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Biomedical subjects

Y Kasai

Publications and source records attributed to Y Kasai.

At least 127 records · Page 7Linked to original sources
PubMed1990

Immunohistochemical evidence of the extracellular localization of calcium-activated neutral protease (CANP) in rabbit skeletal muscle, lung and aorta.

The subcellular localization of calcium-activated neutral protease requiring a millimolar calcium concentration (m-CANP) was examined by light and electron microscopy in various tissues of the rabbit, using an immunoperoxidase method with a monoclonal antibody (1C6D1). In skeletal muscles, specific staining for m-CANP was recognized on collagen fibrils (ca 40 nm in diameter) with a periodic banding pattern. In the lung, dense reaction products were precipitated on elastic fibers under the bronchial epithelia. In the aorta, tunica intima and adventitia were intensely stained. Dense reaction products were observed on collagen fibrils and elastic fibers. Basal laminae, on the other hand, were not stained by anti m-CANP antibody in these tissues. These findings suggest that m-CANP may be involved in the regulation of the structure and function of the extracellular matrix.

Animals↗
PubMed1990

Failure to visualize bilateral adrenal glands in a patient with primary aldosteronism.

Failure to visualize either adrenal gland by adrenal imaging was experienced in a patient with biochemical evidence of primary aldosteronism. Visualization of the adrenal glands was not possible after the administration of ACTH-Z (1 mg/day) for 3 days. The administration of ACTH and dexamethasone elicited an increase in blood pressure. Although the reason for this failure to visualize the adrenal glands by scanning and for the rise in blood pressure brought on by ACTH and dexamethasone remain unclear, we think that the case herein reported is a rare type of primary aldosteronism.

Adosterol↗
PubMed1990

Interaction of endothelin and Ca++ entry blockers on renal circulation in anesthetized rabbits.

We examined an interaction of endothelium-derived vasoconstrictor endothelin and Ca++ entry blockers on renal blood flow in anesthetized rabbits. A bolus intrarenal arterial injection of endothelin at doses of 10, 25 and 50 ng produced a decrease in renal blood flow with a dose-dependent fashion, while there was no change in systemic arterial pressure. A similar extent of the decrease in renal blood flow was produced at doses of endothelin 50 ng(2.0 x 10(-11)M), angiotensin II 10 ng (9.7 x 10(-12)M) and norepinephrine 250 ng (1.5 x 10(-9)M), although the decrease in renal blood flow by endothelin was sustained in contrast to angiotensin II or norepinephrine. Pretreatment with Ca++ entry blocker nifedipine (1.0 microgram/kg/min) or diltiazem (20 micrograms/kg/min) attenuated the decrease in renal blood flow and reduced the duration time. These results suggest that exogenous endothelin produces a renal vasoconstriction in vivo. However, it seems that endothelin is less potent than angiotensin II in renal circulation in anesthetized rabbits. It is also indicated that the decrease in renal blood flow by endothelin could be mediated through a common Ca++ channel pathway in renal vasculatures.

Anesthesia↗
PubMed1989

Induction of cells with a chondrocyte-like phenotype by treatment with 1 alpha,25-dihydroxyvitamin D3 in a human salivary acinar cell line.

A clonal cell with an acinar cell phenotype, which was induced by 5-azacytidine treatment of a neoplastic human salivary intercalated duct cell line, was cultivated in the presence of 1 alpha,25-dihydroxyvitamin D3. Morphological changes occurred; large cells that were polygonal or round in shape and had numerous vacuoles in their cytoplasm appeared in the treated cells, whereas the same concentration of 1 alpha,25-dihydroxyvitamin D3 did not affect the morphology of the parental cells. Major alterations, such as expression of type II collagen, alpha and beta chains of S-100 protein, and sulfated proteoglycans, were observed in these cells with a phenotype similar to chondrocytes. After the removal of 1 alpha,25-dihydroxyvitamin D3 from the culture, the treated cells returned rapidly to the phenotype of the untreated cells. These findings indicate that the reversible differentiation into chondrocyte-like cells of a human salivary acinar cell line occurs in growth medium containing 1 alpha,25-dihydroxyvitamin D3.

