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Biomedical subjects

J Misumi

Publications and source records attributed to J Misumi.

At least 55 records · Page 3Linked to original sources
PubMed1983

[An experimental study on electrophysiological and histopathological changes in 2,5-hexanedione-intoxicated rats].

An experimental study of neuropathy due to 2,5-hexanedione (2,5-HDione) was performed in rats by using simultaneously both electrophysiological and histopathological methods. Seven rats were given subcutaneously five days a week 200 mg/kg of 2,5-HDione for first 3 weeks and then 300 mg/kg for the next 5 weeks. Nerve conduction velocities in the tail were measured every week and after the respective measurement times one animals was sacrificed for histological study. At the 2nd week of the experiment, 2,5-HDione-treated rat showed a slight morphological changes with swollen axons in the posterior spinal root fiber and tail nerve. A slowing of motor and sensory conduction velocity (MCV and SCV) in the tail was observed in the treated group at the 4th week. Weakness of hindlimbs was apparently seen at the 5th week. At the 6th and 7th week, histological changes including giant axonal swelling, fiber loss, thinning of myelin and demyelination, were prominent in the various regions of the peripheral nervous system. Additionally, degenerative changes of the spermatogenic cells, especially the formation of multinucleated giant spermatids, were markedly observed in the treated rats at the 6th and 7th week.

Animals↗
PubMed1983

Vascular effects and metabolism of angiotensins and their metabolites in the isolated perfused rat kidney.

The vascular effects of the injection of angiotensin I (AI), des-Asp1-angiotensin I (des-Asp1-AI), angiotensin II (AII), des-Asp1-angiotensin II ( (2-8)AII) and des-Asp1-Arg2-angiotensin II ( (3-8)AII) have been investigated in an isolated perfused rat kidney model, using a closed circuit system. The apparent half-life of these peptides was measured by AI and AII radioimmunoassays. Des-Asp1-AI is less potent than AI and has a shorter duration of action on perfusion pressure and renal flow. Up to 7.6% of circulating AI and 12.4% of circulating des-Asp1-AI are converted by the kidney to AII, (2-8)AII and other AII immunoreactive materials. This intrarenal conversion entirely explains the vasoconstrictor effects of these two peptides. The vasoconstrictor effects of (2-8)AII is similar to that of AII, but (2-8)AII has a shorter duration of action. At the doses injected, renin secretion is completely inhibited by AII and (2-8)AII, it is partially inhibited by AI, an effect which disappears when converting enzyme is inhibited. Des-Asp1-AI is a less potent inhibitor of renin secretion than AI, and (3-8)AII is devoid of any action on renin secretion. The apparent half-life of AI is 24.3 +/- 1.1 minutes, des-Asp1-AI: 20 to 23 minutes, AII: 19.6 +/- 1.8 minutes, (2-8)AII: 12 to 14.5 minutes and (3-8)AII: 12.5 to 13.5 minutes. Differences in the metabolism of these peptides may contribute to the differences of magnitude and duration of their vascular effects.

Angiotensin I↗
PubMed1983

Effects of circulating renin substrate on renal function in isolated perfused rat kidney.

The effects of two different amounts of pure rat angiotensinogen were investigated in a closed circuit isolated perfused rat kidney. In response to angiotensinogen, circulating levels of angiotensin I (AI) and angiotensin II (AII) immunoreactive materials were found to increase in a time and dose-dependent manner. Vasoconstrictor and renin inhibitory effects were observed in parallel with the increase in AII. Glomerular filtration rate decreased after administration of angiotensinogen to a greater extent than renal flow and filtration fraction. The characterization by high performance liquid chromatography of peptides generated showed the liberation of AI, des-Asp1AI, AII and des-Asp1AII (AIII). These findings demonstrate that administration of angiotensinogen in an isolated perfused kidney model generates AI and that renal converting enzyme and aminopeptidases are able to convert AI to AII, AI to des-Asp1AI, and des-Asp1AI and/or AII to AIII. Changes in circulating level of angiotensinogen influence the activity of the renin-angiotensin system and, therefore, renal function.

Angiotensin I↗
PubMed1982

[An experimental study on the neurotoxicity of 2-octanone and 2-hexanol, a metabolite of n-hexane].

