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Biomedical subjects

K Ogino

Publications and source records attributed to K Ogino.

At least 217 records · Page 12Linked to original sources
PubMed1979

Pathophysiological studies on hypertension induced in rats by kidney extract and salt.

The renin-angiotensin-aldosterone system, electrolyte and water balance, body fluid, and neurogenic tone and reactivity of the vasculature were studied in hypertension induced in uninephrectomized rats by repeated injection of renin-rich kidney extract and 1% saline drinking. The control rats were injected with physiological saline. Various measurements were made in conscious rats on the 10th day of the treatment. As compared with the control, plasma renin concentration and serum sodium increased significantly, while plasma aldosterone and renal excretory function did not differ. Blood volume (BV) expressed as per body weight increased significantly, but absolute BV, absolute or body weight-related plasma volume and hematocrit were not significantly different. The hypotensive effect of 1-Sar-8-Ile-angiotensin II was negligible 12 hours after the preceding injection of kidney extract. It was small but significant 1 hour after the injection. Increase in water turn-over and fractional sodium excretion occurred during the development of hypertension. Spironolactone did not significantly modify the developmental course. We observed increased depressor response to hexamethonium and increased reactivities to noradrenaline and angiotensin II (A II); these response curves relatively resembled those of spontaneously hypertensive rats. Hypertensive vascular changes were seen in the kidney and heart by histology. Thus, it was suggested that a direct vascular action of A II played a partial role in this hypertensive process while aldosterone played little role. The significance of BV increase and possible contribution of A II's other actions were discussed.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1979

Cryoactivation of inactive renin in human plasma.

The mechanism of the increase in renin activity in human plasma which had been kept -5 degrees C for 4 days (cryoactivation) was investigated. From the results of clinical studies, it is likely that the controling mechanism of inactive renin has something in common with that of active renin. The experimental data showed that the increase in renin activity of human plasma by cryoactivation was closely correlated to the increase obtained by incubation with trypsin (r = 0.88, p less than 0.001, n = 10). Soybean trypsin inhibitor, aprotinin and di-isopropylfluorophosphate (DFP) inhibited cryoactivation, indicating that the cryoactivation is due to the action of a trypsin-like serine enzyme. Trypsin which had no effect on plasma renin activity in the presence of the same amount of soybean trypsin inhibitor at 37 degrees C, activated the renin activity during cold incubation, suggesting that the dissociation of the trypsin-inhibitor complex may have taken place at a low temperature. Endogenous trypsin inhibitor is also likely to lose its affinity to endogenous trypsin-like enzyme at a low temperature.

Cold Temperature↗
PubMed1979

[Treatment of Diphyllobothrium latum and Taenia saginata infections with aminosidine (author's transl)].

Recently, it has been known that the aminosidine has marked anthelmintic efficacy against tapeworm. In this investigation, aminosidine was used for treating 14 cases with Ciphyllobothrium latum infection and 5 cases with Taenia saginata infection. Aminosidine was administered orally in a single dose of 50 mg/kg, followed by a purge after the treatment. Fourteen patients with D. latum infection and 5 patients with T. saginata infection expelled long strobila in all cases. Although only 7 scolices of 18 worms of D. latum were found in the stool and no scolex of T. saginata was found, follow-up examination for a long period showed no evidence of remaining infection with one exception of D. latum. Mild nausea, vomiting and abdominal pain were observed in only one of 19 cases given aminosidine. But in the other 18 cases, no side effects were encountered. It was concluded that aminosidine is safe, effective therapeutic agent for the treatment of cestodiasis in man.

Adolescent↗
PubMed1978

Cryoactivation of plasma renin.

1. The mechanism of increased renin activity after human plasma had been kept at -5 degrees C for 4 days (cryoactivation) was investigated. 2. The increase in renin activity of human plasma by cryoactivation was closely correlated to the increase obtained by incubation with trypsin (r = 0.88, P less than 0.001, n = 10). 3. An inhibitor of thiol enzyme, N-ethylmaleimide did not inhibit cryoactivation. 4. Soyabean trypsin inhibitor and di-isopropylflurophosphate (DFP) inhibited cryoactivation, suggesting that the cryoactivation may be due to the action of a trypsin-like serine enzyme. 5. In an experiment in the rat haemorrhagic shock caused parallel and cryoactivated plasma, the renin activity being about two times higher in the latter. No significant differences were found in the concentrations of renin and renin substrate between the non-cryoactivated and cryoactivated plasma samples. 6. The results may indicate that a destruction of an inhibitor of the renin-renin substrate reaction is responsible for the increase of renin activity after exposure of rat plasma to low temperature. A trypsin-like enzyme in plasma might have destroyed the inhibitor during this procedure.

Animals↗
PubMed1977

Effects of beta-adrenergic blocking agents on the blood pressure, plasma renin activity and hemodynamics of hypertensive patients.

Changes in blood pressure, plasma renin activity, and hemodynamic components were studied in 23 patients with essential hypertension treated with oral pindolol or propranolol. These beta-adrenergic blocking agents effectively lowered the blood pressure in the majority of the patients. Although plasma renin activity was not significantly changed, the higher was the pretreatment level, the more it tended to be decreased. Systemic vascular resistence was significantly decreased, while changes in cardiac index and circulating blood volume were variable. Pindolol showed less effect in reducing the heart rate than propranolol. The antihypertensive effect of these drugs had no correlation with the change in plasma renin activity or in any one of hemodynamic components.

