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Biomedical subjects

K Naruse

Publications and source records attributed to K Naruse.

At least 181 records · Page 10Linked 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

Cloning and characterization of cDNAs for 70-kDa heat-shock proteins (Hsp70) from two fish species of the genus Oryzias.

cDNA corresponding to two hsp70-related genes (OLHSC70 and CEHSC70) were isolated from two lines of cultured fish cells derived from the genus Oryzias. OLHSC70 was 2,261 bp in length and encoded a protein of 686 amino acids with a predicted molecular mass of 76,120 daltons. CEHSC70 was 2,114 bp in length and it lacked the 5' region found in OLHSC70. Two-dimensional electrophoresis revealed that Oryzias latipes has at least three heat-inducible proteins with molecular masses of about 70,000 daltons. One of these proteins (Hsp70.1) was barely expressed under normal conditions but its high-level expression was induced by hyperthermia. The other two proteins (Hsc70.1, and Hsc70.2) were constitutively expressed under normal conditions and only slightly enhanced levels were induced by hyperthermia. Transfection with the cloned sequence, RNA dot-blot analysis and the two-dimensional electrophoresis of proteins showed that OLHSC70 encoded Hsc70.1.

Amino Acid Sequence↗
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↗
PubMed1995

An aldose reductase inhibitor, TAT, reduces ADP-induced platelet hyperaggregation in streptozotocin-induced diabetic rats with neuropathy.

To investigate the relationship between metabolic and vascular factors, especially polyol pathway and platelet aggregation, in the pathogenesis of diabetic neuropathy, the effects of a novel potent aldose reductase inhibitor, TAT ((5-(3-thienyl) tetrazol-1-yl) acetic acid monohydrate) on adenosine diphosphate-induced platelet aggregation, polyol contents in platelets, motor nerve conduction velocity (MNCV), and sciatic nerve blood flow (SNBF) were examined in streptozotocin-induced diabetic rats. Diabetic rats demonstrated hyperaggregation in response to adenosine diphosphate, accompanied by sorbitol and fructose accumulation and myoinositol depletion in platelets. Treatment with TAT improved these abnormalities in diabetic rats. A delayed MNCV and a reduced SNBF in diabetic rats were normalized by the administration of TAT. These observations suggest that increased polyol pathway activity plays an important role in platelet aggregation in the development of diabetic neuropathy and that aldose reductase inhibitor is useful for the treatment of diabetic neuropathy from the viewpoint not only of metabolic factors but also of vascular factors.

Adenosine Diphosphate↗
PubMed1995

Genetic linkage map of a fish, the Japanese medaka Oryzias latipes.

In the Japanese medaka, Oryzias latipes, 227 informative random amplified polymorphic DNA markers were detected. Segregations of a total of 170 loci, which included three pigment-pattern loci, five enzyme-coding loci, and one male-determining factor, were examined using intraspecific backcrosses of three inbred strains, two of which were highly polymorphic with respect to the remaining strain. The results were used to prepare a genetic linkage map of and medaka. The map consists of 28 linkage groups and spans about 2480 contiguous centimorgans (cM) with an average of 323 kilobase pairs (kb)/cM.

Animals↗
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

[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

Relationship between the induction of proteins in the HSP70 family and thermosensitivity in two species of Oryzias (Pisces).

A cultured fish cell line, CE, derived from Oryzias celebensis, which lives in a tropical zone, was more heat-resistant than the OL32, which were derived from the Japanese medaka, Oryzias latipes which lives in a temperate zone. Protein synthesis in OL32 cells was also more heat-sensitive than that in CE cells. The relative levels in proteins of the HSP70 family and the ability of cells to tolerate severe heat treatment after a conditioning heat treatment were examined. Twenty-four hours after conditioning heat treatment, both cell lines retained thermotolerance even though three proteins in the HSP70 family had returned to their control levels.

Animals↗
PubMed1994

Long-term inhibition of NO synthesis promotes atherosclerosis in the hypercholesterolemic rabbit thoracic aorta. PGH2 does not contribute to impaired endothelium-dependent relaxation.

We examined whether prostaglandin (PG) H2, as an endothelium-dependent contracting factor, or the disturbed production of endothelium-derived relaxing factor, impairs endothelium-dependent relaxation and whether long-term inhibition of nitric oxide (NO) synthesis aggravates atherosclerosis in hypercholesterolemic rabbits. Male New Zealand White rabbits were fed one of the following diets: (1) standard chow; (2) 2% cholesterol-supplemented chow; (3) standard chow with 80 micrograms/mL N omega-nitro-L-arginine methylester (L-NAME), an NO synthetase inhibitor, in their drinking water; or (4) 2% cholesterol-supplemented chow with 80 or 160 micrograms/mL L-NAME in their drinking water. The rabbits were fed these diets for 8 or 12 weeks. Then aortic rings were obtained, and changes in isometric tension were recorded. Intimal atherosclerotic areas of the thoracic aortas were subsequently measured by planimetry. The cholesterol-supplemented diet significantly impaired endothelium-dependent aortic relaxation to acetylcholine. Pretreatment with the thromboxane A2/PGH2 receptor antagonist ONO-3708 did not reverse this impaired response. Vessels from both normocholesterolemic and hypercholesterolemic rabbits given L-NAME showed more impaired endothelium-dependent relaxation than those from their dietary counterparts not given L-NAME. Morphometric analysis revealed marked enlargement of intimal atherosclerotic areas in aortas from L-NAME-treated hypercholesterolemic rabbits compared with those from untreated hypercholesterolemic rabbits. These findings suggest that PGH2 does not contribute to impaired endothelium-dependent relaxation and that long-term administration of L-NAME promotes atherosclerosis by inhibition of NO synthesis in the hypercholesterolemic rabbit thoracic aorta.

Animals↗
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↗
PubMed1993

Involvement of stretch-activated ion channels in Ca2+ mobilization to mechanical stretch in endothelial cells.

Endothelial cells are subjected to shear stresses by blood flow, normal stresses by blood pressure, and stretch by vessel expansion. These forces are known to induce secretions of several vasoactive substances probably via internal calcium mobilization (R. F. Furchgott. Circ. Res. 53: 557-573, 1983; M. J. Peach, A. L. Loeb, H. A. Singer, and J. Saye. Hypertension Dallas 7, Suppl. I: I-94-I-100, 1985). Here we report that stretching cellular membranes increased intracellular Ca2+ concentration ([Ca2+]i) in human umbilical endothelial cells cultured on silicon membranes. Upon application of a stretch pulse (3-s duration), [Ca2+]i increased rapidly and decayed slowly. The following results suggest that this increase arises from Ca2+ entry through stretch-activated (SA) channels: 1) the Ca2+ response disappeared when extracellular Ca2+ was removed; 2) gadolinium (Gd3+), a blocker for cation-selective SA channels, blocked the response but nifedipine did not; and 3) externally applied Mn2+, which is known to permeate mechanosensitive channels but not Ca2+ channels, entered the intracellular space immediately after an application of mechanical stretch. The increase in [Ca2+]i was found to consist of at least two components: an initial fast component and a delayed slower component. Ryanodine inhibited the slow component. It is suggested that stretching the membrane primarily induced extracellular Ca2+ entry through SA channels followed by Ca2+ releases from intracellular Ca2+ stores.

Calcium↗