An electrophysiological study of the neurotoxicity of 2-octanone (an analogue of methyl n-butyl ketone) and 2-hexanol (a metabolite of n-hexane) was conducted on rats as a part of the study to determine the specific molecular arrangement required for the development of peripheral neuropathy. The compound 2-octanone or 2-hexanol was administered subcutaneously in the daily dose of 400 mg/kg of each compound into the back of seven rats, weighing 290 g, 5 days per week for a period of 21 weeks. Animals treated with 2-octanone for 21 weeks failed to exhibit apparent clinical and neurophysiological evidence except a slight inhibition of weight gain and narcotic effects after treatment with the compound. The same doses of 2-hexanol for 21 weeks caused hypersalivation, gait disturbances, crossing phenomena of hind limbs and a failure of normal growth. Retardation of the conduction velocity in the motor and sensory nerve fibers and the prolonged motor latencies of the tail nerves (distal part) began to appear at the 14th week of the experiment when 9.6 g in the total dose had been given to each animal. These changes were intensified in the subsequent course of the experiment. Our previous experiments and the present results showed that n-hexane barely produced peripheral neuropathy in doses over 10.5 g, and that 2-hexanone (MBK), 2,5-hexanediol or 2,5-hexanedione never failed to produce a neuropathy even in doses less than 9.6 g of each compound. The above results suggest that the neurotoxic potency of 2-hexanol is greater than that of n-hexane but less than that of MBK, 2,5-hexanediol or 2,5-hexanedione.

Animals↗
PubMed1982

Diuretic and natriuretic effects of nifedipine on isolated perfused rat kidneys.

The effects of nifedipine, a vasodilating drug which acts through calcium antagonism, were studied in vitro using isolated perfused rat kidneys. Most of the nifedipine was neither metabolized nor excreted by this preparation. Four doses were tested: 50, 250, 500 and 750 nM. The two higher concentrations enhanced urine flow and sodium (UNaV) and potassium excretion. Tubular reabsorption of sodium was reduced compared to untreated control kidneys. The glomerular filtration rate was not modified but the filtration fraction decreased. The magnitude of urine volume, UNaV, urinary potassium excretion and filtration fraction changes were related to the dose of nifedipine. The decrement of total renal resistance and the increment of UNaV were correlated for 500 and 750 nM nifedipine (n = 13; r = -0.77; P less than .001), suggesting that it acted by dilating the renal vascular bed. Nifedipine at 250, 500 and 750 nM significantly increased the renin secretion rate compared to that of untreated control kidneys. When renin secretion was enhanced by 50 nM isoproterenol, this stimulatory effect was enhanced in kidneys concomitantly treated with 500 and 750 nM nifedipine. Dihydralazine, another vasodilating drug, was tested at a comparable molar dose (500 nM) and induced similar changes in urine volume, UNaV, urinary potassium excretion and Na reabsorption. The variations in total renal resistance and UNaV were also inversely correlated (n = 8; r = -0.68; P less than .05). Dihydralazine did not modify renin secretion rate significantly. These results suggest that: 1) both nifedipine and dihydralazine increase diuresis, natriuresis and kaliuresis in the isolated perfused rat kidney and 2) nifedipine enhances basal renin release from the juxta-glomerular cells and potentiates renin release caused by beta receptor stimulation.

Animals↗
PubMed1981

Effect of adrenalectomy and aldosterone on the modulation of mineralocorticoid receptors in rat kidney.

Adrenalectomized rat kidney is commonly used for the study of mineralocorticoid mechanism of action in mammals. In this model, aldosterone is known to bind to two classes of binding sites: type I (mineralocorticoid) and type II (glucocorticoid). The study of the aldosterone binding in normal rat kidney requires the elimination of endogenous hormones bound to each type of receptor. Thus, a suitable technique was developed using in situ perfusion of the kidneys. The efficacy of this method was of about 85 to 90% at the level of both cytoplasm and nucleus. Aldosterone binding capacity was checked in normal rat kidney after in situ perfusion and was found to be 300 to 500% lower than in adrenalectomized rat kidney, both in cytoplasm and nuclei. Computer analysis of aldosterone binding parameters in the cytoplasm (30,000 X g supernatant) of rat kidney suggested that adrenalectomy might induce an important rise in the number of mineralocorticoid receptors (congruent to 260%). An increase in the number of glucocorticoid receptors was also observed but appeared to be lower. Aldosterone, when perfused during 24 h in adrenalectomized rats, lowered the number of type I sites to the same level as observed in normal rat kidney. This effect was fully reversible after interruption of aldosterone perfusion. These results suggested an aldosterone-induced down regulation of mineralocorticoid receptors.

