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Biomedical subjects

R Nakamura

Publications and source records attributed to R Nakamura.

At least 487 records · Page 27Linked to original sources
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↗
PubMed1980

Dependence of EMG-reaction times of the rectus femoris on position changes of the hip joint--role of the joint capsule.

EMG-reaction times (EMG-RTs) of the rectus femoris in midposition (M) and internally rotated position (IR) of the right hip joint were examined in nine control subjects and nine patients who had lost most of the capsule of a hip joint after total hip joint replacement procedure. In both groups EMG-RTs of the rectus femoris were faster at IR than at M. The difference of EMG-RTs between M and IR was essentially the same in the two groups. It is assumed that information from proprioceptors in the joint capsule may not play an important role in postural dependence of EMG-RTs of the muscle.

Adult↗
PubMed1980

Dependence of reaction times on movement patterns in patients with Parkinson's disease and those with cerebellar degeneration.

Premotor times (PMTs) of both biceps muscles in flexion and supination of the forearms were examined in 13 patients with Parkinson's disease (PD), 10 with cerebellar degeneration (CD) and 14 control subjects. Compared with the control, PMT of CD increased definitely but that of PD was within normal range. The difference of PMTs between flexion and supination was lost in PD, but not in CD. It is assumed that the basal ganglia and the right cerebral cortex are functioning for the selection of movement patterns at the initiation of movements.

Adult↗
PubMed1980

Interaction of parotid saliva basic glycoprotein with Streptococcus sanguis ATCC 10557.

It is postulated that an initial step in dental plaque formation is the adherence of oral bacteria to the salivary pellicle. Recently, we have found that a proline-rich and basic glycoprotein (MGP) from human parotid saliva, which is successfully purified by Concanavalin A-Sepharose affinity chromatography, binds to some oral streptococci such as S. mitis and S. sanguis. This paper deals with some inhibitors which affect the binding of the MGP to S. sanguis ATCC 10557. The assay for the binding ability of the radioactive MGP to the bacterial cells was performed by incubation of the reaction mixture containing 10 microgram of [3H]MGP (6000 dpm) and about 4.5 mg of bacterial cells (dry weight) in 0.5 ml of 0.05 M Tris-HCl buffer containing 0.05 M NaCl, pH 8.0 with a final volume of 0.51 ml. After 1 hour standing at 4 degrees C, the cells were washed five times with the same buffer. The resulting sediment was solubilized in 0.5 ml of NCS tissue solubilizer and the radioactivity was measured. The binding of the radioactive MGP to bacterial cells was specifically inhibited by galactose, lactose and N-acetyllactosamine. Applications of heat and trypsin on the cell surface, strikingly reduced the binding ability. These findings strongly suggested that a lectin-like substance may be present on the bacterial cell surface.

Adult↗
PubMed1980

Influence of 6 alpha-methylprednisolone 21-sodium succinate on the pituitary, adrenal glands, and the gastrointestinal tract in rats. (Comparative toxicity study with hydrocortisone 21-sodium succinate).

A comparative toxicity study with 6 alpha-methylprednisolone 21-sodium succinate (MPS) and hydrocortisone 21-sodium succinate (HCS) was carried out on male rats of the Wistar strain. MPS and HCS were administered intravenously to rats in dose levels of 20 or 100 mg/kg/day for 14 days. There were no significant differences in the pituitary weights in MPS and HCS groups, but weight of the adrenal glands decreased with increasing dose levels of MPS and HCS. Histopathological examination of MPS and HCS treated rats revealed atrophy of the zona fasiculata in the adrenal cortex which correlated with dose levels. The decline of serum corticosterone levels in rats correlated with increasing dose levels of MPS and HCS. It can be concluded that the inhibitory effect of MPS on the pituitary-adrenal system in rats was the same as HCS. No ulceration was observed in the gastro-intestinal tract of MPS of HCS treated rats.

Adrenal Glands↗
PubMed1980

Bacteremia in post-Cesarean section endomyometritis: differential response to therapy.

