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Biomedical subjects

R Nakamura

Publications and source records attributed to R Nakamura.

At least 505 records · Page 28Linked to original sources
PubMed1978

Renin and the juxtaglomerular apparatus in diabetic nephropathy.

In order to study the role of the renin-angiotensin system in patients with diabetic nephropathy, renin release and the juxtaglomerular apparatus were studied in 17 diabetic patients with proteinuria and in 23 without proteinuria; 8 normal subjects were used for conctrls. Despite hypertension and marked arteriosclerosis, plasma renin activity (supine posture) was normal; however, the renin response to salt restriction and upright posture was less in the diabetic patients with proteinuria than in the controls. Renal renin content, determined at autopsy, was also normal. Examination of the juxtaglomerular apparatus in the diabetic patients with proteinuria revealed hyalinization of the afferent and efferent arterioles in most of the glomeruli and various degrees of destruction of the juxtaglomerular cells. The findings suggest that renin production is not increased in diabetic patients with proteinuria plus marked vascular damage, and that the renin-angiotensin system in patients with diabetic nephropathy apparently does not play an important role in the exacerbation of hypertension or the degree of vascular damage.

Adult↗
PubMed1978

Serum uric acid and the renin-angiotensin system in hypertension.

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.

Adolescent↗
PubMed1978

Hypertension induced by adrenocortical dysfunction--hypertension in 17 alpha-hydroxylase deficiency and metopirone-induced hypertension.

Hypertension in 17 alpha-hydroxylase deficiency was studied by comparing it with hypertension in Cushing syndrome or that in primary aldosteronism. Furthermore, the role of endogenous increases of ACTH, deoxycorticosterone, and 18 alpha-hydroxy-deoxycorticosterone upon blood pressure was studied in rats by administerating metopirone. Hypertension in 17 alpha-hydroxylase deficiency was considered to be more similar to that in primary aldosteronism from the studies on renin components, pressor responses to angiotensin II and norepinephrine, and renin responses to stimulations. Plasma catecholamines were slightly decreased in 17 alpha-hydroxylase deficiency. The hypertension was alleviated by the administeration of dexamethasone in 2 of 3 patients with 17 alpha-hydroxylase deficiency. However, in the remaining one who had an accelerated hypertension and normal renin, the hypertension was not alleviated by dexamethasone. In the animal studies, hypertension induced by metopirone was accelerated by salt loading of uni-lateral nephrectomy plus salt loading. In those rats, plasma ACTH, and deoxycorticosterone were markedly increased.

Adrenal Hyperplasia, Congenital↗
PubMed1978

Role of renin-angiotensin system in the controls of blood pressure and aldosterone in patients with cirrhosis and ascites.

In an attempt to evaluate the role of renin-angiotensin system in the contols of blood pressure and aldosterone secretion in the patients with cirrhosis and asictes, 7 patients were infused of an antagonist of angiotensin II, Sar-1 Ile-8 angiotensin II, intravenously to inhibit the action of renin-angiotensin system and to observe changes in arterial pressure and plasma aldosterone. In 1 patient with recent onset of severe ascites and high plasma renin activity, blood pressure and plasma aldosterone decreased during the infusion. In contrast, mild rise in blood pressure and various changes in plasma aldosterone were observed in the other 6 patients with normal plasma renin activity. These results suggest variable angiotensin dependency in the controls of blood pressure and plasma aldosterone in the patients with cirrhosis and ascites according to the stage of the disease, the states of sodium and water balance and/or palasma renin activity.

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↗
PubMed1978

Disturbances of rhythm formation in patients with Parkinson's disease: part I. Characteristics of tapping response to the periodic signals.

A tapping test in which the tasks required a synchronous response to a periodic sound signal by the finger tapping was performed by 27 normal subjects and 146 patients with Parkinson's disease. Some patients could not maintain a synchronous response at a critical frequency of 2.5 or 5 Hz (taps per second) and showed a hastened tapping of 5 6 Hz, independent of the input signal frequencies, i.e., the 'hastening phenomenon.' The other patients and normal subjects could respond synchronously up to 5 7 Hz. Autocorrelational analysis of the sequential tapping intervals suggested that the synchronized response was performed by a feedback control with the input signal as target except at 2.5 and 5 Hz, whereas the hastened tapping of patients was a random process. The frequency-dependence of the error in the tapping was interpreted as representing an intrinsic oscillation in the central nervous system, which would be masked in normal subjects but released in patients with Parkinson's disease. Around 2.5 or 5 Hz the error or response becomes so large that some patients can no longer maintain the synchronized response and show a hastened tapping due to this intrinsic oscillation.