Calcitriol↗
PubMed1989

Role of renal kallikrein in the regulation of blood pressure in the rat remnant kidney model of chronic renal failure.

We studied urinary excretion of active and inactive kallikrein every day for 3 weeks in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) subjected to 5/6 nephrectomy (5/6), 1/2-nephrectomy (1/2) or sham-operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). In the SHR group, blood pressure was significantly elevated in 5/6-animals as compared with 1/2 or sham, whereas in the WKY group blood pressure was not changed after either operation. Urinary active and total kallikrein excretion were decreased in 5/6-SHR to 34% and 59%, respectively, as compared with values of sham-SHR, and in 1/2-SHR to 70% and 70%, respectively. Similarly, they were also decreased in 5/6-WKY to 36% and 55%, respectively, as compared with values of sham-WKY. In 1/2-WKY urinary active kallikrein excretion was decreased to 88% as compared with the value of sham-WKY, but urinary total kallikrein excretion was not different from that of sham-WKY. Thus, the suppressed renal kallikrein activity due to reduced renal mass was not associated with any significant change in blood pressure in WKY, although it induced an elevation of blood pressure in SHR. These results indicate that the decreased production of renal active kallikrein may not play a significant role in the regulation of blood pressure in the rat remnant kidney model of chronic renal failure. In addition, it is suggested that the elevation of blood pressure in this model of SHR may be due to other factors than renal kallikrein.

Animals↗
PubMed1989

Role of renal kallikrein in the increased fractional sodium excretion in the rat remnant kidney model of chronic renal failure.

To assess the potential role of renal kallikrein-kinin system in enhancing sodium excretion per nephron in chronic renal failure, we studied urinary excretion of active and inactive kallikrein for 3 weeks in Wistar-Kyoto rats subjected to 5/6 nephrectomy (5/6), 1/2 nephrectomy (1/2) or sham operation (Sham). We determined urinary active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Fractional sodium excretion was significantly increased in 5/6-rats as compared with 1/2- or sham-rats. On the contrary, urinary active kallikrein excretion per nephron was not different in the three models whereas a significant rise in urinary inactive kallikrein excretion per nephron was found in 5/6-rats as compared with 1/2- or sham-rats. Urinary total kallikrein excretion per nephron was significantly increased in 5/6-rats as compared with sham-rats. In addition, no correlation was found between fractional sodium excretion and urinary active kallikrein excretion corrected for creatinine clearance (Ccr) in 5/6-rats. These results indicate that decreased excretion of renal active kallikrein may not play a significant role in the increased sodium excretion per nephron in the rat remnant kidney model of chronic renal failure. Furthermore, it is suggested that in this model of rat there might be impaired production of renal active kallikrein although its exact mechanism remains to be determined.

Animals↗
PubMed1989

PGE2 synthesis in cultured renal papillary collecting tubule cells from young and aged spontaneously hypertensive rats.

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the capacity of PGE2 synthesis in cultured renal papillary collecting tubule cells from young (4-week-old) and aged (16-week-old) SHR and control Wistar-Kyoto rats (WKY). Basal levels of PGE2 synthesis were lower in young SHR cells than in WKY cells (p less than 0.001). Arachidonic acid-stimulated PGE2 synthesis, however, had a slight tendency to be higher in SHR cells than in WKY cells. Bradykinin- and A23187-stimulated PGE2 synthesis were similar in both strains. Basal levels of cyclic AMP were also lower in young SHR cells than in WKY cells (p less than 0.001), but the cAMP response to exogenous PGE2 was equal between the strains. In papillary collecting tubule cells from aged rats, basal levels of PGE2 and cyclic AMP as corrected for cellular protein were significantly lower than those in young rats, but there was no difference between the strains. Urinary excretion of PGE2 and thromboxane B2 was equal in aged SHR and WKY. These results suggest that papillary collecting tubule of young SHR and WKY may differ in the metabolism of PGE2 and cyclic AMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Acute and chronic effects of synthetic atrial natriuretic factor on blood pressure and sodium excretion in spontaneously hypertensive rats.