Presented are blood culture results obtained from 200 patients with post-cesarean section endomyometritis treated with either penicillin-gentamicin or clindamycin-gentamicin. Their clinical course is correlated to their blood culture results by the fever index. Fifty-three percent of the 60 organisms isolated from 48 patients were anaerobic bacteria. Patients from whose blood cultures anaerobic bacteria were recovered had higher fever indexes than did those with aerobic isolates (P less than .05). Clindamycin-gentamicin patients from whose blood cultures anaerobic organisms were isolated had less febrile morbidity than did comparable penicillin-gentamicin patients. Patients with Bacteroides fragilis bacteremia had the highest fever indexes overall. Therefore, patients with post-cesarean section endomyometritis have less febrile morbidity if they are initially treated with a drug effective against anaerobic bacteria, especially B fragilis.

Anti-Bacterial Agents↗
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

Active and inactive renin in pregnancy and in women on estrogen-containing oral contraceptives.

Total and active renin concentrations (TRC and ARC) were determined in pregnant women and in women on estrogen-containing oral contraceptives to study the variation of plasma renin forms in pregnancy. TRC was already elevated in the first trimester. After that TRC increased consistently reaching the maximum in the third trimester. The ratio of inactive renin concentrations (IRC) to TRC was between 20 and 30% throughout gestation. Therefore, it was supposed that the development of the placenta or the enlargement of the uterus do not affect the ratio of IRC to TRC too much. In women on oral contraceptives in whom plasma renin activity was increased due to elevation of renin substrate, the ratio of IRC to TRC was almost the same as that in normal controls. From these results, it was suggested that the development of the placenta and the enlargement of the uterus do not play an important role in the variation of plasma renin forms, although remarkable changes are observed in the renin substrate and total amounts of renin in pregnancy.

Adult↗
PubMed1979

Central hypertensive actions of angiotensin I, II and III in conscious rats.

The effects of intracerebroventricular administrations of three natural angiotensins, angiotensin I (ANG I 3.8 X 10-11-9.4 X10-10 mol/kg body weight), II (9.6 X 10-12-2.4 X 10-10 mol/kg body weight) and III (2.7 X 10-10 2.5 X 10-9 mol/kg body weight) on systemic blood pressure were investigated in conscious rats. Angiotensin II (ANG II), ANG I and angiotensin III (ANG III), increased blood pressure in a dose-related manner. The order of potency of angiotensins was ANG II greater than ANG I greater than ANG III. The intraventricular administration of a converting enzyme inhibitor (SQ 14225, 6.9 X10-8 mol/kg) abolished the central effect of ANG I, while an angiotensin II analogue ([Sar1-Ala8]ANG II, 1.1 X 10-8 mol/kg) administered intraventricularly inhibited the central pressor effects of these three angiotensins. These results suggest that ANG II is a main mediator of the renin-angiotensin system in the central nervous system.

Angiotensin I↗
PubMed1979

Responses of aldosterone-producing adenomas to ACTH and angiotensins.

To elucidate the control mechanism of aldosterone production in primary aldosteronism, in vivo and in vitro studies were done in 7 patients with aldosterone-producing adenomas. In the in vivo study, plasma aldosterone was stimulated more significantly by (Formula: see text), synthetic ACTH than by angiotensin II or furosemide. Diurnal variations of plasma aldosterone, which were studied in 4 patients, were similar to those seen in normal controls. In agreement with the results in the in vivo study, the in vitro study also revealed ACTH stimulated aldosterone and deoxycorticosterone (DOC) from the adenoma more markedly than angiotensin II or III. There was no adenoma which was more sensitivie to angiotenion II or III than to ACTH. From these results it is considered that changes in plasma aldosterone induced by the exogenous administration of angiotensin II or ACTH in patients with aldosterone-producing adenoma are mainly based on changes in aldosterone production in the adenoma. Furthermore, in patients with an aldosterone-producing adenoma in whom diurnal variations of plasma aldosterone similar to those in normal subjects are observed, responses of aldosterone to angiotensin II are supposed to be less than those to ACTH.

Adenoma↗