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Biomedical subjects

M Naruse

Publications and source records attributed to M Naruse.

At least 127 records · Page 7Linked to original sources
PubMed1995

Modulation of vascular natriuretic peptide receptor gene expression in hypertensive and obese hyperglycemic rats.

Receptors for natriuretic peptide (NP) consist of three subtypes: NP-A, NP-B, and NP-C. Recent studies in cultured aortic cells have suggested a phenotype-related switching of the vascular NP receptor from NP-A to NP-B. To ascertain the biological significance of the phenomenon in vivo, we developed a sensitive and reproducible ribonuclease protection assay and determined each receptor messenger RNA (mRNA) level in the vascular vessels of stroke-prone spontaneously hypertensive rats, deoxycorticosterone acetate-salt hypertensive rats, and genetically hyperglycemic. Wistar fatty rats and in cultured aortic smooth muscle cells. The aortic NP-A receptor mRNA level was significantly up-regulated in both types of hypertensive rats, whereas the NP-B receptor mRNA level did not show any significant change. Both NP-A and NP-B receptor mRNA levels were significantly up-regulated in Wistar fatty rats compared with the control values. There was no significant up-regulation of NP-A receptor mRNA in the inferior vena cava of the stroke-prone spontaneously hypertensive rats. Although the NP-A receptor was always the predominant subtype in rat aortic tissue, NP-B receptor was the predominant subtype in aortic smooth muscle cells in culture. These findings suggest that up-regulation of the NP-A receptor, but not the subtype switching, is the major modulation of receptor gene expression in both hypertensive and diabetic rats.

Animals↗
PubMed1995

Lysine vasopressin stimulation of cortisol secretion in patients with adrenocorticotropin-independent macronodular adrenal hyperplasia.

We present two patients with Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia who showed marked plasma cortisol response to lysine-8-vasopressin (LVP) injection (from 930 and 731 pmol/L to 2177 and 1920 pmol/L, respectively), while plasma ACTH levels remained undetectable. The ACTH independence of cortisol secretion in the two patients was determined from the following endocrinological findings. Plasma cortisol levels were not increased by corticotropin-releasing hormone injections and were not suppressed by high dose (16 mg) dexamethasone administrations. The plasma ACTH levels, measured by two independent sensitive immunoassays, were persistently undetectable even after corticotropin-releasing hormone injection, metyrapone administration, and bilateral adrenalectomy. The particular pathological finding of the two cases, atrophic lesions in nonnodular parts of the adrenal cortexes, also indicated ACTH independence of the macronodular hyperplasia. In vitro examination revealed a direct effect of LVP on cortisol secretion from the adrenal cells of the macronodules. We also examined seven patients with Cushing's syndrome caused by adrenal adenoma and found a statistically significant plasma cortisol response to LVP injection. The direct effect of LVP was also demonstrated in cultured adenoma cells. In conclusion, we discovered a direct adrenal effect of LVP on cortisol secretion in patients with ACTH-independent macronodular hyperplasia and, to a lesser extent, in patients with cortisol-producing adrenal adenoma. The cortisol response to LVP may serve to facilitate their diagnosis and choice of therapy.

17-Hydroxycorticosteroids↗
PubMed1995

Dopaminergic regulation of aldosterone secretion: its pathophysiologic significance in subsets of primary aldosteronism.

Although aldosterone (Aldo.) secretion is regulated by various humoral factors, evidence has accumulated to support an involvement of dopaminergic system in its regulation. The pathophysiological significance of the dopaminergic system in primary aldosteronism (PA) however remains unknown. In the present study, we examined the effects of metoclopramide (MCP) on Aldo. secretion in normal subjects (n = 11) and patients with essential hypertension (EH, n = 8), aldosterone-producing adenoma (APA, n = 10), and idiopathic hyperaldosteronism (IHA, n = 6). Plasma Aldo., prolactin (PRL), renin, cortisol, serum sodium, and serum potassium levels were determined before and 30 min after i.v. bolus injection of 10 mg MCP at 9 a.m. Plasma Aldo. showed a significant increase after MCP in normal subjects, EH, and APA, but not in IHA. The incremental response of plasma Aldo. was largest in APA and smallest in IHA. The percentage increase in plasma Aldo. from the basal level was significantly attenuated in IHA, while no significant difference was seen among other groups. Although plasma PRL showed a significant increase in response to MCP, no difference of the change was seen among the groups. There was no significant change in plasma cortisol, renin, serum sodium, and serum potassium levels in response to MCP. In addition, the response of Aldo. to MCP was normalized in APA after unilateral adrenalectomy, while that of PRL did not change. These results indicate that the adrenal dopaminergic activity is enhanced in APA and attenuated in IHA and suggest an involvement of the dopaminergic system in the pathogenesis of IHA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1995

Pathophysiological significance of plasma total renin and prorenin in patients with diabetes mellitus.

