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T Saruta

Publications and source records attributed to T Saruta.

At least 361 records · Page 20Linked to original sources
PubMed1992

Effects of antihypertensive agents on arterial baroreceptor reflexes in conscious rats.

The effects of antihypertensive treatment with four currently used agents (trichlormethiazide, atenolol, nicardipine, and enalapril) on the arterial baroreceptor reflex control of renal sympathetic nerve activity and heart rate were investigated in 45 conscious spontaneously hypertensive rats and 37 age-matched Wistar-Kyoto rats. Antihypertensive agents were administered for 2 weeks beginning at 8 weeks of age to treat and prevent the development of hypertension. Blood pressure was reduced to a similar level (-13 +/- 3 mm Hg, p < 0.05) by each antihypertensive agent. Blood pressure, heart rate, and renal sympathetic nerve activity were recorded in the conscious state during phenylephrine and nitroglycerin ramp infusion. The gain in the baroreceptor reflex was determined from the maximum slope of logistic function curves. Untreated spontaneously hypertensive rats exhibited decreased sensitivity of reflex control of renal sympathetic nerve activity and heart rate (-1.78 +/- 0.07% of control/mm Hg and -2.16 +/- 0.05 beats per minute/mm Hg, respectively) compared with untreated Wistar-Kyoto rats (-3.62 +/- 0.18% of control/mm Hg, p < 0.01, and -3.46 +/- 0.11 beats per minute/mm Hg, p < 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Importance of atrial natriuretic hormone in an exaggerated natriuresis during acute sodium load in primary aldosteronism.

To elucidate the factors which contribute to the exaggerated natriuresis in primary aldosteronism, hemodynamic and hormonal changes induced by saline infusion (at a rate of 0.5 l/h for 3 h) were examined in 6 patients with primary aldosteronism, 13 with essential hypertension, and 8 normotensive subjects. After saline infusion, increases in urinary sodium excretion, glomerular filtration rate, atrial natriuretic hormone, and urinary dopamine excretion along with suppression of plasma renin activity and aldosterone were compared in the three groups. All three groups demonstrated similar increases in glomerular filtration rate, but patients with primary aldosteronism did not show changes in urinary dopamine excretion, plasma renin activity, and aldosterone, despite their increased excretion of sodium. The increase in plasma atrial natriuretic hormone was significantly greater in primary aldosteronism than in essential hypertension or normotensive subjects. No changes in blood pressure or heart rate were seen. These findings suggest that atrial natriuretic hormone might play a role in the exaggerated excretion of sodium in patients with primary aldosteronism.

Aldosterone↗
PubMed1992

Presence of aldosterone-like immunoreactivity in cerebrospinal fluid in normotensive subjects.

Accumulating evidence, including a wide distribution of specific receptors for aldosterone in the brain, has revealed a potential role of aldosterone in the central nervous system. However, whether or not aldosterone is present in cerebrospinal fluid remains unclear. We attempted to detect aldosterone in cerebrospinal fluid in 14 normotensive subjects. Cerebrospinal fluid was obtained by lumbar puncture. Aldosterone-like immunoreactivity was detected in cerebrospinal fluid (163 +/- 5 pmol/l, range 139-211 pmol/l) and was found to significantly correlate to both plasma aldosterone (r = 0.70, p less than 0.01) and plasma renin activity (r = 0.68, p less than 0.01). However, no significant relationship was found between aldosterone-like immunoreactivity in cerebrospinal fluid and the level of sodium or potassium in cerebrospinal fluid or mean blood pressure. Although we confirmed the presence of aldosterone-like immunoreactivity in cerebrospinal fluid of normotensive subjects, the physiological role of aldosterone in cerebrospinal fluid has yet to be elucidated. Further study will thus be needed to determine the role of cerebrospinal fluid aldosterone.

Adult↗
PubMed1992

Alpha-2 adrenergic agonism stimulates islet glucagon release from perfused rat pancreas: possible involvement of alpha-2A adrenergic receptor subtype.

