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Biomedical subjects

N Sugino

Publications and source records attributed to N Sugino.

At least 19 recordsLinked to original sources
PubMed1992

Endothelin-specific antibodies decrease blood pressure and increase glomerular filtration rate and renal plasma flow in spontaneously hypertensive rats.

OBJECTIVE: Studies were undertaken to clarify the pathophysiologic significance of endogenous endothelin in the control of blood pressure and renal hemodynamics in spontaneously hypertensive rats (SHR). DESIGN: The technique of passive immunization was used to neutralize endogenous endothelin in order to estimate the contribution of endothelin to the in vivo control of blood pressure and renal hemodynamics. METHODS: Endothelin-specific antibodies were administered intravenously into anesthetized SHR and Wistar-Kyoto (WKY) rats, and the effects upon blood pressure and renal function (renal plasma flow and glomerular filtration rate) assessed. Using the same antibodies, baseline plasma levels of endothelin in both strains of rats were determined by radioimmunoassay. RESULTS: Infusion of endothelin-specific antibodies into SHR decreased mean arterial pressure by approximately 10% and renal vascular resistance and renal vascular resistance by approximately 35%. Glomerular filtration rate and renal plasma flow both increased by approximately 50% over control. In contrast, infusion of normal rabbit serum into SHR or of endothelin-specific antibodies into WKY rats did not result in any significant change in renal hemodynamics or arterial blood pressure. Baseline plasma levels of immunoreactive endothelin in SHR were significantly lower than those in WKY rats. CONCLUSION: These results suggest that endothelin plays an important role in the modulation of systemic blood pressure and renal function in SHR.

Animals↗
PubMed1992

[Increased serum levels of human cardiac myosin light chain 1 in patients with renal failure].

In this study, we measured cMLC1 concentration in serum and urine from patients with acute myocardial infarction (AMI), chronic renal failure (CRF), and various grades of renal dysfunction (RD) in comparison with normal controls, by using enzyme immunoassay (EIA) with monoclonal antibody, and attempted to elucidate the mechanism of increased serum level of cMLC1 in patients with renal failure. The serum level of cMLC1 of CRF patients under maintenance hemodialysis (HD) was 20.3 +/- 19.6 ng/ml, markedly higher than normal controls (0.54 +/- 0.55 ng/ml). The patients with RD and CRF under conservative therapy had higher serum cMLC1 level than normal controls especially in advanced CRF, while each value not correlating with their creatine clearance (Ccr). cMLC1 in urine was detectable in only two cases with AMI accompanied with CRF or RD. In addition, immunohistological studies of renal biopsy specimens from RD patients did not show cMLC1 deposits in glomerulus. These results suggest that cMLC1 is assumably filtered through the glomerulus, and then absorbed in the renal tubule.

Humans↗
PubMed1992

Comparison of converting enzyme inhibitor and calcium channel blocker in SHR with nephrotoxic serum nephritis.

In order to compare the protective effects of angiotensin converting enzyme inhibitors (ACEI) and calcium channel blockers (CCB) on the renal function in experimental nephritis, nephrotoxic serum nephritis was induced in male spontaneously hypertensive rats (SHR). The above drugs were then chronically administered to different groups, as follows: the ACEI-treated group (n = 7) received captopril (150 mg/kg/day), and the CCB-treated group (n = 6) was given both nifedipine (40 mg/kg/day) and nisoldipine (20 mg/kg/day). The control group (n = 8) received a placebo. Although the control group developed marked hypertension and proteinuria, the rats treated with either ACEI or CCB demonstrated a significant and equivalent decrease in mean arterial pressure and urinary protein excretion. At 15 weeks after the injection of nephrotoxic serum, all rats were anesthetized with Inactin, and the glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured. In the control group, GFR and RPF were markedly attenuated. However, both were preserved at much higher levels in the ACEI-treated group, and GFR was also maintained to a similar degree in the CCB-treated group. Histological studies were carried out after the clearance studies. As a result, it was found that the ACEI treatment significantly limited the development of glomerulosclerosis, whereas CCB modestly ameliorated the glomerular structural lesions. Moreover, ACEI significantly reduced the serum cholesterol, while CCB did not exert such an effect. These results suggest that both ACEI and CCB have a therapeutic effect in experimental glomerulonephritis models which are accompanied by hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Molecular form of immunoreactive endothelin in plasma and urine of normal subjects and patients with various disease states.

To elucidate the pathophysiologic significance of the family of endothelin (ET) peptides, we have investigated plasma and urinary immunoreactive (ir-) ET levels and its molecular forms in normal and pathological conditions. Plasma and urine ET were extracted with an Amprep C2 column. The molecular form of ET was determined by a combination of radioimmunoassay and reverse-phase high-performance liquid chromatography. Although plasma ir-ET was composed mainly of big ET and endothelin-1 (ET-1) in normal subjects, that in acute myocardial infarction, chronic renal failure (CRF), essential hypertension, and vasospastic angina pectoris was characterized by an increase of high molecular ir-ET in addition to increases in big ET and ET-1. Urinary ir-ET in both normal subjects and patients with CRF was composed mainly of a high molecular form in addition to big ET and ET-1. These results suggest that the biosynthetic and/or degradation process of ET under pathological conditions appears to be different from that under normal conditions.