To seek the pathophysiologic significance of measuring the concentration of total renin instead of prorenin, we determined the plasma total renin concentration by immunoradiometric assay and correlated the results with various clinical features and laboratory parameters of diabetic complication in 108 patients with diabetes mellitus. The plasma prorenin concentration was estimated as the difference between the total and active renin concentrations. The plasma total renin and prorenin concentrations were high in patients with diabetes mellitus, in contrast to the active renin concentration which was slightly decreased. In addition, the plasma total renin and prorenin concentrations were higher in patients with diabetic complications than in patients without any complication. Multiple regression analysis showed that the presence of orthostatic hypotension, diabetic retinopathy, and proteinuria is significantly associated with the increased plasma total renin and prorenin concentrations. In addition, there was a significant positive correlation between the total renin and prorenin concentrations. These results suggest that both the plasma total renin concentration and the prorenin concentration are closely related to diabetic complications. Determination of the plasma total renin concentration by immunoradiometric assay as a substitute for prorenin could be a powerful tool in elucidating the mechanism for the increased plasma prorenin in diabetes mellitus.

Adult↗
PubMed1995

Effects of acute hyperinsulinemia on plasma atrial and brain natriuretic peptide concentrations.

Impaired renal sodium excretion and increased plasma atrial natriuretic peptide (ANP) levels have been reported in patients with hypertension associated with insulin resistance and hyperinsulinemia. To clarify the interrelationship between hyperinsulinemia and plasma natriuretic peptides, we investigated the effects of physiological and non-physiological hyperinsulinemia on the plasma ANP and brain natriuretic peptide (BNP) levels. Plasma immunoreactive insulin (IRI), ANP and BNP levels were determined by a euglycemic-hyperinsulinemic glucose clamp in 20 patients with non-insulin-dependent diabetes mellitus, by a glucose challenge test in 22 normal subjects and by an insulin challenge test in six normal subjects. Both in the glucose clamp and the glucose challenge test, plasma ANP showed a significant increase in association with increased plasma IRI and plasma volume. However, there was no significant correlation between the changes in plasma ANP levels and plasma IRI levels in view of the peak values and the area under the curve of their responses. In addition, the plasma ANP did not show any significant change despite the marked elevation of plasma IRI in the insulin challenge test. There was no significant change in plasma BNP under any of the hyperinsulinemic conditions. These findings provide in vivo evidence for the lack of a direct effect of acute hyperinsulinemia on natriuretic peptides, although the chronic effects of hyperinsulinemia remain to be elucidated.

Acute Disease↗
PubMed1994

Angiotensin converting enzyme inhibitor but not calcium blocker down-regulates gene expression of vascular natriuretic peptide receptor in hypertensive rats.

We have recently found that vascular natriuretic peptide (NP)-A receptor mRNA is upregulated in genetically hypertensive (SHR-SP/Izm) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In the present study, we examined the effects of antihypertensive treatments on aortic NP-A receptor mRNA expression in these hypertensive rats using ribonuclease protection assay. Oral administration of an angiotensin converting enzyme inhibitor, derapril, but not a calcium channel blocker, manidipine, produced a significant decrease of the NP-A receptor mRNA level after 4 weeks, while both antihypertensive agents showed similar hypotensive effects. Plasma renin was high in SHR-SP/Izm and low in DOCA-salt rats. These results suggest that the vascular renin-angiotensin system rather than the blood pressure has an important role in the regulation of the vascular NP-A receptor.

Animals↗
PubMed1994

Effect of dithiothreitol on angiotensin II receptor type II in rat ovarian cultured granulosa cells.