Adrenergic beta-Antagonists↗
PubMed1977

Effect of propranolol on blood pressure and plasma renin concentration in renovascular hypertensive rats.

The effect of chronic oral administration of propranolol (39--80 mg/Kg/day, for 21--27 days) on blood pressure, plasma renin concentration, and heart rate were studied in 2 types of renovascular hypertensive rats; one-kidney type with normal plasma renin and two-kidney type with high plasma renin. No significant change was observed in the blood pressure of either model during the administration of propranolol in spite of a significant reduction of heart rate. Plasma renin concentration showed a trend of suppression in two-kidney type rats, but this change was not significant. There was no suppression in one-kidney type rats. These results suggest that the beta-adrenergic system may not play a major role either in regulating plasma renin level or in maintaining the blood pressure in renovascular hypertensive rats.

Animals↗
PubMed1976

Vascular lesions in hypertensive rats under salt loading: kidney renin and lysosomal enzymes.

1. Renal and cerebral vascular lesions occurred more often and earlier in spontaneously hypertensive rats (SHR) given a high salt diet than in SHR given a normal diet. 2. Kidney renin activity was low during high salt loading; the kidney renin activity of rats with hypertensive renal vascular lesions was moderately elevated. Kidney renin activity or cathepsin D activities were higher in stroke-prone SHR (SHRSP) aged 9 months than in stroke-resistant SHR (SHRSR). 3. beta-Glucuronidase, cathepsin D and deoxyribonuclease activities were greater in the kidney of Wistar/Kyoto (WK) rats or SHR when there were hypertensive vascular lesions. These three enzyme activities were also greater in the aorta of SHR aged 13-14 months than in the aorta of WK rats. 4. It was supposed that kidney renin activity and lysosomal enzyme activities were related to hypertensive vascular lesions.

Animals↗
PubMed1976

Column chromatographic analysis of relationship between hypertension-inducing potency and renin content of kidney extract.

The relationship between hypertension-inducing potency and renin content of kidney extract was analyzed in rats using Sephadex G-100, CM-Sephadex C-50, DEAE-Cellulose or Concanavalin A-Sepharose column chromatography. Hypertension-inducing potency of each fraction obtained was evaluated in the basis of the final blood pressure level attained by repeated injections into the test animals for 10 days. Hypertension-inducing potency was found mainly in the renin-contaning fractions. And it seems reasonable to conclude that renin is implicated in the pathogenesis of hypertension produced by kidney extract. However, there were significant discrepancies between hypertension-inducing potency and renin content of subdivided fractions of these renin-containing eluates. Possible explantations for the discrepancies disclosed--including the possibility of the involvement of an unknown substance(s)--have been discussed. In addition, it was suggested from the results of Concanavalin A-Sepharose chromatography that rat renal renin has a glycoprotein nature.

Animals↗
PubMed1976

Plasma renin and vascular complications in substrains of the spontaneously hypertensive rat, with a reference to water and electrolyte balance.

The stroke-prone and stroke-resistant substrains of the spontaneously hypertensive rat (SHR) were employed for an evaluation of possible role of reninangiotensin system and of water and electrolyte balances in inducing hypertensive vascular lesions. Serial study on plasma renin level and vascular changes did not support the hypothesis that plasma renin is a major risk factor in the development of cardiovascular complications. The high plasma renin level seen in advanced stages of hypertension appeared to be a result of severe vascular damages, indicating malignant transformation of hypertension. In this state, water turnover was enhanced without any abnormality in electrolyte balances. A possible mechanism involved in the malignant course of hypertension is discussed.

Animals↗
PubMed1976

Irreversible inhibitory effect of atropine on contractile responses to drugs in isolated rabbit ileum.

Effect of atropine sulfate (atropine) on the contractile responses to acetylcholine chloride (ACh), potassium chloride (K) and barium chloride (Ba) was investigated in isolated rabbit ileum. Tension of the strips suspended in the bath medium (Locke solution, 30 degrees C) was isotonically recorded. The K(ED50)- and Ba(ED50)-induced contractions were not affected by atropine at 3.0 X 10(-4) mM, which reversibly abolished the ACh(ED100)-contraction. After washout of 6.0 X 10(-4) mM atropine, the phasic, but not the tonic, component of ACh(ED50)-, K(ED50)- and Ba(ED50)- contractions was to some extent inhibited irreversibly. On the contrary, such irreversible inhibition of the phasic component was not produced by atropine methylbromide even in the high concentration of 3.0 X 10(-3) mM. The irreversible inhibitions by atropine of 6.0 X 10(-4) mM on the phasic component of ACh- and K-contractions were protected by pretreatment with a high concentration of ACh or K. Further, these irreversible inhibitions by atropine were potentiated by the absence of Ca and were abolished by the increase of Ca content in bath media. These results suggest that the irreversible inhibition of the contractile responses to drugs by atropine in high concentration may be due to the interference with the mobilization of Ca in the deep layer of the membrane, rather than by a blockade of muscarinic receptor sites.

Animals↗