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S Akabane

Publications and source records attributed to S Akabane.

47 records · Page 3Linked to original sources
PubMed1984

Intrarenal beta-adrenergic stimulation enhances excretion of urinary lysosomal enzyme in anesthetized dogs.

The effects of intrarenal administration of isoproterenol on excretion of urinary enzymes were examined in dogs. Urinary N-acetyl-beta-D-glucosaminidase (NAG) and glutamyl transpeptidase (gamma-GTP) originated from lysosomes and the brush border membrane of the kidney, respectively. NAG excretion was elevated for 10 min by isoproterenol (0.2 microgram/kg/min) without a drastic change in glomerular filtration rate and renal blood flow. This elevation was inhibited by pretreatment with d,l-propranolol (0.6 mg/kg bolus injection 0.3 mg/kg/30 min) but less so by d-propranolol. Urinary gamma-GTP excretion was little affected by isoproterenol. In light of these findings, the possibility that beta-receptors may be involved in the excretion of NAG has to be considered.

Animals↗
PubMed1984

Roles of endogenous angiotensin II or kinin in the mechanism of altered renal vascular responsiveness to angiotensin II following acute blood volume expansion in the dog.

To examine the role of endogenous angiotensin II or kinins in the mechanism of the increased renal vascular reactivity to exogenous angiotensin II following acute blood volume expansion, we examined whether captopril, a converting enzyme inhibitor, can prevent the increase in renal vascular response in anesthetized dogs. Pretreatment of dogs with captopril increased plasma renin activity, but it did not affect systemic blood pressure, renal blood flow and renal vascular resistance. Acute blood volume expansion with saline suppressed plasma renin activity in dogs with or without pretreatment with captopril. Basal level of renal vascular reactivity to angiotensin II was increased by pretreatment with captopril. In the control animals, acute blood volume expansion enhanced renal vascular reactivity to angiotensin II but not norepinephrine. The enhanced renal vascular reactivity to angiotensin II, however, was not prevented by the captopril treatment. The failure of captopril to prevent an increase in renal vascular reactivity to angiotensin II following acute blood volume expansion was associated with an increase in urinary excretion of bradykinin. These data suggest that endogenous angiotensin II level is not necessarily a determinant for vascular reactivity to exogenous angiotensin II, especially in the case of acute blood volume expansion.

Angiotensin II↗
PubMed1983

The inactive to active renin ratio in the kidneys and the plasma in diabetic nephropathy.

We examined the inactive to active renin ratio in the renin granules of the cadaver kidneys and the plasma in patients with diabetic nephropathy. The inactive renin in the break-through fraction when the plasma or the renin from the renin granules was put into a pepstatin column was determined. The inactive renin in this fraction was activated by trypsin. Concerning plasma, the inactive to active renin ratio was 90 in the patients and 9 in the normal subjects. On the other hand, this ratio was 0.29 in the patients' kidneys and 0.28 in the control kidneys. These results suggest that the increase of the inactive to active renin ratio in plasma of diabetic nephropathy does not result from the change of the renin storage in the kidneys.

Blood Proteins↗
PubMed1983

The existence of inactive (trypsin-activated) renin in dog plasma and renin granules from the kidney.

Trypsin-activated renin (inactive renin) was detected in the break-through fraction when dog plasma or renin extracted from renin granules (stored renin) was applied to a pepstatin column, respectively. The appearance of the renin activity by trypsin treatment was not due to acid protease. Production of angiotensin I from homologous renin substrate by the trypsin-activated renin was proportional to the time of incubation. The trypsin-activated renin had an affinity for the pepstatin column. The maximum amount of trypsin-activated renin was obtained with incubation for 15 min at 37 degrees C at 1000 micrograms/ml in plasma or at 100 micrograms/ml in case of stored renin. The ratio of inactive to active renin was calculated to be 1.6 or 0.002 in plasma or stored renin, respectively, under conditions of a standard sodium diet.

Animals↗
PubMedDate not supplied

The storage form of human renal renin.