Dithiothreitol markedly increased the ligand binding affinity of angiotensin II (AII) receptor type II (AT2) without affecting its antagonist selectivity in cultured ovarian granulosa cells, demonstrating that this AT2 is of the dithiothreitol-sensitive type. Dithiothreitol is useful for specifically detecting low levels of the AT2 in the ovary, where it plays roles that are probably related to atresia.

Angiotensin II↗
PubMed1994

[Clinical significance of nitric oxide in hypertension].

Vascular endothelial cells produce various biologically active factors regulating blood pressure, coagulation, and possibly cell growth of the vascular wall. Of the factors, nitric oxide (NO) has been the object of attention because of its quite simple molecular structure and variety of biological functions. In the present review, we focused on the physiologic and pathologic aspects of NO in hypertension. In experimental animals, both acute and chronic inhibition of NO synthase (NOS) with arginine derivatives produce a significant rise in blood pressure, indicating that tonic production of NO regulates basal vascular tonus. The chronic hypertension caused by NOS inhibitor is associated with cardiac hypertrophy and renal insufficiency. Sodium retention, though transient, and the plasma and tissue renin/angiotensin system in addition to the reduced production of NO have been implicated in the development of hypertension. Hypertension and the associated target organ failure can be reversed by co-administration of L-arginine or blockades of the renin/angiotensin system. Studies in which L-arginine as the substrate of NO or NOS inhibitor was administered demonstrated an important role of NO in the regulation of tonic vascular tonus also in normal subjects. In hypertensive subjects, however, endothelium-dependent vasorelaxation and production of NO are impaired, possibly due to a deficiency of L-arginine and/or a disorder of its utilization. Recent advances in the methods of detecting NO enabled us to demonstrate its diminished production from endothelial cells of hypertensive rats in vitro, although no definite biochemical evidence has been obtained in hypertensive subjects. The endothelial dysfunction, however, is not a primary cause of hypertension but a secondary result since it is commonly observed in various types of hypertension and can be reversed by correcting the blood pressure. Other common diseases including atherosclerosis and diabetes mellitus are also associated with similar abnormalities of the endothelium. NO has anti-atherogenic actions: inhibition of platelet functions and proliferation of vascular smooth muscle cells. Therefore, potentiation of endogenous NO and/or supplement of exogenous NO donors could be novel therapeutic approaches for the treatment of hypertension and atherosclerosis, while potential adverse effects of NO including cytotoxicity, immunosuppressibility, and hypotensive shock should be taken into account.

Amino Acid Oxidoreductases↗
PubMed1994

Mercury, not sulphur dioxide, poisoning as cause of smelter disease in industrial plants producing sulphuric acid.

Several episodes of "smelter disease", previously assumed to be caused by sulphur dioxide (SO2) poisoning, have been reported in workers replacing pipes in sulphuric acid manufacturing plants. One such incident, affecting 20 men, was recorded in Akita, Japan, in July, 1993, but the protection these workers used suggested that some cause other than SO2 needed to be looked for. 10 workers were affected despite wearing respirators with SO2 cartridges, the symptoms including dyspnoea, diarrhoea, colicky pain, muscle pain and eczema with erythema. Subsequently 10 other workers using face masks with supplied air were affected, though without respiratory symptoms. Sludge in the piping contained mercuric sulphate, and mercury fumes resulted when pipes were cut with gas burners. Blood and urine measurements confirmed heavy exposure to the metal, and simulation experiments in rats showed that skin absorption was likely too. The masks with supplied air ought to have excluded both SO2 and mercury fumes. The only way to avoid smelter disease reliably is to wear an encapsulated suit that prevents inhalation and skin absorption of industrial toxins.

Acute Disease↗
PubMed1994

Does plasma immunoreactive ouabain originate from the adrenal gland?