Angina Pectoris↗
PubMed1991

Different mechanisms for the inhibition of progesterone secretion by ACTH and corticosterone in pregnant rats.

The present study investigated possible sites through which ACTH or corticosterone inhibit progesterone secretion in pregnant rats, and the role of placental factors in blocking the inhibitory effect. The number of conceptuses was adjusted to one (IC group) or more than ten (FC group) on day 7 of pregnancy by aspirating the desired number. Serum concentrations of progesterone, testosterone and oestradiol were significantly (P less than 0.01) lower on day 15 in the 1C group than in the FC group. Corpora lutea (CL) obtained on day 15 were incubated for 6 h with corticosterone or ACTH. Corticosterone (1 mumol/l) significantly (P less than 0.05) inhibited progesterone secretion in the 1C group but not in the FC group. The inhibitory effect of corticosterone in the 1C group was completely blocked by co-addition of 1 mumol testosterone/l or 1 mumol oestradiol/l but not by 1 mumol dihydrotestosterone/l. ACTH (1 microgram/l-1 mg/l) had no direct effect on progesterone secretion in either the 1C or the FC groups, although ACTH apparently decreases progesterone secretion in vivo. Placentae obtained from rats of the FC group on day 15 were incubated for 24 h with or without ACTH (1 mg/l). The supernatant after placental incubation without ACTH significantly (P less than 0.01) increased progesterone secretion by the CL in both the 1C and FC groups, and also eliminated the inhibitory effect of corticosterone in the 1C group. The supernatant after placental incubation with ACTH also increased progesterone secretion in the FC group as effectively as the supernatant from the control incubation, but it had no effect in the 1C group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1991

Effect of dietary chloride on spontaneously hypertensive rat.

The anionic component of sodium salt has been reported to contribute to hypertension in some animal models and hypertensive patients. In the present study, the anionic effects on exacerbation of hypertension in spontaneously hypertensive rat (SHR) were investigated by chronic loading tests with two sources of sodium, viz. sodium chloride (NaCl; 0.9% solution) and sodium bicarbonate (NaHCO3; 1.28% solution), using SHRs with normal renal function (NRF) and with chronic renal failure (CRF; produced by cryosurgery). In addition, extracellular fluid volume (ECFV: inulin space) was measured in SHRs with NRF and CRF. In the NRF groups, systolic blood pressure (SBP) reached 230 mmHg at Week 13, and there was no significant difference in SBP between the NaCl and NaHCO3 groups. In the CRF groups, SBP of the NaCl group was significantly higher (p less than 0.01) than that of the NaHCO3 group (280 mmHg vs. 230 mmHg at Week 15). ECFV was also greater in the NaCl group than in the NaHCO3 group (ECFV: NaCl vs. NaHCO3, 15.9 +/- 1.7 vs. 14.0 +/- 0.9 at Week 13; and 16.2 +/- 1.1 vs. 14.2 +/- 1.2 at Week 15, respectively). These results indicate that chloride ion plays an important role in the pathogenesis of hypertension in SHR with CRF. Expansion of ECFV is considered to be one of the mechanisms whereby the hypertension is exacerbated.

Animals↗
PubMed1991

[Improvement of malnutrition indices in adult patients with end stage renal disease by recombinant human growth hormone].

Recombinant human growth hormone (r-hGH), 1 U/kg body weight/week, was administered subcutaneously for 2-4 weeks to two end stage renal disease patients with severe malnutrition. Following r-hGH, there were significant increase in hematocrit level and serum concentration of albumin, IGF-1 and GH, and decrease of urea nitrogen. It was concluded that r-hGH exerts a therapeutic effect to nutritional status in renal failure patients by improving severe hypoalbuminemia, susceptibility to infectious disease, intractable ascites and so on.

Adult↗
PubMed1991

Tubuloglomerular feedback resetting in different models of acute volume expansion.

Our results revealed that renal blood flow (RBF) increased during both isooncotic and hypooncotic plasma expansion by 4% of body weight (BW). Tubuloglomerular feedback (TGF) sensitivity assessed by the measurement of proximal stop-flow pressure at loop perfusion rates of 0 to 40 nl/min and RBF autoregulation were not substantially affected by this degree of volume expansion, provided plasma oncotic pressure did not change. This upward shift of the TGF response curve together with maintenance of an RBF autoregulation during plasma expansion lead to the conclusion that the TGF mechanism apparently plays a significant role in the control of glomerular hemodynamics, despite the marked vasodilation occurring during acute volume expansion.

Animals↗
PubMed1990

[Treatment of liver metastatic ovarian cancer with sequential administration of OK-432 and etoposide].

OK-432 and etoposide were administered intravenously to a patient with liver metastasis of ovarian cancer. OK-432 induced IFN-gamma and TNF. SuPS and PPD skin reaction became positive after the therapy. The size of metastatic lesions was reduced significantly (partial response). It is suggested that the combination therapy of OK-432 and etoposide may be effective to the liver metastasis of ovarian cancer.

Adult↗