To assess possible roles of atrial natriuretic factor (ANF) in the regulation of blood pressure in spontaneously hypertensive rats (SHR), we performed two series of experiments. First, we studied acute hypotensive, natriuretic and diuretic effects of ANF in pentobarbital-anesthetized SHR and age-matched Wistar-Kyoto rats (WKY). A synthetic ANF of 25 amino acid residues was intravenously administered as a bolus at doses of 0.1, 1.0, 2.5 and 5.0 micrograms/kg. In SHR group, a significant decrease in mean arterial pressure (MAP) was observed at a dose of 1.0 micrograms/kg, and the decrease was dose-dependent. On the other hand, in WKY group, the hypotensive effect of ANF was not observed until a dose of 5.0 micrograms/kg. The diuretic and natriuretic effects of ANF were observed at a dose of 2.5 micrograms/kg in SHR and 5.0 micrograms/kg in WKY, respectively. Second, we also studied chronic effect of ANF on the development of hypertension in 6-week-old SHR. The SHRs, on regular diet or given 1% NaCl solution for drinking, were continuously infused into the jugular vein by osmotic minipumps with ANF (15, 75 and 150 micrograms/kg/day) or vehicle (physiological saline) as controls for up to 14 days. ANF at a dose of 150 micrograms/kg/day attenuated transiently the development of hypertension in the sodium-loaded SHR. However, the blood pressure returned to control levels by day 5. ANF at doses of 15 and 75 micrograms/kg/day did not affect the development of hypertension. In SHR on regular diet, ANF at a dose of 150 micrograms/kg/day did not affect the development of hypertension. In addition, ANF did not induce any significant changes in urine volume, fluid intake, and urinary excretion of sodium and potassium in SHR, whether they were sodium-loaded or not, when compared to those in vehicle-infused SHR. These results indicate that there may be a significant difference in the sensitivity to diuretic, natriuretic and hypotensive actions of ANF between SHR and WKY. Moreover, it is suggested that ANF may play significant roles by its vascular effect at the early stage of development of hypertension in sodium-loaded SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Blood pressure and renal responses to synthetic rat atrial natriuretic factor in deoxycorticosterone acetate-salt hypertension.

To assess possible roles of atrial natriuretic factor (ANF) in the regulation of blood pressure in deoxycorticosterone acetate (DOCA)-salt hypertensive rats, we performed two series of experiments. First, we studied acute hypotensive, and natriuretic and diuretic effects of ANF in pentobarbital-anesthetized DOCA-salt hypertensive rats and age-matched controls. A synthetic rat ANF was intravenously administered as a bolus at doses of 0.5, 2.5 and 5.0 micrograms/kg. In DOCA-salt rats, a significant decrease in mean arterial pressure was observed at a dose of 5.0 micrograms/kg, whereas at a dose of 2.5 micrograms/kg in control rats. On the other hand, the diuretic and natriuretic effects of ANF were observed at a dose of 2.5 micrograms/kg in DOCA-salt rats and 5.0 micrograms/kg in control rats. Second, we examined chronic effect of ANF on the development of hypertension in DOCA-salt rats. The DOCA-salt rats, given 1% NaCl solution for drinking, were continuously infused with ANF (15, 75 and 150 micrograms/kg/day) or vehicle (physiological saline) into the jugular vein by osmotic minipumps for up to 14 days. In DOCA-salt treated rats, ANF at doses of 75 and 150 micrograms/kg/day attenuated significantly the development of hypertension, although at a dose of 15 micrograms/kg/day did not. The hypotensive effect of ANF was sustained throughout the experimental period and the effect of ANF at a dose of 150 micrograms/kg/day was more prominent than that of this peptide at a dose of 75 micrograms/kg/day. ANF did not induce any significant changes in urine volume, fluid intake and urinary excretion of sodium and potassium in DOCA-salt rats when compared to those in vehicle-infused DOCA-salt rats. These results indicate that DOCA-salt rats are more sensitive to ANF in diuretic and natriuretic effects, and less sensitive to ANF in hypotensive effect compared to control rats. Moreover, it is suggested that ANF can affect the regulation of blood pressure by its vascular effect in the development of hypertension in DOCA-salt rats.