It was reported recently that the endogenous digitalis-like factor ouabain may mainly originate from the adrenal gland. To ascertain the pathophysiological significance of endogenous ouabain and to examine if it originates in the adrenal gland, we determined plasma immunoreactive ouabain levels in patients with various cardiovascular and endocrine diseases. Plasma immunoreactive ouabain levels were also determined in the adrenal venous blood by adrenal venous sampling. Plasma immunoreactive ouabain levels were significantly increased in patients with essential hypertension, primary aldosteronism, Cushing's syndrome, pheochromocytoma, acromegaly, and chronic renal failure. Plasma immunoreactive ouabain levels were decreased in patients with primary aldosteronism after unilateral adrenalectomy, acromegaly after pituitary adenomectomy, and chronic renal failure after hemodialysis. Plasma immunoreactive ouabain levels in patients after bilateral adrenalectomy were similar to those in healthy subjects. There was no significant step-up of immunoreactive ouabain levels in the adrenal vein from the peripheral vein in three patients, whereas one patient with hypertension and right adrenal tumor but without any known adrenal hormone excess showed higher plasma immunoreactive ouabain levels in the right adrenal vein than those in the peripheral vein. These results suggest an important pathophysiological significance of endogenous ouabain in various cardiovascular and endocrine diseases. It is unlikely that the adrenal gland is a major source of plasma ouabain, although a possible excess production of ouabain by the adrenal tumor remains to be elucidated.

Adrenal Gland Neoplasms↗
PubMed1994

Atrial and brain natriuretic peptides in cardiovascular diseases.

The human heart secretes both atrial natriuretic peptide and brain natriuretic peptide. This study attempts to clarify the pathophysiological significance of the peptides in cardiovascular diseases. Using immunoradiometric assay, plasma brain natriuretic peptide and atrial natriuretic peptide levels in essential hypertension, various secondary hypertension, chronic renal failure, chronic heart failure during cardiac pacing, and acute myocardial infarction were determined. Mean plasma brain natriuretic peptide and atrial natriuretic peptide levels in healthy subjects were 3.7 +/- 0.3 and 5.7 +/- 0.3 pmol/L, respectively, and increased as a function of age. Plasma brain natriuretic peptide levels showed a larger increase than atrial natriuretic peptide levels in various cardiovascular diseases. In chronic renal failure, whereas plasma atrial natriuretic peptide levels decreased significantly after hemodialysis and were correlated with the changes in body weight, changes in plasma brain natriuretic peptide levels were less prominent and did not show such a correlation. In chronic heart failure, both basal plasma brain natriuretic peptide and atrial natriuretic peptide levels were also significantly elevated. However, in response to acute ventricular or atrial pacing, brain natriuretic peptide levels did not show any increase in contrast to the marked increase of atrial natriuretic peptide levels. In acute myocardial infarction, brain natriuretic peptide levels showed more prominent changes than atrial natriuretic peptide levels and were correlated with serum levels of creatine kinase and cardiac myosin light chain I in most patients. These results suggest that both brain and atrial natriuretic peptides play an important role in the regulation of cardiovascular homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗
PubMed1994

Recent advances in endothelin research on cardiovascular and endocrine systems.

Recent advances in ET research on the cardiovascular and endocrine systems were reviewed. Considering the potent vasculotropic actions, strategically advantageous localization, and recent findings with the specific receptor antagonist, ET is potentially involved in the regulation of hemodynamic homeostasis and in the pathogenesis of essential and secondary hypertension. The mitogenic action on the vascular smooth muscle cells suggests its more chronic effect on the vascular structure. In addition to the hypertensinogenic aspects, the role of ET in maintaining blood pressure in a hypotensive condition should not be overlooked. The development of specific antagonists which block the action of locally operating ET in vivo will be a powerful tool in elucidating the pathophysiological significance of ET and will provide a new therapeutic approach for hypertension. The roles of ET in the endocrine system are also fascinating. Accumulating evidence supports the notion that ET modulates the secretion of pituitary and adrenal hormones. The mode of action is likely to be paracrine/autocrine rather than endocrine, although a possible role of circulating ET cannot be ruled out. The pathophysiological role of ET in the endocrine tissues remains to be clarified. The diversity of the action of ET on the blood pressure and endocrine functions provides further evidence of the complexity of the homeostatic mechanisms, leaving us an intriguing subject for future study.

Adrenal Glands↗
PubMed1994

Immunoreactive endothelin-1 in the neural lobe of the rat pituitary following hemorrhage and dehydration.

