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T Saruta

Publications and source records attributed to T Saruta.

At least 415 records · Page 23Linked to original sources
PubMed1990

Aromatic L-amino acid decarboxylase activity along the rat nephron.

Extraneural dopamine is thought to be synthesized by an aromatic L-amino acid decarboxylase (L-AADC) activity in tubular cells. However, the previous histochemical studies of this enzyme's localization in the nephron were not consistent. To determine the localization of L-AADC and whether changes in Na intake regulate this enzyme, L-AADC was measured in microdissected nephron segments from rat kidneys. Dopamine formed by isolated tubules incubated with exogenous L-dopa was quantitated by high-performance liquid chromatography (HPLC) and with the more sensitive radioenzyme assay (REA). L-AADC activity was present only in proximal convoluted (PCT, 208 +/- 19 ng.cm-1.h-1) and proximal straight tubules (PST, 81 +/- 9 ng.cm-1.h-1), whereas no significant activity was detected in other nephron segments by either HPLC or REA. Maximal velocity (Vmax) of L-AADC in a low-salt diet group (246 +/- 4 ng.cm-1.h-1) showed a small but a significant decrease (P less than 0.05) compared with control and high-salt diet groups (311 +/- 6 and 293 +/- 4 ng.cm-1.h-1, respectively), whereas the apparent Michaelis constant (Km) was similar in these three groups. These results show that L-AADC is present only in the PCT and PST of the rat nephron, and suggest that the changes in L-AADC activity may contribute to the regulation of extraneural dopamine production in the kidney during low-salt intake.

Animals↗
PubMed1990

Baroreflex control of renal sympathetic nerve activity is potentiated at early phase of two-kidney, one-clip Goldblatt hypertension in conscious rabbits.

Conscious normotensive and two-kidney, one-clip Goldblatt hypertensive rabbits were studied to determine the sensitivity of the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate. The relations of the mean arterial pressure-RSNA and mean arterial pressure-heart rate were examined over a wide range of blood pressures produced by infusions of phenylephrine and nitroglycerin. The maximum slope obtained by logistic function analysis was considered to represent the baroreflex sensitivity. In the early hypertensive group (n = 8; mean arterial pressure +/- SEM, 88 +/- 2 mm Hg) on day 5 after renal clip application, the maximum slope of the mean arterial pressure-RSNA relation was -11.3 +/- 1.2, which was significantly greater than that of the sham normotensive group (-6.9 +/- 0.3, p less than 0.05). The maximum slope (-4.3 +/- 0.2) of the mean arterial pressure-RSNA relation in the late hypertensive group (n = 8; mean arterial pressure, 96 +/- 3 mm Hg) on day 21 after renal clipping was significantly smaller than that of another sham group (-7.2 +/- 0.2, p less than 0.05). In contrast to these changes in the baroreflex control of RSNA, the control of heart rate was attenuated according to the magnitude of mean arterial pressure. To elucidate the mechanisms underlying the potentiated baroreflex, the effects of endogenous neuropeptides were investigated. First, plasma concentrations of angiotensin II and arginine vasopressin that are known to affect the baroreflex were determined. Plasma concentrations of vasopressin (3.1 +/- 0.6 pg/ml) as well as of angiotensin II (34 +/- 7 pg/ml) were increased in the early hypertensive group, and the plasma vasopressin returned to a similar level to the sham group in the late hypertensive group (1.3 +/- 0.4 pg/ml). Second, to study endogenous effects of these neuropeptides on the baroreflex, the maximum slopes of the baroreflex curves during infusions of antagonists for the peptides were determined in the early hypertensive group. The maximum slope of mean arterial pressure-RSNA during intravertebral arterial [Sar1, Ala8]-angiotensin II (-16.4 +/- 1.5) was significantly greater (p less than 0.05), whereas the maximum slope during intravertebral arterial infusion of d(CH2)5Tyr(Me)arginine vasopressin (-4.7 +/- 0.5) was significantly smaller (p less than 0.05) than that during vehicle infusion (-11.3 +/- 1.2).(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin II↗
PubMed1990

Effect of captopril on plasma prolactin in patients with essential hypertension.

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.

Adult↗
PubMed1990

Na+, K(+)-ATPase inhibitory activity of fractionated urine during changes in dietary sodium intake in man.

