (pHi) of cultured aortic cells were measured using the fluorescent probe 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The initial maximal reaction velocity of Na(+)-dependent alkalinization was significantly higher in SHR and Wistar than WKY cells. Similar results were obtained for the maximal velocity of the proton equivalent efflux: SHR, 7.51 +/- 0.71; Wistar, 9.14 +/- 0.85; WKY, 4.38 +/- 0.55 mmol H+/liter x 10 s. There were no differences in the basal pHi or cellular buffering power among the three rat strains. These findings indicate that the activity of the Na(+)-H+ antiport is higher in SHR vascular smooth muscle cells than in WKY cells. However, by itself, this difference cannot explain the hypertensive process in the SHR, since this transport system is also higher in vascular cells of the Wistar rat.

Animals↗
PubMed1990

Na(+)-H+ antiport activity in skin fibroblasts from blacks and whites.

The predisposition of black people to salt (NaCl)-sensitive essential hypertension may relate to racial differences in cellular Na+ metabolism. This tenet was investigated by examining the Na(+)-H+ antiport in serially passed skin fibroblasts from blacks and whites. Na(+)-dependent stimulation of the Na(+)-H+ antiport by cellular acidification resulted in a greater maximal velocity (Vmax) (mean +/- SEM) of this transport system in quiescent fibroblasts from blacks than fibroblasts from whites; the Vmax for recovery from cellular pH (pHi) of 6.6 was 5.84 +/- 0.50 versus 4.39 +/- 0.34 mmol H+/l X 20 seconds for blacks and whites, respectively (p less than 0.05). Although the Na+ concentration producing 50% stimulation of the Na(+)-H+ antiport for blacks (35.1 +/- 5.7 mM) was greater than for whites (24.1 +/- 3.5 mM), this difference was not statistically significant. No racial differences were observed in the Hill coefficient (n, 1.35 +/- 0.21 for blacks and 1.46 +/- 0.28 for whites). Compared with whites, cells from blacks exhibited a greater response to cytoplasmic acidification over the range of pHi values 6.20-6.60, as exhibited by an augmented rate of recovery in the pHi. These differences were not due to different basal pHi values or cellular buffering capacities, which were similar for blacks and whites. Na(+)-H+ antiport activity was not correlated with family history of hypertension. Increased activity of the Na(+)-H+ antiport in fibroblasts from blacks was confirmed without cellular acidification by stimulating quiescent cells with 10% human serum. This study demonstrates innate racial differences in cellular membrane Na(+)-H+ antiport activity.

Adult↗
PubMed1990

Variations in the apparent pH set point for activation of platelet Na-H antiport.

To explore the role of the Na-H antiport in essential hypertension, we studied the kinetics of cytosolic pH and external sodium activation of this transport system in platelets from 65 normotensive and essential hypertensive subjects on and off antihypertensive medications. Subjects included both blacks and whites, as well as men and women. The fluorescent dye 2'7-bis(carboxyethyl)-5,6-carboxyfluorescein was used to monitor the cytosolic pH in these cells. Platelets from black (hypertensive and normotensive) men and hypertensive white men demonstrated a highly significant alkaline shift in the apparent cytosolic pH set point for activation of the Na-H antiport. For the hypertensive subgroups, the cytosolic pH set point values (mean +/- SEM) were: white men, 7.45 +/- 0.052; white women, 7.04 +/- 0.089; black men, 7.66 +/- 0.148; and black women, 7.20 +/- 0.082. For the normotensive subgroups, the cytosolic pH set point values were: white men, 7.13 +/- 0.034; white women, 7.05 +/- 0.036; black men, 7.50 +/- 0.110; and black women, 7.20 +/- 0.176 (p = 0.0016 for race and p = 0.0001 for gender, using a three-way analysis of variance by race, gender, and hypertension). There were no race-, gender-, or blood pressure-related differences among the various cohorts in the kinetics of sodium activation of the Na-H antiport, the cellular buffering power, and basal pH. These results suggest that at basal pH the Na-H antiport is quiescent in platelets from both black and white women and normotensive white men.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1990

Refined estimation of kinetic parameters of the Na+/H+ antiport in human fibroblasts and platelets.