Although insulin release is known to be inhibited by alpha-2 adrenergic agonism, the effect of alpha adrenergic agonism on islet glucagon release remains controversial. Alpha-2 adrenoceptors are subdivided into alpha-2A and alpha-2B subtypes using receptor binding methods or cloning methodology. This study was designed to confirm the involvement of the alpha-2 adrenoceptor and its subtypes in glucagon release from the isolated, perfused rat pancreas. Both the alpha-2A preferential agonist oxymetazoline and the non-subtype-selective alpha-2 agonist clonidine induced concentration-dependent stimulation of glucagon release, starting at 10(-8) and 10(-7) mol/l, respectively (p < 0.01). In contrast, neither of the two alpha-1 selective agonists, methoxamine and phenylephrine, at concentrations up to 10(-6) mol/l affected glucagon release. Furthermore, the non-subtype-selective alpha-2 antagonist rauwolscine at concentrations of 10(-6) and 10(-5) mol/l and the alpha-1 and alpha-2A selective antagonist WB-4101 at 10(-5) mol/l showed significant antagonism of 10(-7) mol/l clonidine-induced glucagon release versus corresponding controls. Neither the alpha-1 and alpha-2B selective antagonist prazosin nor the alpha-2B preferential antagonist chlorpromazine, at concentrations up to 10(-5) mol/l, antagonized the effects of clonidine. None of the eight drugs, at the concentrations tested, affected insulin release with 5.5 mmol/l glucose. These results suggest that in rats islet glucagon release induced by alpha adrenoceptor agonism is mediated through alpha-2 adrenoceptors, possibly the alpha-2A subtype.

Adrenergic alpha-Agonists↗
PubMed1992

Effect of systemic L-arginine administration on hemodynamics and nitric oxide release in man.

The effects of L-arginine administration on systemic hemodynamics and plasma concentrations of neuro-endocrine hormones and amino acids were investigated in 10 normotensive healthy volunteers. Nitrite/nitrate in urine and cyclic guanosine monophosphate (c-GMP) in plasma were also measured as indicators of release of nitric oxide (NO). L-arginine administration (30 g/300 ml/30 min) caused hypotension (mean arterial pressure; 79.3 +/- 3.9 mmHg fell to 68.8 +/- 2.2 mmHg) with tachycardia (62.3 +/- 2.3 beats/min increased to 67.5 +/- 1.9 beats/min). The plasma concentration of L-arginine before administration was 98.8 +/- 8.2 mumol/l and increased to 7263 +/- 567 mumol/l 20 min after administration. Cardiac output also increased to 127.2 +/- 3.9% by L-arginine administration. Total peripheral resistance was calculated to fall to 65.9 +/- 2.0%. L-arginine administration slightly changed several hormones, but all values were within normal ranges. Nitrite/nitrate in urine increased 142.1 +/- 12.4% compared to the values before L-arginine administration. Plasma concentrations of c-GMP and L-citrulline, the by-product of NO from L-arginine, were also significantly increased by L-arginine administration. All our results provide evidence for the first time that systemically administered L-arginine releases NO in man.

Adult↗
PubMed1992

Glycyrrhizin induces mineralocorticoid activity through alterations in cortisol metabolism in the human kidney.

It has been suggested that the mineralocorticoid action of glycyrrhizin is caused by a defect in the conversion of cortisol to cortisone through inhibition of the enzyme 11 beta-dehydrogenase (11 beta-DH). We investigated the functional significance of the inhibition of this enzyme as a mechanism of the mineralocorticoid action of glycyrrhizin. Eighteen healthy volunteers were divided into three groups of six and treated as follows: (1) 225 mg glycyrrhizin/day, (2) 0.1 mg 9 alpha-fluorocortisol (FC)/day and (3) 225 mg glycyrrhizin and 1.5 mg dexamethasone/day, all of which were given for 7 days. The administration of glycyrrhizin or FC induced a similar mineralocorticoid effect; specifically, suppression of plasma renin activity, hypokalaemia and kaliuresis. During the concomitant administration of glycyrrhizin and dexamethasone, however, these mineralocorticoid effects were significantly attenuated. During the administration of glycyrrhizin, urinary excretion of cortisol increased without change in the plasma levels of cortisol, while both plasma level and urinary excretion of cortisone decreased. Changes in cortisol metabolism were not observed during the administration of FC. These results demonstrated the functional significance of the inhibition of 11 beta-DH in the mineralocorticoid activity of glycyrrhizin in man.

Cortisone↗
PubMed1992

Effects of manidipine on blood pressure and renal function in salt-loaded, spontaneously hypertensive rats.