Adrenalectomy↗
PubMed1980

[Release of platelet activating factor (P.A.F.-acether) by isolated perfused rat kidney].

Platelet-activating factor (a 1-0-alkyl-2-acetyl glyceryl-3-phosphorylcholine, P.A.F.-acether) causes the aggregation of platelets from various Mammalian species and the release of their granule content. P.A.F.-acether activity has been recovered in vitro from perfused isolated Rat kidneys, stimulated by the ionophore A 23187. The maximum release was reached 10 min. after addition of the ionophore. P.A.F.-acether from kidney exhibited the same physico-chemical and biological characteristics as P.A.F.-acether from leucocytes. These data demonstrate that the kidney secretes a mediator of immediate hypersensitivity (P.A.F.-acether) in the veinous vasculature. Therefore the kidney itself has the ability of inducing intravascular platelet aggregation with subsequent local increase in vasopermeability.

Animals↗
PubMed1980

A comparison of multiple forms of renin in rat renal perfusate with those in renal extract.

1. Physicochemical properties of renin secreted by isolated perfused rat kidney were examined and the results compared with those obtained for the renin in renal extract. 2. In renal extract, two high-molecular-weight renins (molecular weight 65 000 and 55 000) and one low-molecular-weight renin (molecular weight 39 000) were found. Their relative proportion varied depending on extraction conditions. By acidification, high-molecular-weight renins were converted into low-molecular-weight renin without marked changes in activity. 3. In renal perfusate only low-molecular-weight renin was found after renin stimulation by isoprenaline or anoxia. Inactive renin was not found. 4. Renin in renal extract and perfusate samples were both found to consist of at least four isoenzymes having different isoelectric points (pI). The pI patterns were identical in renal extract and perfusate samples: pI 5.7 (60-70%), 5.5 (15-25%), 5.3 (5-10%) and 5.0-5.2 (2-5%). 5. These results indicate that the native renin secreted by rat kidney consists entirely of the low-molecular-weight and active form comprising multiple isoenzymes with a stable pI pattern.

Animals↗
PubMed1980

Mechanism of renin inhibition by beta adrenergic blocking agents. Effects of dl-, d-, l-propranolol and pindolol on renin release.

In order to reveal the mechanism of renin inhibition by beta adrenergic blocking agents, the effects of dl-, d-, l-propranolol and pindolol on renin release were studied. This was done by injecting them intraperitoneally or by using an in vitro system of rat kidney slices. In the in vivo study, dl-, d-, and l-propranolol inhibited plasma renin activity and renal renin content significantly in normal rats. Furthermore, in the in vitro study, the basal levels of renin in the media and that in the kidney were significantly inhibited by these agents. Pindolol also inhibited renin release, but its effects were significantly less than those of other agents. The finding that d-propranolol which has little beta adrenergic blocking action inhibited renin release, and that the effects of pindolol which displays strong beta adrenergic blocking action but little membrane stabilizing action, were less than those of other agents, may suggest that the inhibitory effects of beta adrenergic blocking agents on renin release are dependent mainly on the membrane stabilizing action rather than the beta adrenergic blocking action.

Adrenergic beta-Antagonists↗
PubMed1980

Effects of converting enzyme inhibitor (SQ 20881) on changes in blood pressure and plasma aldosterone induced by angiotensin I or acute hemorrhage in rabbits.