Animals↗
PubMed1989

Difference between the effects of atrial natriuretic peptide and calcium antagonist on cytosolic free calcium in cultured vascular smooth muscle cells.

The effect of atrial natriuretic peptide (ANP) on cytosolic free calcium ([Ca2+]i) was studied in monolayers of cultured vascular smooth muscle (VSM) cells loaded with a fluorescent calcium indicator, fura-2. ANP (atriopeptin III, 10(-8) M) decreased the resting level of [Ca2+]i and sustained rises in [Ca2+]i following peak levels induced by vasoconstrictive hormones (angiotensin II or vasopressin). ANP also decreased a rise in [Ca2+]i induced by high potassium (high K+) depolarization. The initial rise in [Ca2+]i induced by vasopressin was not inhibited by ANP. On the other hand, calcium antagonists (nicardipine or nifedipine) inhibited the high K+-induced rise in [Ca2+]i, whereas there was no effect on rises in [Ca2+]i induced by vasopressin. These results suggest that calcium antagonists inhibit voltage-dependent calcium channels, while ANP can decrease [Ca2+]i presumably through a stimulation of calcium-extrusion active transports in vascular smooth muscle cells.

Animals↗
PubMed1989

Calcium-dependent proteolytic activity in hypoxic rat brain.

The effect of hypoxia (7% oxygen in nitrogen) on Ca2+-activated protease (/u- and mCANP) in the rat brain has been studied. Hypoxia changed the intracellular distribution of CANPs without affecting the total calcium dependent proteolytic activity. The 3-fold rise of the activity of mCANP bound to synaptosomal membranes and less pronounced elevation in mitochondrial and microsomal fractions is compensated by corresponding drop of mCANP activity in cytosol. The changes of /uCANP under hypoxia were less expressed and their direction was opposite to mCANP. Additionally the susceptibility of brain membrane proteins to mCANP was tested. Our results show that proteins from the brains of animals submitted to hypoxic conditions are more susceptible to CANP than those from control animals. Thus, it is suggested that hypoxia results in some physico-chemical changes of membranes which render the membranes more sensitive to CANP.

Animals↗
PubMed1989

[Extended aortic arch anastomosis for aortic coarctation in neonate and early infancy--experience in 5 patients].

The aortic coarctation (CoA) was repaired with extended aortic arch (AA) anastomosis in 5 consecutive patients, 2 in neonate and 3 in infancy, ranging in age from 3 to 106 days. The associated lesions were ventricular septal defect in 2, atrial septal defect in 2 and complete atrioventricular canal in 1. Patent ductus was found in 4 and prostaglandin E1 was required in 2 with response in 1 patient. The AA was hypoplastic in 2 patients with arch to descending aorta diameter ratio below 0.5. The CoA repair was performed as the first procedure in all. The primary anastomosis was possible in all between AA and the descending aorta without undue tension after removal of the all ductus tissue and extensive mobilization of the aorta. Aortic clamp time was 28 minutes in average. The intraoperative pressure gradient after repair across AA was 0 to 10 mmHg (average 4.6 mmHg). All except 1 with preceding hepatic dysfunction tolerated the procedure without complication or operative death. Postoperative evaluation at 1 to 11 months showed no significant pressure gradient between upper and lower extremities. This method appears to be useful for CoA in early infancy particularly when AA is hypoplastic.

Anastomosis, Surgical↗