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Biomedical subjects

T Noshiro

Publications and source records attributed to T Noshiro.

46 records · Page 3Linked to original sources
PubMed1988

A plasma inhibitor of sodium and potassium activated adenosine triphosphatase in patients with essential hypertension.

The purpose of this study is to evaluate the plasma Na, K-ATPase inhibitor (NKI) in patients with essential hypertension and to compare the mode of its biochemical actions on the Na, K-ATPase with that of ouabain. Plasma NKI was extracted through a reversed-phase cartridge column and its inhibitory action on hog brain Na, K-ATPase was measured in vitro. Plasma NKI activity was significantly greater in patients with essential hypertension (44 +/- 2.8% (S.E.), n = 28, p less than 0.01) than in normotensive controls (25 +/- 2.4%, n = 21). No significant correlation was demonstrated between the values of plasma NKI and mean arterial pressure in either group. Both plasma NKI and ouabain showed a dose-dependent inhibition on the Na, K-ATPase reaction. An action of ouabain was competitively antagonized by increased concentration of potassium in the reaction mixture, while plasma NKI showed a constant inhibition on the Na, K-ATPase independently of potassium concentrations. The action of plasma NKI was of rapid onset and linear with time, while ouabain showed a delayed onset of the reaction over 30 sec, followed by a progressively increasing inhibition on the enzyme reaction. Finally, the inhibitory action of plasma NKI on Na, K-ATPase was completely abolished in the presence of bovine serum albumin even at the concentration of 500 micrograms/ml in the reaction mixture, which did not have any influence on the actions of ouabain. To sum up, the results showed a markedly different nature of plasma NKI from ouabain in the mode of biochemical actions on the Na, K-ATPase in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

The baroreflex-mediated changes in plasma norepinephrine and heart rate in patients with essential hypertension.

Baroreflex sensitivity was evaluated in 19 patients with essential hypertension (EH), 8 patients with borderline hypertension (BH) and 12 age-matched normal controls (N), by measuring the reflex-mediated changes in plasma norepinephrine (NE) and heart rate (RR interval) while a phenylephrine hydrochloride or a sodium nitroprusside solution was infused in graded doses for a total of 24 minutes. Changes in RR interval and plasma NE showed a significant linear correlation to those in mean arterial pressure (MAP) in every subject studied. The slopes of RR/MAP and %NE/MAP tended to be reduced in EH and BH patients during both pressor and depressor stimulations. There was a significant (p less than 0.01) inverse correlation between the basal MAP levels and RR/MAP or %NE/MAP except for %NE/MAP during pressor stimulation. Fifteen minutes after the pressor stimulation was stopped, MAP and RR interval in each group tended to be greater than their baselines. Plasma NE remained significantly (p less than 0.01) depressed in N and BH subjects while those in EH returned to their baselines. When pressor stimulations were repeated twice at intervals of 15 minutes in hypertensive subjects, the second response curves of MAP-RR interval tended to shift slightly to the right while the slopes of the second response curves of plasma NE were significantly (p less than 0.05) reduced compared with the first ones. These findings indicate that an inability of the baroreflex to produce a sustained suppression of sympathetic nerve activity associated with an efficient ability to reset at the higher pressure levels in EH patients results in a continued tendency for blood pressure to rise and contributes to the development of hypertension.

Adult↗
PubMed1986

[Plasma dopamine concentrations in various types of hypertension].

The concentrations of unconjugated plasma dopamine (PDA) were studied in patients with various types of hypertension. Catecholamines were extracted from plasma specimens (1.0-3.0 ml) through an Amberlite CG50 (Li+-form) microcolumn and eluted by a magnesium sulfate - ethanol solution. The elute was then desalinated and deproteinized by the ethanol-treated precipitation procedure and dried in a vacuum oven at 25 degrees C. A fraction of catecholamines was assayed with the modified procedures of the COMT-mediated radio-enzymatic method. This assay system was sensitive enough to permit an accurate measurement of PDA as low as 6.0 pg per ml of plasma without any detectable contamination of the conjugated dopamine. The resting levels of PDA were 10.1 +/- 1.0 pg/ml (mean +/- SEM), 9.5 +/- 1.0 and 13.7 +/- 0.6 in patients with borderline hypertension (BH, n = 25), essential hypertension (EH, n = 22) and renovascular hypertension (RVH, n = 8), respectively. The values in EH patients were significantly smaller than those in age-matched normal controls (13.0 +/- 1.4, n = 14, p less than 0.05). Remarkably increased PDA values were observed in patients with pheochromocytoma (76.5 +/- 25.4, n = 9, p less than 0.01). Significantly raised PDA values were also found in patients with primary aldosteronism (PA, 27.8 +/- 9.0, n = 6, p less than 0.05), while their plasma norepinephrine levels (PNE, 169 +/- 39 pg/ml) tended to be lower than those of normal controls (206 +/- 20), showing an apparent dissociation between the values of PDA and PNE. Upright posture for 15 minutes induced a significant rise in PDA (p less than 0.05) in all subjects except PA patients. The postural changes of PDA, however, were invariably smaller than those of PNE (p less than 0.05). The resting values of PDA in normal, BH and EH patients showed a significant negative correlation with their mean arterial pressures (r = -0.301, n = 61, p less than 0.05) and a positive correlation with those of PNE (r = 0.381, p less than 0.01). There was no correlation between PDA and age in any group studied. These findings indicate that PDA might not be only a precursor fraction of neurotransmitters released from the sympathetic nervous system but could also represent a physiological function of the dopaminergic regulatory system. The varied but distinctive features of PDA status in various types of hypertension suggest the possibility that the peripheral dopaminergic mechanisms play an inherent role in the pathogenesis of hypertension.