Na+, K(+)-ATPase inhibitory activity in urine fractionated by HPLC was quantified in 7 normotensive male subjects during changes in dietary sodium intake. Subjects were studied on free sodium intake for 2 days, on low sodium intake (2 g/day) for 3 days, on high sodium intake (22 g/day) for 4 days and subsequently on normal sodium intake (6 g/day) for 2 days. Na+, K(+)-ATPase inhibitory activity in fraction 10 eluted with 17% acetonitrile by reverse-phase HPLC was 12.3 +/- 5.2% (mean +/- S.D.) on free sodium intake, 8.7 +/- 9.8% on the 3rd day of low sodium intake, 61.2 +/- 6.6% on the 4th day of high sodium intake, and 20.5% +/- 0.7% on the 2nd day of the normal sodium intake. Changes in Na+, K(+)-ATPase inhibitory activity of fraction 10 were closely associated with those in urinary sodium excretion. These results suggest that an endogenous Na+, K(+)-ATPase inhibitor(s) which plays a physiological role in the control of sodium and water balance may exist in this particular fraction.

Adult↗
PubMed1990

Effects of angiotensin II, ACTH, and KCl on the adrenal renin-angiotensin system in the rat.

Angiotensin II, ACTH and potassium chloride were administered to rats for 6 days and the effects on adrenal renin-like activity and adrenal angiotensin II/III immunoreactivity were investigated. Rats infused with angiotensin II (140 pmol/min) either ip or sc showed increases in adrenal angiotensin II/III immunoreactivity (p less than 0.05) and plasma aldosterone concentration (p less than 0.05), but no change in adrenal renin-like activity. Captopril treatment of angiotensin II-infused rats caused a slight decrease in angiotensin II/III immunoreactivity which did not reach statistical significance. In contrast, rats treated with ACTH (Cortrosyn-Z, 3 IU/day, sc) showed an increase in adrenal renin-like activity (p less than 0.01), but no significant change in adrenal angiotensin II/III immunoreactivity. Rats treated with KCl in drinking water showed increases (p less than 0.05) in adrenal renin-like activity, adrenal angiotensin II/III immunoreactivity, and plasma aldosterone. These results suggest that angiotensin II, ACTH and potassium, three major regulators of aldosterone secretion by the adrenal gland, have different effects on the adrenal renin-angiotensin system when administered in vivo.

Adrenal Glands↗
PubMed1990

Role of intrarenal renin-angiotensin system on pressure-natriuresis in spontaneously hypertensive rats.

The pressure-natriuresis relationships in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were characterized with or without intrarenal renin-angiotensin system (RAS) blockade. The pressure-natriuresis relationship in SHR was shifted toward higher pressure in comparison to WKY. The inhibition of intrarenal RAS by MK-422 (0.3 ug/kg/min) in SHR enabled to excrete more sodium at the same pressure (P less than 0.05), whereas no significant changes were observed in WKY. In SHR, during administration of Thi5,8, D-Phe7-bradykinin (50 micrograms/kg/min), the natriuretic responses to MK-422 were maintained. Intrarenal infusion of Sar1, Ile8-angiotensin (70 ng/kg/min) into SHR increased sodium excretion accompanied by an increase in renal plasma flow. Intrarenally administered angiotensin I (10 ng/kg/min) into WKY showed antinatriuretic effects with minimal changes in renal hemodynamics. These results indicate that alteration of intrarenal RAS in SHR might contribute to reset the pressure-natriuresis relationship.

Angiotensins↗
PubMed1990

[Toxic activities of the Ga-Sn alloy (Adlloy-OH) on nutritional condition and dental caries development in rats].

The toxic activities of Ga-Sn alloy (Adlloy-OH) in experimental rats, its relations to the nutritional condition and dental caries development, were studied for three months. Adlloy, 0.3 g or 3 g per body weight (kg), was fed orally with the basal diet consisting of casein, sucrose, bean oil, mineral, and vitamin mixtures. Biochemical assays of serum was carried out for total protein, albumin, calcium, inorganic phosphate, glucose, urea, creatine, alkaline phosphatase, GOT, and GPT. There was no convincing evidence of toxic effects on growth and biochemical data by the oral feeding of Addloy-OH.

Animals↗
PubMed1990

Interrelationships among the renin-angiotensin system, sympathetic nervous system and atrial natriuretic peptide in end-stage renal failure.