Acoustic Stimulation↗
PubMed1978

Disturbances of rhythm formation in patients with Parkinson's disease: part II. a forced oscillation model.

The origin of the characteristic disturbances of rhythm formation in patients with Parkinson's disease (the hastening phenomenon) was discussed, using a second-order system of the periodic response. The input signal was regarded as a pulse series of a Dirac function. The output process of the system had maximal errors of response at input frequencies of f = omega0/n (n = 1, 2, . . .), where omega0 was the intrinsic frequency of the system. Damping coefficient epsilon represented a function of an inhibitor against these maximal errors and the errors diverged to infinity when epsilon = 0. The solution of this forced oscillation system indicated that the intrinsic oscillation of the system has a possibility to be excited at these critical frequencies f = omega/n. Inferred from data on the tapping test, the frequency of an intrinsic oscillation was 5 Hz in the central nervous system, then the critical frequencies were predicted 5/n = 5, 2.5, . . . Hz. On the tapping test the errors of response become maximum around 2.5 and 5 Hz (taps per second), and their peak heights increased from the minimum in well trained normal subjects to the maximum in patients. An inhibitory mechanism against the maximal error would function well, i.e. epsilon greater than 0, in normal subjects but so insufficiently (epsilon leads to 0) in patients that the excited intrinsic oscillation would control their response directly. Thus some patients could no longer maintain a synchronous tapping response at 2.5 Hz or 5 Hz and showed a hastened tapping of 5 6 Hz independent of the signal frequency.

Central Nervous System↗
PubMed1977

Lactose synthase activity of galactosyltransferase from human parotid saliva.

Galactosyltransferase is human parotid saliva catalyzed the transfer of galactose from uridine 5'-diphospho (UDP)-galactose to D-glucose in the presence of exogenous alpha-lactalbumin. Some albumins other than alpha-lactalbumin did not have an effect on the appearance of lactosesynthesizing activity.

Galactosyltransferases↗
PubMed1977

Effects of angiotensin III (DES-1-asp-angiotensin II) and angiotensin III analogue (DES-1-asp-8-ile-angiotensin II) upon adrenal steroidogenesis and blood pressure.

Effects of angiotensin III and angiotensin III analogue upon adrenal steroidogenesis and blood pressure were studied in rats, rabbits and a man. Pressor effect of angiotensin III was about one fifth of that of angiotensin II in all the species. Degradation rate of pressor effect of angiotensin III in plasma was more rapid than that of angiotensin II. Different from the effects of angiotensin III upon blood pressure, its effect upon aldosterone was similar to that of angiotensin II. The effect of angiotensin III upon other adrenal steroids, such as DOC and cortisol, however, seemed to be slightly less than that of angiotensin II. Angiotensin III producted an additive effect to that of ACTH, but it didn't produce an additive effect to that of angiotensin II. Angiotensin III analogue, itself, stimulated adrenal steroidogenesis, but it inhibited the effects of angiotensin III and angiotensin II upon aldosterone. Effects of ACTH upon plasma DOC and cortisol were not inhibited by angiotenesin III analogue, but the effect of ACTH upon aldosterone was blunted slightly.

Adrenal Cortex↗
PubMed1977

Reaction time in simultaneous motions.

EMG-RTs of biceps and triceps brachii muscles were measured in 3 different tasks: isolated motions, flexion or extension of either forearm; bilateral symmetrical motions, flexion or extension of both forearms; bilateral opposite motions, flexion of a forearm and extension of the other. EMG-RTs of opposite motions were slower than those of isolated and symmetrical motions, EMG-RTs of symmetrical motions were nearly equivalent to those of isolated motions. Simplicity and complexity of simultaneous motions are discussed.

Adult↗