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Biomedical subjects

T Takabatake

Publications and source records attributed to T Takabatake.

At least 91 records · Page 5Linked to original sources
PubMed1988

Resetting of tubuloglomerular feedback in acute volume expansion in rats.

Loss of sensitivity or "resetting" of tubulo-glomerular feedback has been reported after both acute and chronic volume expansion in rats. In chronic volume expansion due to dietary salt loading, resetting was found to result from the appearance of an inhibitory factor in tubular fluid. The aim of the present study was to test the possibility that resetting after acute isooncotic volume expansion may also be due to such an inhibitor. Rats were acutely volume expanded (4.5% of body weight) by infusion of a solution of fresh plasma and Ringer's solution. Tubuloglomerular feedback activity was assessed in expanded and control animals by measuring early proximal flow (EPF) rate during perfusion of the loop of Henle at varying rates with proximal tubular fluid harvested from the control (control TF) and expanded animals (AVE TF). When loops of Henle in control animals were perfused with control TF at 10, 20 or 40 nl min-1, EPF fell from (mean +/- SD) 29.8 +/- 5.6 at zero loop flow to 27.5 +/- 7.5, 21.1 +/- 4.2 and 15.5 +/- 4.5 nl min-1 gKW-1 respectively. Perfusion at the same rates with control TF in expanded animals reduced EPF from 39.5 +/- 9.6 (at zero loop flow) to 35.9 +/- 11.3, 31.6 +/- 4.3 and 22.9 +/- 6.8 nl min-1 gKW-1 respectively. When loops of Henle in control animals were perfused with AVE TF, EPF fell from 28.6 +/- 9.5 (zero loop flow) to 23.5 +/- 8.6, 19.9 +/- 8.2 and 15.6 +/- 6.5 nl min-1 gKW-1 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Increased tubuloglomerular feed-back mediated suppression of glomerular filtration during acute volume expansion in rats.

1. Volume expansion is currently believed to change the intrinsic properties of the juxtaglomerular apparatus such that the sensitivity of the tubuloglomerular feedback (TGF) mechanism is reduced, thus allowing glomerular filtration rate, and hence salt and water excretion, to rise. Recent studies conflict with this view and indeed the older literature reveals that the rise in glomerular filtration rate (GFR) under these conditions is far more modest than would be expected if TGF control were eliminated. 2. To investigate this problem, TGF control of filtration rate was examined by measuring single-nephron glomerular filtration rate (SNGFR) during loop of Henle perfusion at varying rates in rats under control conditions, after acute, moderate (4% of body weight), iso-oncotic volume expansion and in rats treated with antibodies to atrial natriuretic peptide (ANP) prior to the acute volume expansion. 3. With TGF control of filtration interrupted by filtrate collection from the proximal tubule, SNGFR in the expanded rats was massively increased compared with controls, although SNGFR measured in the distal tubule, and hence with TGF control intact, was only modestly increased, as was whole-kidney filtration rate. Loop perfusion at increasing rates up to 30 nl min-1 progressively decreased SNGFR in controls, and in the expanded rats the range over which control was exerted extended up to 60-80 nl min-1. For changes in loop flow around the spontaneous operating point, the sensitivity of the TGF mechanism, defined as delta SNGFR/delta loop flow, was similar in both groups. Treatment of rats with ANP antibodies prior to volume expansion substantially blunted the changes in renal salt and water excretion and the increase in SNGFR seen in the absence of loop perfusion. 4. These results are not consistent with a diminution of TGF function after volume expansion, rather with an enhancement. The latter is best accounted for by vasodilation of preglomerular resistance vessels on volume expansion, a result predicted by calculations from a model based on the serial arrangement of preglomerular and TGF-controlled vascular resistance elements and the established pharmacological actions of ANP.

Animals↗
PubMed1988

Low serum creatinine levels in severe hepatic disease.

For five years, eight patients had abnormally low serum concentrations of creatinine. All patients presented with severe hepatic failure, which was due to fulminant hepatitis in seven patients and to advanced primary biliary cirrhosis in one patients. The serum urate (as uric acid) concentration was also low in seven patients. Endogenous creatinine clearance was increased in all patients (2.38 to 14.75 mL/s [143 to 885 mL/min]). However, inulin clearance measured in four patients was reduced (25 to 32 mL/min) and the creatinine-to-inulin clearance ratio ranged from 4.5 to 9.9. This range can be explained largely by an increased tubular secretion of creatinine related to body fluid expansion caused by a large fluid infusion. Renal function would be extremely overestimated when assessed from serum concentrations or clearance of creatinine in such patients.

Creatinine↗
PubMed1987

Effect of the calcium antagonist nilvadipine on haemodynamics at rest and during cold stimulation in essential hypertension.