Since it remains unclear how the regulatory mechanism of blood pressure and volume is associated with the renin-angiotensin system, the sympathetic nervous system, and atrial natriuretic peptide (ANP), we examined the changes in blood pressure and vasoactive hormones occurring in 12 patients with end-stage renal failure. They were divided into two groups, those who were anuric (group A, n = 7), and those who had a daily urine volume of more than 700 ml (group B, n = 5). The changes in the mean blood pressure (MBP) and these vasoactive hormones were observed during hemodialysis with water removal in group A and without water removal in group B, and during blood pressure reduction with sodium nitroprusside in group A. The basal levels of ANP in groups A and B were twice as high as those of normotensive subjects. During hemodialysis, MBP did not reveal any changes in both groups. In group A, ANP and body weight (BW) decreased, whereas the plasma renin activity (PRA) and norepinephrine (NE) increased. In group B, ANP remained stable during the first 3 hr and decreased at the end of hemodialysis. However, BW, PRA, and NE were unchanged. In group A, significant correlations were observed between the changes in BW and those in ANP (r = 0.52, p less than 0.05), PRA (r = -0.57, p less than 0.01), and NE (r = -0.76, p less than 0.01). During blood pressure reduction, MBP decreased with accompanying increases in NE and PRA. However, ANP did not show any change.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1990

Effects of antihypertensive agents on blood pressure and the progress of renal failure in partially nephrectomized spontaneously hypertensive rats.

The purpose of this study was to investigate the effects of antihypertensive agents on blood pressure and the development of glomerular changes in salt-loaded, 5/6 nephrectomized spontaneously hypertensive rats (SHR). Thirty-two spontaneously hypertensive rats with 5/6 nephrectomy were divided into 4 groups: a control group (N = 8), and group treated with 10 mg/kg/day trichlormethiazide. (N = 8), 30 mg/kg/day captopril (N = 8), and 200 mg/kg/day nicardipine (N = 8). Each of these antihypertensive drugs was added to the drinking water for 10 weeks and the rats were given the drugs and a high-salt diet (5% NaCl). During the experiment, body weight and systolic blood pressure were measured every 2 weeks. At the end of the study, blood was collected for determination of serum creatinine, blood urea nitrogen, serum protein, serum sodium and potassium, and plasma renin activity and aldosterone concentration. Also renal tissues were obtained for light and electron microscopic examination at the end of the study. Systolic blood pressure in 5/6 nephrectomized SHR loaded with a high salt was significantly reduced by administration of trichlormethiazide (155 +/- 12 versus 204 +/- 12 mm Hg), but not by administration of either captopril or nicardipine. However, levels of serum creatinine were not significantly elevated in rats treated with captopril and nicardipine (control: 0.93 +/- 0.11 mg/dl, captopril: 0.62 +/- 0.01 mg/dl, nicardipine: 0.55 +/- 0.05 mg/dl). In contrast to changes in blood pressure, marked glomerular sclerosis with hyalinosis, which was found in the control group was not ameliorated by treatment with trichlormethiazide. However, these changes were not observed in rats treated with either captopril or nicardipine in spite of the absence of a prominent fall in blood pressure. These data suggest that captopril and nicardipine ameliorated glomerular injury regardless of the level of systolic blood pressure through the direct and/or indirect actions on the glomerulus.

Animals↗
PubMed1990

Response of plasma immunoreactive active renin, inactive renin, plasma renin activity, and aldosterone to hemodialysis in patients with diabetic nephropathy.

Several alterations in plasma active renin, inactive renin (prorenin), and aldosterone have been described in patients with diabetes mellitus. Such changes could be of some importance for patients on hemodialysis treatment, who must undergo severe changes in fluid and electrolyte status during each dialysis session. Therefore we studied the response of renin and aldosterone to hemodialysis in uremic diabetic nephropathy patients, using direct immunometric assays to measure plasma active renin concentration (ARC), inactive renin concentration (IRC), total renin concentration (TRC), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) in 11 male patients aged 39-69 (mean 53 +/- 2) with diabetic nephropathy and 11 male age-matched non-diabetics who had been on maintenance hemodialysis for 1-10 years. Although baseline values of IRC were slightly higher, and values of PAC lower in diabetics compared to non-diabetics, the results did not reach statistical significance. During hemodialysis, significant increases in ARC (p less than 0.01), TRC (p less than 0.05), and PRA (p less than 0.01), and a significant decrease (p less than 0.05) in PAC were seen in non-diabetic patients but no significant changes were observed in patients with diabetic nephropathy. IRC did not change during hemodialysis in either group of patients. There were no significant differences in body weight, blood pressure, or electrolyte changes in the two groups. These results suggest an altered response of plasma renin and aldosterone to hemodialysis in patients with diabetic nephropathy compared to non-diabetics. The reduced renin response could not be explained by a defect in conversion from inactive renin, but may be caused by decreased secretion of active renin in these patients.