The effects of angiotensin converting enzyme inhibitor (CEI) upon blood pressure and plasma aldosterone (PA) were studied in rabbits with a simultaneous infusion of angiotensin I (ANG I) or with hemorrhagic hypotension. Pretreatment with CEI (SQ 20881), 1.0 mg/Kg, inhibited the effects of infused ANG I, 30 ng/Kg/min, upon PA and blood pressure at 30 min of the infusion, but the inhibition on PA was not significant at 60 min of the infusion. The same dose of CEI was ineffective in blocking the effect of 100 ng/Kg/min of ANG I on PA and blood pressure even at 30 min of the infusion. In rabbits with hemorrhagic hypotension, injection of CEI resulted in the decrement in blood pressure, whereas no decrement in blood pressure was observed in normal control rabbits. This study suggests that CEI exerts it's effect in part by inhibiting conversion of ANG I to angiotensin II (ANG II), but this can't exclude other mechanisms.

Aldosterone↗
PubMed1979

Effect of prostaglandin E2 on vascular reactivity to norepinephrine in isolated rat mesenteric artery, hind limb and splenic artery.

The effects of prostaglandin E2 (PGE2) and indomethacin on the vascular reactivity to norepinephrine were tested in three different isolated rat vascular beds (mesenteric artery, hind limb and splenic artery) perfused with the Krebs bicarbonate solution. In these vascular beds PGE2 (0.1-64 ng/ml) or indomethacin (09.1-96 microgram/ml) in the perfusate did not change the basal pressure. In the mesenteric vascular bed and the hind limb, PGE2 dose-dependently potentiated the vascular response to norephinephrine, whereas PGE2 dose-dependently inhibited the vascular response to norepinephrine in the splenic artery. In these three vascular beds indomethacin in the perfusate dose-dependently attenuated the vascular response to norepinephrine. In the mesenteric artery and the hind limb PGE2 restored the effect of indomethacin, but in the splenic artery PGE2 did not restore the inhibitory effect of indomethacin. These results indicate that the modulating effect of exogenously administrated PGE2 on the vascular action to norepinephrine varies in different vascular beds. It is also suggested that the contribution of endogenous PGE2 synthesized in the vascular wall to the vascular reactivity to norepinephrine is, as well as the effect of exogenous PGE2, different in different vascular beds.

Animals↗
PubMed1979

Follow-up studies on the distribution of haemoglobin levels in female farm workers.

Haemoglobin concentrations in about 1000 women agricultural workers in Japan were measured every year, except in 1972, during the period 1967-77. Improvements were noted in the course of this investigation, and these were predominantly associated with the fact that those in the study community began to pay attention to the problem of low haemoglobin levels and to improve their diet, with an increase in daily food intake, particularly of animal protein and iron. In addition, a marked decrease in anaemia caused by hookworm also played an important role. In this paper, the change in haemoglobin concentration during the period of study are described and the aetiology is discussed.

Adult↗
PubMed1978

Effect of estrogen upon the juxtaglomerular apparatus and the renin-angiotensin system in rats.

Administration of 1.5 mg/kg of estriol intramuscularly and 15 mg/kg of stilbestrol disulfate intraperitoneally daily for 15 days caused an increase in plasma renin substrate (PRS), accompanied by an increase in plasma renin activity (PRA) and a slight decrease in plasma renin concentration (PRC). Contrary to the slight suppression of PRC, juxtaglomerular granulation index (JGI) was significantly increased in rats treated by estrogen. In the rats which developed hypertension by estrogen PRA, PRC and JGI were a little higher than those in the rats which remained normotensive after the same estrogon treatment, but these differences were not statistically significant. Therefore, it seems rather difficult to attribute the development of estrogen hypertension only to the quantitative changes in the renin-angiotensin system.

Angiotensins↗
PubMed1976

Effects of furosemide and chlorothiazide on blood pressure and plasma renin activity.

Short (2 weeks) and long (12 weeks) term effects of furosemide and chlorothiazide on blood pressure, plasma renin activity, and uric acid concentration were studied in 69 hypertensive patients. Both treatments caused significant reductions in blood pressure and increases in plasma renin activity and uric acid at 2 and 12 weeks in 6) normal renin patients; there was no difference between the effects of furosemide and that of chlorothiazide. Reduction in blood pressure in eight low renin patients who showed smaller changes in plasma renin activity and uric acid was not significant at 2 weeks but significant after 12 weeks of treatment.

Adult↗