The immediate haemodynamic effects of the calcium antagonist nilvadipine have been studied in ten patients with established mild essential hypertension. Nilvadipine 4 mg p.o. reduced both the systolic and diastolic blood pressures within 60 min, associated with a fall in total peripheral resistance and an increase in heart rate and cardiac index. The peak of blood pressure and total peripheral resistance reached during a cold pressor test were reduced by nilvadipine, but it did not affect the haemodynamic responsiveness to cold stimulation. Plasma renin activity was unaltered and the plasma noradrenaline concentration was increased only slightly. Thus, nilvadipine lowered blood pressure at rest and during cold stimulation as a result of arteriolar dilatation. The hypotensive effect at rest was associated with a reflex increase in heart rate and cardiac index.

Adult↗
PubMed1987

Effect of angiotensin blockade and converting enzyme inhibition on renovascular hypertension: comparison between unilateral and bilateral renal artery stenosis.

The response to angiotensin II analog infusion during sodium deletion and the effects of a one-month captopril treatment were compared between 15 renovascular hypertensive patients with unilateral and 6 with bilateral renal artery stenosis. Plasma renin activity, its response to sodium depletion, and the renal vein renin ratio during sodium depletion were greater in unilateral than in bilateral stenosis. A fall in diastolic blood pressure induced by analog infusion during sodium depletion was correlated with the preinfusion plasma renin activity and with the renal vein renin ratio. Treatment with captopril showed a comparable hypotensive effect in unilateral and bilateral stenosis. The reduction in blood pressure was not correlated with the pretreatment renin levels or changes in blood pressure observed during analog infusion. Plasma renin activity rose and plasma aldosterone level fell in all patients. These results indicate that the mechanism maintaining high blood pressure is more renin dependent in unilateral than in bilateral stenosis and that the long-term effect of captopril does not depend solely on the suppression of the renin-angiotensin-aldosterone system.

Adult↗
PubMed1986

Pharmacokinetics of TZU-0460, a new H2-receptor antagonist, in patients with impaired renal function.

We have studied pharmacokinetics of a new H2-receptor antagonist, TZU-0460, in patients with varying degrees of renal impairment. The apparent volume of distribution at steady-state was 1.70 l/kg, and the plasma protein binding of TZU-0460 or its active metabolite, desacetyl TZU-0460 was less than 10% in normal subjects. These variables were not altered with renal impairment. Sixty percent of TZU-0460 given orally was excreted via the kidney, mainly by tubular secretion. The half-time of elimination was 3.94 h in normal subjects, and was prolonged to 12.13 h in severe renal failure (creatinine clearance below 30 ml/min/1.48 m2). Dosage adjustment of TZU-0460 is necessary in renal failure.

Adult↗
PubMed1986

The long term effects of percutaneous transluminal angioplasty for treating patients with renovascular hypertension: case studies.

Percutaneous transluminal angioplasty was performed on 10 patients with unilateral renovascular hypertension (7 with atheromatous and 3 with fibromuscular stenoses) who were then followed for an average of 42 months (range, 24 to 67 months). Dilation of the stenosis was initially successful in all patients except one who had severe atheromatous stenosis. Among patients with atheromatous disease, normotension was attained for 40, 25 and 24 months in 3 patients given no antihypertensive medication and for 67 and 55 months in 2 patients given only nicardipine. The remaining one patient had a recurrent stenosis 3 months after angioplasty. All patients with fibromuscular dysplasia have been normotensive without any hypotensive medication for more than 4 years. Plasma renin activity declined within one week after angioplasty and remained unchanged thereafter in all patients except the one case suffering from a recurrent stenosis. Renal blood flow and glomerular filtration rate remained increased after angioplasty. These results suggest that hypertension can be controlled and renal dysfunction in patients with renal artery stenosis caused by atheroma or fibromuscular dysplasia improved for long periods by percutaneous transluminal angioplasty. The antihypertensive effect obtained by this procedure was more valuable for the patients with fibromuscular dysplasia than in those with atheromatous disease.

Adolescent↗
PubMed1985

Pharmacokinetics of famotidine, a new H2-receptor antagonist, in relation to renal function.

The pharmacokinetics of a new, potent H2-receptor antagonist, famotidine, 20 mg i.v. was studied in 7 subjects with normal renal function and in 24 patients with varying degrees of renal impairment. The volume of distribution at steady state was 1.141/kg in normal subjects and was not altered in renal failure. The half-life of elimination was 2.59 h in normal subjects and was unchanged in mild renal failure (creatinine clearance, CLCR 90-60 ml/min/1.48 m2) but was increased to 4.72 h in moderate renal failure (CLCR 60-30 ml/min/1.48 m2), and to 12.07 h in severe renal failure (CLCR below 30 ml/min/1.48 m2). The cumulative urinary excretion and renal clearance of famotidine were correspondingly reduced in patients with impaired kidney function. In normal subjects and in patients with mild to moderate renal failure, about 70% of famotidine was excreted through the kidney, mainly by tubular secretion. In patients with a CLCR above 60 ml/min/1.48 m2 the normal daily dose of famotidine can be employed, but in those with a CLCR between 60 and 30 ml/min/1.48 m2 the dose should be reduced by half, and in patients with a CLCR below 30 ml/min/1.48 m2 a reduction by three quarters of the normal dose is recommended.