Adult↗
PubMed1985

Effects of dietary potassium on the hemodynamics and plasma norepinephrine kinetics in patients with essential hypertension.

The effects of dietary potassium on the hemodynamics and plasma norepinephrine (NE) kinetics were studied in 10 patients with borderline hypertension. Potassium supplement (96 mEq daily for 5-7 days) induced a significant (p less than 0.05) fall in blood pressure and a slight decrease in cardiac output. Both urine volume and urinary sodium excretion increased significantly (p less than 0.05) for a first few days following the potassium supplement. The baseline values of the half-time of the rapid NE removal from plasma was significantly delayed in the hypertensive patients (1.05 +/- 0.06 min, p less than 0.05) when compared with those (0.88 +/- 0.04) in normal controls. Potassium supplement induced a significant rise in both plasma NE levels and NE outflow rate (p less than 0.01) in the hypertensive patients, while their half-times were significantly shortened (0.89 +/- 0.07 min, p less than 0.01). The pressor responsiveness to exogenously infused NE tended to diminish during the potassium supplement. These findings indicate that a high potassium intake might accelerate the slowed neuronal NE uptake in the hypertensive patients, while a potassium-induced fall in blood pressure might exert a baroreflex stimulation of NE release. As a net result, an increased NE outflow into the circulation has been confirmed. It is likely that a natriuresis-induced volume contraction might be a predominant factor responsible for the early reduction of blood pressure during the high potassium intake.

Adult↗
PubMed1983

The effect of sodium depletion on plasma norepinephrine kinetics in patients with essential hypertension.

The effects of sodium depletion on plasma norepinephrine (NE) kinetics were studied in 14 patients with essential hypertension using the steady state NE infusion technique on the theoretical basis of a two-compartmental open model. The calculated half time of rapid removal phase (t 1/2 alpha) of plasma NE was significantly delayed in the hypertensives (1.20 +/- 0.22 min, mean +/- SD) than in normal subjects (0.89 +/- 0.14) (p less than 0.01). The total clearance rates were comparable between the 2 groups (47 +/- 7 vs 48 +/- 11 ml/kg/min). The rates of the endogenous NE outflow into the circulation (RE-NE) were not significantly different between normal (5.29 +/- 1.68 ng/kg/min) and hypertensives (7.69 +/- 5.42), although 5 hypertensive patients (36%) showed an increased RE-NE above the normal range. The prolonged half time (t 1/2 alpha) in the hypertensives tended to be shortened after sodium depletion induced by either low sodium diet or diuretics (1.04 +/- 0.22, p less than 0.001). Both plasma NE and RE-NE were significantly increased after sodium depletion. A close correlation was observed between plasma NE and RE-NE (r = 0.907, p less than 0.001) in these subjects. These results suggest the slowed neuronal uptake of NE at the sympathetic nerve terminals in some patients with essential hypertension, occurring in part as a sodium-mediated consequence.

Adolescent↗
PubMedDate not supplied

Effects of isotonic saline loading on renal tubular and neurogenic dopamine release in conscious rabbits.

1. This study was designed to investigate the effects of isotonic saline loading on renal tubular and neurogenic dopamine (DA) in conscious rabbits. 2. Isotonic saline loading did not affect mean arterial pressure, heart rate or renal blood flow but markedly increased urine volume, sodium excretion and DA excretion. 3. Renal DA spillover was not affected by venous emptying, while renal noradrenaline (NA) spillover tended to decrease during saline loading. The ratio of % renal DA spillover to % renal NA spillover increased to 2.3 +/- 0.6 (P < 0.05) 3 h after saline loading. 4. Isotonic saline loading increased renal tubular DA production but had little effect on neurogenic DA release.

Analysis of Variance↗