A technique is presented to estimate the initial rates of Na(+)-dependent alkalinization of acidified human fibroblasts and platelets and assess the kinetics of the Na+/H+ antiport in these cells. Cytosolic pH (pHi) exhibits an exponential recovery following cellular acidification. Thus, the length of the time interval selected to monitor changes in pHi (delta pHi) is critical to estimating the kinetics of the Na+/H+ antiport. We compared kinetic parameters of the Na+/H+ antiport, using computed and observed changes in delta pHi, for arbitrarily selected time intervals following Na(+)-dependent activation. In both cells, significant increases in both the [Na+] for half-maximal activation (K0.5) and maximal velocities (Vmax) were observed as delta pHi was decreased. We conclude that kinetic parameters derived from initial rate determinations enable a more accurate characterization of the Na+/H+ antiport.

Biological Transport, Active↗
PubMed1985

Changes in bone remodeling after palatal surgery.

It is generally well known that an infant with a cleft palate will have facial underdevelopment after corrective surgery. In such a case, we can suppose that the internal remodeling of the facial bone becomes abnormal postoperatively. The purpose of this study was to observe the changes in palatal bone remodeling after palatal surgery and the external bone growth inhibition using the microradiography and hard tissue labeling method. In this investigation we had 4 experimental groups and used large undecalcified ground sections to observe the whole palatal bone. Our experiments showed that the changes resulting from surgery include not only external bone growth inhibition, but also considerable abnormal remodeling in the interior of the bone. When the mucoperiosteum was removed, the changes continued to occur for an especially long period.

Animals↗
PubMedDate not supplied

Stimulatory effect of serum on 86Rb washout from vascular smooth muscle cells in culture.

In order to elucidate the effect of serum on passive K permeability of vascular smooth muscle cells (VSMC) membrane, outward passive K permeability yielded as washout rate constant (Kc) of 86Rb washout, was measured in the presence and in the absence of cation transport modulators using VSMC in culture. The overall Kc of 86Rb washout subjected to 1% serum was significantly larger than that in controls. This stimulated Kc was substantially blunted in the presence of 10(-4) M amiloride and was partially inhibited with 5 x 10(-4) M bumetanide. Angiotensin II of 10(-5) M exerted to a lesser extent, a similar significant stimulatory effect on Kc of 86Rb washout, which effect was inhibited with application of amiloride. Additionally, Ca-antagonist, 10(-5) M nifedipine reduced serum-stimulated Kc to the basal level. It is concluded that both serum and angiotensin II increase K permeability in cultured VSMC. A part of this effect of serum may be attributable to angiotensin II in the serum. Furthermore, it is suggested that the stimulatory effect of serum on membrane permeability may be exerted, at least in part, via activation of both Na-H antiport and Na-K co-transport, possibly through mechanisms in conjunction with intracellular Ca.

Angiotensin II↗
PubMedDate not supplied

Tranexamic acid increases peritoneal ultrafiltration volume in patients on CAPD.

OBJECTIVE: The preservation of ultrafiltration (UF) capacity is crucial to maintaining long-term continuous ambulatory peritoneal dialysis (CAPD).The aim of the present study was to investigate whether the antiplasmin agent tranexamic acid (TNA) increases UF volume in CAPD patients. PATIENTS AND METHODS: Fifteen patients on CAPD, 5 with UF loss and 10 without UF loss, were recruited for the study. The effect of TNA was evaluated with respect to changes in UF volume, peritoneal permeability, peritoneal clearance, bradykinin (BK), and tissue plasminogen activator (tPA) concentration. SETTING: Dialysis unit of the Saiseikai Central Hospital. RESULTS: In patients with UF loss, 2 weeks of treatment with oral TNA produced a significant increase in UF volume in all subjects (5/5).TNA also produced a significant increase in peritoneal clearances of urea and creatinine (Cr). However, the peritoneal equilibration test (PET) revealed that TNA had no effect on dialysate/plasma (D/P) Cr, Kt/V, or the protein catabolic rate (PCR).TNA also had no effect on net glucose reabsorption. In contrast, significant decreases in BK and blood tPA concentrations in response to TNA treatment were noted. BK concentration in drainage fluid was also reduced. In the case of patients without UF loss,TNA produced an increase in UF volume in 70% (7/10). However, no differences were found in blood and drainage BK and tPA concentrations between theTNA treatment and nontreatment periods in these patients. A comparison of basal BK and tPA concentration showed that there were no differences in these parameters between patients with UF loss and those without loss of UF. Furthermore,TNA given intraperitoneally to a patient also produced a marked increase in UF volume. CONCLUSION: The present study suggests thatTNA enhances UF volume in patients both with and without UF loss. SinceTNA did not affect peritoneal permeability and glucose reabsorption, the mechanism by which TNA exerts an enhancing action on UF is largely unknown. We speculate that it may be associated with suppression of the BK and/or tPA system, at least in patients with UF loss.

Absorption↗