Adult↗
PubMed1985

A case of one-kidney hypertension: contrasting effects of angioplasty and treatment with captopril.

A patient with hypertension is shown to have both a renal artery stenosis due to fibromuscular dysplasia and a hypoplastic contralateral kidney, a condition comparable to that of the one-kidney Goldblatt hypertension. Both blood volume and plasma renin activity were increased. Blood pressure was lowered either by an angiotensin II analog or by captopril. Secretion of excess renin was observed only from the stenotic kidney. A 4-week period of captopril treatment was accompanied by an acute, reversible deterioration of renal function. Transluminal angioplasty corrected the abnormalities in renin and in blood volume and has kept blood pressure and renal function normal for over 2 years.

Adult↗
PubMed1985

Blood pressure variability and hemodynamic response to stress in patients with paroxysmal elevation of blood pressure.

Blood pressure variability during 24 hours and hemodynamic response to stress were studied in essential hypertensive patients, displaying paroxysmal hypertension and pheochromocytoma-type symptoms (PH). Hemodynamics at rest, in response to mental arithmetic, bicycle ergometer exercise or the cold together with baroreflex sensitivity were not different between these patients and other essential hypertensives (EH). Average waking systolic blood pressure was lower but variabilities of both systolic and diastolic blood pressure were greater in PH than in EH. During sleep, these differences disappeared. Thus, the greater variability in blood pressure seen only in waking PH patients cannot be estimated from the hemodynamic patterns at rest and is not likely to be related to an excessive response to stress or impaired baroreflex.

Adrenal Gland Neoplasms↗
PubMed1985

The effect of muzolimine on the tubuloglomerular feedback mechanism in the rat kidney.

Inhibition of tubuloglomerular feedback (TGF) by loop diuretics can enhance the diuretic response by attenuating the fall in GFR to be expected with the diuretic-induced rise in distal salt delivery. To establish whether such a mechanism contributes to muzolimine (M)-induced diuresis, TGF activity was tested in male Wistar rats by measuring early proximal flow rate in nephrons, the loops of Henle of which were perfused with M at various concentrations in the presence or absence of M systemically. Since M inhibited TGF only at concentrations far in excess of those adequate to produce substantial diuresis, it is concluded that TGF inhibition by M plays no significant role in the diuretic response to this agent.

Animals↗
PubMed1985

Acute renal failure and transient, massive proteinuria in a case of pheochromocytoma.

Severe renal impairment and massive proteinuria are rare in pheochromocytoma. We report the case of a patient with pheochromocytoma who repeatedly developed episodes of acute renal deterioration and transient, massive proteinuria. Each episodes followed hypotensive periods, two of which seemed to be induced by administration of metoclopramide. The pathogenetic mechanisms of acute renal deterioration and proteinuria are discussed.

Acute Kidney Injury↗
PubMed1984

Effects of long-term prazosin therapy on lipoprotein metabolism in hypertensive patients.

Prazosin administration caused a significant and continuous antihypertensive effect when given as a single agent for 12 months. The daily dose was stabilized after three months at 6.0 mg per day. After 12 months of prazosin treatment, high-density lipoprotein cholesterol increased by 17 percent (p less than 0.005) and the cholesterol ratio increased by 19 percent (p less than 0.05), but total cholesterol was not significantly changed. There were no statistically significant changes in triglycerides, plasma renin activity, and plasma aldosterone concentration following treatment when compared with baseline levels. Prazosin monotherapy is concluded to have favorable effects on serum lipids and can be considered suitable for long-term antihypertensive therapy.

Adult↗
PubMed1983

Disparity between surface and deep nephron function early after renal ischemia.

Experiments were performed using a variety of methods to assess the functional status of different nephron populations following 45 min of renal ischemia in the rat. Micropuncture techniques revealed that SNGFR and reabsorption in the surface nephrons are only modestly reduced after ischemia, whereas kidney GFR and reabsorption are more severely affected. Determinations of bolus velocity with the Hanssen technique or of glomerular blood flow with the microsphere method confirmed that both were highest in the surface nephrons, lower in the middle nephrons and lowest of all in the juxtamedullary nephrons after ischemia. It is concluded that surface nephron function is well-maintained following ischemia and that it is the functional deficiency of the deeper nephrons that is predominantly responsible for the impairment in whole kidney function. Although the pathogenic mechanism is not yet clear, neither tubular obstruction nor tubular leakage in the deeper nephrons seems to be involved. The present findings suggest that micropuncture of the surface nephrons is a technique of questionable validity for studying this type of acute renal failure, they explain the inability of the kidney to concentrate the final urine, and they predict a more pronounced deficiency in medullary than in outer cortical blood flow.

Acute Kidney Injury↗