We isolated renin granules from cadaver kidneys using discontinuous sucrose density gradient centrifugation, and investigated the storage form of the renin from these granules. Approximately 23% of the total renin activity in the original homogenate was obtained from the surface phase between 1.6 and 1.7 M sucrose (Fraction 6). Granule renin extracted from the granules in Fraction 6 was separated into active and inactive renin using pepstatin affinity chromatography. Only the active renin had an affinity for pepstatin. The inactive renin, albeit activated by trypsin, was little activated by acidification. The proportion of inactive renin was about 25% of the total granule renin (active renin + inactive renin). Trypsin concentrations over 10 micrograms/ml resulted in a decrease in the renin activity of the trypsin-activated renin, but the enzymatic activity of active renin was decreased by trypsin. With gel filtration, the inactive renin revealed a single peak, and the molecular weight (MW) was 48,000. The active renin had a MW of 44,000. The inactive renin could be activated by trypsin without an apparent change in molecular weight.

Aged↗
PubMedDate not supplied

Effects of sodium depletion on inactive and active renin from dog kidney and plasma.

The relationship of active renin and inactive renin (trypsin-activated angiotensin-I-forming enzyme) to sodium depletion was examined in renal and peripheral plasma and at the subcellular level in the kidneys of dogs. Subcellular fractionation was carried out by discontinuous sucrose density (1.5 and 1.6 M) centrifugation. Sodium depletion selectively caused a six- to sevenfold increase in the renal content of inactive and active renins in the original homogenate, while the subcellular distribution patterns of these enzymes were little changed. Of the total granule fractions of 1.5 M sucrose (F1), 1.6 M sucrose (F2), and sediment (F3), approximately 80% of inactive renin was recovered in F1, which was rich in microsomes, while about 50% of active renin was in F2. The ratio of inactive to active renin was 0.02 in F1 and 0.003 to 0.004 in F2. Sodium depletion also caused a 20-fold increase in active renin and a twofold increase in inactive renin in peripheral plasma. The renal venous-arterial concentration difference of inactive renin was statistically significant in low-sodium dogs, although it was not significant in controls. The ratio of inactive to active renin was 0.2 to 0.4 in plasma from low-sodium dogs, while it was 1.5 to 3 in plasma from control dogs. These results suggest that plasma inactive renin originates, at least in part, in the kidney.

Animals↗
PubMedDate not supplied

Effects of taurine on stress-evoked hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.

Cardiovascular hemodynamics (microspheres) and plasma norepinephrine and epinephrine levels at rest and during short-term shaker stress were investigated in conscious spontaneously hypertensive rats and Wistar-Kyoto rats, with or without oral taurine (1.5%) treatment for 8 weeks. Taurine effects were evaluated by comparing data on the taurine-treated and untreated rats. Taurine affected neither the resting hemodynamics nor the resting plasma catecholamine levels in spontaneously hypertensive and Wistar-Kyoto rats. Taurine slightly but significantly reduced the left ventricular/body weight ratio in the spontaneously hypertensive rats (p less than 0.05) and caused an insignificant 10 mm Hg decrease in the resting mean arterial pressure. Spontaneously hypertensive and Wistar-Kyoto rats responded in a qualitatively similar manner to stress, as evidenced by resistance-dominated increases in mean arterial pressure and increases in heart rate, with a blood flow redistribution from splanchnic, cutaneous, and testicular to skeletal muscle and cerebral circulations and by increases in plasma norepinephrine and epinephrine levels. These changes were more marked in the spontaneously hypertensive rats. Taurine significantly reduced the stress values of mean arterial pressure (untreated, 189 +/- 4 (SE) mm Hg; treated, 166 +/- 4 mm Hg in the spontaneously hypertensive rats; p less than 0.05), while it significantly reduced stress values of heart rate in spontaneously hypertensive and Wistar-Kyoto rats (p less than 0.05). Taurine also blunted the stress values of splanchnic, testicular, and cutaneous vascular resistance in the spontaneously hypertensive rats. There were no or only slight regional effects in the Wistar-Kyoto rats. Taurine substantially decreased plasma levels of norepinephrine (untreated, 615 +/- 76 pg/ml; treated, 383 +/- 49 pg/ml) and epinephrine (untreated, 892 +/- 187 pg/ml; treated, 232 +/- 59 pg/ml) during stress in the spontaneously hypertensive rats. These results indicate that chronic taurine treatment attenuates short-term shaker stress-induced hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.

Animals↗