Adult↗
PubMed1989

Characterization of subclones of Madin-Darby canine kidney renal epithelial cell line.

Heterogeneity in Madin-Darby canine kidney (MDCK) epithelial cells has been reported, however, its details have not been well described. In the present study, we show that subclones obtained from a MDCK cell line could be divided into two morphologically and biochemically distinct cell types with different hormonal responsiveness. Clones of the first type, motile clones, which had extended and flattened cytoplasm, were devoid of carbonic anhydrase activity. Clones of the second type, nonmotile clones, formed colonies of cuboidal cells and showed carbonic anhydrase activity. Motile clones synthesized cAMP in response to arginine vasopressin, prostaglandin E1, and isoproterenol but not glucagon. In contrast, nonmotile clones responded to all of these hormones. These findings suggest MDCK cells have multiple cellular origins. The motile clones have characteristics similar to the principal cells of the collecting system, whereas the nonmotile clones may be derived from the thick ascending limb or the intercalated cell. Our studies also demonstrate a significant influence of culture condition on MDCK cellular behavior (carbonic anhydrase activity, Na+/K+-ATPase activity and vasopressin responsiveness). Therefore, physiologic and biochemical experiments with MDCK cells must be interpreted with reservations about cellular heterogeneity as well as differences induced by culture conditions.

Animals↗
PubMed1989

Effects of nicardipine on blood pressure and renal function in elderly hypertensive patients with renal dysfunction.

The effects of monotherapy with nicardipine, 20 mg three times a day, have been investigated in a 1-year study of 26 elderly (greater than 60 years) patients with hypertension with various types of renal dysfunction and seven without renal dysfunction. Parameters measured included blood pressure, blood chemistry (serum creatinine, uric acid, blood urea nitrogen, blood glucose total cholesterol, and electrolytes), plasma renin activity, and plasma aldosterone concentration. Nicardipine was effective in reducing blood pressure in all patients with diabetic nephropathy, parenchymal renal diseases, or hypertensive nephropathy, and in those without renal dysfunction. Serum creatinine and blood urea nitrogen levels were slightly elevated in some patients whose pretreatment serum creatinine level was greater than 2 mg/dl, regardless of the type of nephropathy. However, it was not determined whether this effect was the result of a reduction in blood pressure induced by nicardipine. Serum sodium, potassium, total cholesterol, and blood glucose levels were unchanged by the administration of nicardipine. Changes in plasma renin activity and aldosterone levels were not significant. These results suggest that nicardipine can be used safely in elderly patients with hypertension with renal dysfunction, regardless of the type of nephropathy.

Aged↗
PubMed1989

Differences in the effects of angiotensin converting enzyme inhibitors with or without a thiol group in chronic renal failure in rats.

1. We have investigated the effects of the non-renin-mediated actions of angiotensin converting enzyme inhibitors on the progression of chronic renal failure accelerated by hypertension. For this purpose, we studied the effects of captopril (a thiol-containing angiotensin converting enzyme inhibitor), enalapril (an angiotensin converting enzyme inhibitor without a thiol group) and cysteine (a thiol-containing amino acid which has no angiotensin converting enzyme-inhibitory action) in adriamycin-treated rats with deoxycorticosterone acetate-salt hypertension, in which the renin-angiotensin system was suppressed. 2. There were no significant differences in blood pressure between these groups and the control group [adriamycin-treated group with deoxycorticosterone acetate-salt loading, 206 +/- 7 mmHg (27.4 +/- 0.9 kPa) at week 10]. 3. Massive proteinuria occurred in all groups. At the end of the experiment (at week 10), urinary protein excretion was significantly reduced in the captopril and cysteine groups compared with the control group. No manifest improvements appeared in the enalapril group. 4. Levels of serum creatinine and blood urea nitrogen increased progressively. At week 10, the increases in the serum levels of creatinine were less in the captopril (87 +/- 16 mmol/l) and cysteine (80 +/- 19 mmol/l) groups than in the control group (124 +/- 27 mmol/l) (P less than 0.01). No marked differences were found between the control and enalapril groups. 5. Captopril and cysteine caused more than a three-fold reduction in the focal glomerulosclerosis score when compared with that in the control group, but enalapril did not decrease the score. The extent of tubulointerstitial change was parallel with the focal glomerulosclerosis score. 6. We conclude that the thiol group is possibly involved in the mechanism of the beneficial effects of some angiotensin converting enzyme inhibitors on the progression of chronic renal failure exacerbated by hypertension.

Angiotensin-Converting Enzyme Inhibitors↗