The purpose of this study was to investigate the effects of 4-week oral administration of manidipine (40 mg daily), a newly developed calcium channel blocker, on blood pressure and renal function in salt-loaded (8% NaCl) spontaneously hypertensive rats. Systolic blood pressure of spontaneously hypertensive rats increased from 167 +/- 4 to 221 +/- 7 mmHg with salt loading for 4 weeks; manidipine completely prevented this elevation in blood pressure. Urinary excretion of sodium in salt-loaded spontaneously hypertensive rats was twelve-fold compared with those receiving a normal diet (0.38% NaCl). The pressure-natriuresis relationship was obtained during week 4 of the metabolic study. At similar renal perfusion pressures, sodium excretion was significantly higher in salt-loaded rats than in rats fed a normal diet. Glomerular filtration rate and renal plasma flow were similar between the two groups. In salt-loaded spontaneously hypertensive rats, treatment with manidipine improved the pressure-natriuresis relationship toward lower pressures. Further, manidipine attenuated the autoregulation of glomerular filtration rate and renal plasma flow. These results indicate that manidipine normalizes the relation between sodium excretion and renal perfusion pressure in salt-loaded spontaneously hypertensive rats by resetting pressure natriuresis.

Animals↗
PubMed1992

[Molecular structure and function of renal adrenergic receptors].

The kidney is the principal organ in the body that mediates the excretion of water and minerals, and also functions as an endocrine organ in producing hormones, enzymes (e.g., renin), and vasoactive molecules (e.g., prostaglandins). Circulating catecholamines and autonomic innervation of the kidney can influence those important functional responses as well as vascular constriction via renal adrenergic receptors. The adrenergic receptors are members of a large family of G protein-coupled receptors. Recent advance of molecular cloning has revealed a growing heterogeneity of adrenergic receptor subtypes. They share a common topographical motif consisting of seven putative transmembrane regions, where. They are thought to be essential for ligand binding. Multiple subtypes of adrenergic receptors may exist in the kidney. Defining the precise role of renal adrenergic receptors in disease states, particularly hypertension, will certainly require the application of new tools of biochemistry and molecular biology.

Glomerular Filtration Rate↗
PubMed1992

Alterations in sex hormones and sexual function of patients with renal failure treated with recombinant human erythropoietin.

Since it has been reported that correction of anemia in long-term hemodialysis patients by using human recombinant erythropoietin (r-HuEPO) is associated with improve sexual function, we conducted the present study to evaluate the changes in sex hormones as well as sexual function after r-HuEPO administration (1500 to 4500 IU per dialysis) for a year in patients on regular hemodialysis. Thirteen patients receiving regular hemodialysis entered this study. Their median age was 43 years. Along with correction of anemia (the hematocrit increased from 20 to 28%), testosterone (T) increased from 2.4 +/- 0.1 to 2.6 +/- 0.2 ng/ml, follicular stimulating hormone (FSH) increased (29 +/- 5 to 73 +/- 7 mIU/ml), luteinizing hormone increased (69 +/- 14 to 160 +/- 21 IU/ml) and prolactin decreased (all changes are significant at p less than 0.05). However, the improvement of sexual function was not remarkable. Only 25% of the uremic patients treated with r-HuEPO showed amelioration of this function. From the present data, it does not seem likely that therapy with r-HuEPO induces directly amelioration of sexual function through changes in sex hormones.

Adult↗
PubMed1992

Histological alterations in renal specimens as indicators of prognosis of IgA nephropathy.

A retrospective clinicopathological study of 66 patients with IgA nephropathy was undertaken to determine the prognostic significance of various renal histopathological alterations and clinical parameters. At the latest follow-up, after a period of 60 to 72 months following biopsy, 18 patients had serum creatinine concentration above 1.8 mg/dl. When the entire patients were evaluated as a whole, the extents of interstitial broadening and glomerular sclerosis were correlated significantly with the final status of renal function: proteinuria of more than 1.0 g per day and mildly impaired renal function at the time of biopsy were also associated with unfavourable outcome. However, when the patients with initially normal renal function, i.e. serum creatinine level below 1.2 mg/dl, were evaluated separately, the initial amount of proteinuria, but none of the other parameters, had a prognostic significance in the subsequent course of renal function. These findings suggest that proteinuria of more than 1.0 g per day as an early event often indicates the progression of IgA nephropathy, and lead to a postulation that renal histopathological changes become more significant prognostic indicators in the relatively advanced stage of the disease.

Adult↗