Previously we found intragranular colocalization of immunoreactive endothelin-1 and neurohypophysial hormones in the axon terminals of the rat neural lobe. To investigate the function of endothelin-1 in the rat neural lobe, immunoreactive endothelin-1 in plasma and the neural lobe was measured by enzyme immunoassay in rats subjected to hemorrhage and in other rats who were deprived of water for 2 days to induce dehydration. Changes in plasma arginine vasopressin were determined by radioimmunoassay. In addition, morphometric analysis was performed in the neural lobe of rats exposed to these stresses. Plasma concentrations of immunoreactive endothelin-1 were unchanged following hemorrhage or dehydration, whereas those of immunoreactive vasopressin were remarkably increased. In the neural lobe, immunoreactive endothelin-1 content and the number of neurosecretory granules decreased significantly after dehydration. However, immunoreactive endothelin-1 in tissue increased nearly three-fold in hemorrhaged rats, whereas the endothelin-1-immunolabeling in the axon terminals was unchanged. These results suggest that endothelin-1 in the hypothalamo-hypophysial system may be involved in the local modulation of vasopressin secretion when an animal is exposed to hypovolemic and/or osmotic stress.

Animals↗
PubMed1994

Effect of luminal Cl- and Ca2+ on tubuloglomerular feedback mechanism.

We dissected and perfused in vitro rabbit cortical thick ascending limbs (CTAL) and distal convoluted tubule with the glomerulus attached intact. Basolateral membrane voltage (Vbl) and intracellular Ca2+ concentration ([Ca2+]i) in macula densa (MD) cells were measured with microelectrodes and microscope photometry, respectively. Our data suggest that the apical membrane of MD cell has a Ca2+ entry pathway, and that the basolateral membrane of MD cell has a Cl- conductance, which may be regulated by the [Ca2+]i in MD cell. We next evaluated by measuring the afferent arteriolar diameter with video camera monitoring whether the change in Ca2+ concentration of macula densa tubular lumen indeed affect tubuloglomerular feedback. The data suggest that the changes in luminal Ca2+ as well as Cl- concentration at macula densa independently alter the afferent arteriolar diameter, thus may affect the single nephron glomerular filtration rate.

Animals↗
PubMed1994

[An approach to home therapy for cancer pain patients].

Recently, in consideration of cost performance and improvement in quality of life (QOL) of the patient, the significance of home care and outpatient treatment has also been recognized in Japan. A terminal cancer patient who had local recurrence in the pelvic region after surgery for rectum carcinoma, was treated for cancer pain by us with a continuous epidural infusion of morphine by means of a prolonged operating continuous infusion device. The treatment made home therapy possible and allowed the patient to return to normal social activities. Based on this case, the significance of and issues regarding home therapy are discussed in this study.

Costs and Cost Analysis↗
PubMed1994

Reversible functional asplenia. Autoimmune hemolytic anemia with thrombocytopenia in chronic lymphocytic leukemia.

An enlarged spleen failed to accumulate Tc-99m-labeled phytate, but it showed normal perfusion and uptake of labeled and heat-denatured red blood cells. A blood cell count demonstrated moderately low hemoglobin and hematocrit levels and a markedly low platelet count, and results of direct Coombs' and antiplatelet-antibody (IgG) tests were positive. Steroid therapy resulted in normal splenic function. This case demonstrates reversible functional asplenia caused by reticuloendothelial dysfunction secondary to pure splenic chronic lymphocytic leukemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1993

Isolation of an endogenous Na-pump specific inhibitor from normal pig urine: characterization and comparison with the inhibitor purified from bovine adrenal glands.

An endogenous Na-pump specific inhibitor has been purified to homogeneity from normal pig urine using Amberlite XAD-2 adsorption chromatography followed by five steps of reverse phase HPLC. Although most of the dose response curves for this purified Na-pump inhibitor, designated uroxin, in the various assay systems paralleled those of authentic ouabain and the specific Na-pump inhibitor previously purified from bovine adrenal glands (designated adrexin C), the cross-reactivity curve with anti-ouabain antibodies did not. The retention times of uroxin on various types of reverse phase HPLC columns were also different from those of plant-derived cardiotonic steroids and adrexin C. The cross-reaction curve of adrexin C was superimposable with that of ouabain, and adrexin C coeluted with ouabain from all of the HPLC columns tested. The results from physical and chemical characterization of both purified inhibitors suggest that uroxin is a novel Na-pump inhibitor which is structurally different from any of the known cardiotonic steroids or other substances previously reported to exhibit Na-pump inhibitory activity. The results also indicate that adrexin C is indistinguishable from ouabain. These results suggest that there are at least two different types of endogenous Na+,K(+)-ATPase inhibitors in the mammalian body.

Adrenal Glands↗