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Biomedical subjects

K Hiwada

Publications and source records attributed to K Hiwada.

At least 307 records · Page 17Linked to original sources
PubMed1989

Calpain proteolysis of free and bound forms of calponin, a troponin T-like protein in smooth muscle.

Calponin, a novel homologue of troponin T, purified from chicken gizzard was found to be one of the most susceptible proteins among smooth muscle contraction-associated proteins to hydrolysis by calpain I purified from human red blood cells. The high susceptibility of calponin was comparable to that reported for troponin T. The rate of degradation of calponin, unlike caldesmon and myosin light chain kinase, was accelerated when bound to calmodulin. When calponin existed as a bound form in both reconstituted actin filament and native thin filament, the rate of proteolysis was markedly retarded, indicating close association of calponin with actin filament. These observations are compatible with the view that calponin is an integral part of the actin-linked contractile machinery in smooth muscle.

Animals↗
PubMed1989

Effect of oral potassium on urinary kallikrein excretion in essential hypertension.

Urinary kallikrein and potassium were excreted in parallel in not only static but also dynamic sodium states. Oral potassium load stimulated the release of urinary kallikrein in normotensive subjects and WHO stage I essential hypertensive patients. Stage II essential hypertensive patients had the lowest value of basal level of urinary kallikrein and showed no increase in urinary kallikrein by oral potassium load. These results suggest that the functional activity of renal kallikrein-kinin system decreases with the development of essential hypertension.

Administration, Oral↗
PubMed1989

Blood pressure elevation caused by inhibition of brain glutathione reductase.

The effect of brain glutathione reductase activity on blood pressure regulation was investigated. The intravenous administration of the glutathione reductase inhibitor, nitrofurantoin (0.1-0.3 mg/rat), to seven normotensive Wistar rats caused dose-dependent rises in blood pressure and the heart rate (delta mean blood pressure 17 +/- 1 mmHg; delta heart rate 89 +/- 7 beats/min for 0.3 mg). Rats treated with 0.3 mg nitrofurantoin showed a 50% decrease in glutathione reductase activity with a twofold increase in the ratio of glutathione disulphide to reduced glutathione in the hypothalamus and brainstem, and a 1.5-fold increase in plasma noradrenaline and plasma renin activity compared with controls. These nitrofurantoin-induced effects were totally abolished by pretreatment with a sympathetic ganglion blocker (4 mg pentolinium tartrate, administered subcutaneously) except for the increased ratio of glutathione disulphide to reduced glutathione and the decreased glutathione reductase activity in the brain. These results suggest that the blood pressure elevation caused by inhibition of brain glutathione reductase activity occurs through activation of the sympathetic nervous system and the renin-angiotensin system.

Animals↗
PubMed1989

Effects of renin inhibitors on the expression of kidney renin gene and tissue renin-like activity.

The effect of renin inhibitor ES-1005 on renin gene expression was investigated in sodium-depleted marmosets. The kidneys were removed after continuous infusion of ES-1005 (12 mg/kg per h) for 2 h. The relative amount of kidney renin messenger (m)RNA was measured by densitometric Northern blot analysis using an alpha-32P-labelled human renin complementary (c)DNA fragment as a hybridization probe. Plasma renin activity was completely inhibited by ES-1005. The level of kidney renin mRNA decreased significantly to about one-third of the normal control value. We also investigated the inhibitory potency of the renin inhibitor ES-6864 on the renin-like activity in dog tissues (adrenal glands, aorta and brainstem). ES-6864 inhibited the tissue renin-like activity with an IC50 of 10(-7) to 10(-8) mol/l in vitro. Renin inhibitors not only inhibit the activity of plasma and tissue renin, but also suppress the synthesis of renin in the kidney.

Animals↗
PubMed1989

Impact of a family history of hypertension on blood pressure levels during early and late adolescence.

The aim of this study was to examine the impact of a family history of hypertension (FHH) on blood pressure levels in Japanese rural adolescents. The study population consisted of 458 and 553 subjects, aged 13 and 16 years, respectively. Particular attention was focussed on subjects with a FHH (13 years old, n = 38; 16 years old, n = 46) and those without a FHH (13 years old, n = 83; 16 years old, n = 97). Significant associations were found between FHH and systolic blood pressure for boys and girls at 16 years old and diastolic blood pressure for girls at 16 years old. The impact of a FHH on blood pressure mainly affected systolic blood pressure in late adolescence (16 years of age). In early adolescence (13 years of age), different physical maturation status may have masked the real impact of a FHH on blood pressure.

Adolescent↗
PubMed1989

Blood pressure distribution and determinants of higher levels of blood pressure in Japanese rural adolescents.

The blood pressures (BP) and anthropometric values of 1,014 Japanese rural school children aged 12-17 years old were measured at one-year interval. The strongest correlation for systolic BP (SBP) was weight and for diastolic BP (DBP) it was age. Larger values of weight, body mass index, triceps skinfold thickness and smaller increment of height showed significant discriminative powers in differentiating the subjects who had been above the age-sex specific 80th percentile value (H-H group) from those who had been below the 20th percentile value (L-L group) for both SBP and DBP. Subjects with a family history of hypertension (FHH) had higher SBP than those without a FHH, and were more prevalent in H-H group for SBP. These results indicate that larger body size and more mature stature are determinants of higher levels of BP during adolescence, and that FHH affects SBP only in this period.

Adolescent↗
PubMed1989

[Molecular forms of plasma atrial natriuretic peptide (ANP) after three kinds of ANP releasing stimulation].

This study analyzed by high performance gel permeation chromatography (HPGC) molecular forms of atrial natriuretic peptide (ANP) in plasma from anesthetized dogs stimulated by balloon inflation at the main pulmonary artery (Group A, n = 4), right atrial pacing (Group B, n = 4) and low-molecular dextran injection to right atrium (Group C, n = 4). Mean pulmonary arterial (PA) pressure, mean right atrial (RA) pressure, mean arterial pressure, heart rate and ECG were monitored by polygraph system Mean PA pressure in Group A, heart rate in Group B and mean RA pressure in Group C increased significantly by the stimulation (p less than 0.01, p less than 0.001 and p less than 0.05 respectively). Other parameters were not changed significantly in the three groups. There were significant increases in ANP concentration after the three stimulations (Group A: 52.4 +/- 5.4 (SD) pg/ml----86.4 +/- 12.2 (SD) pg/ml, Group B: 43.8 +/- 6.7 (SD) pg/ml----72.0 +/- 14.1 (SD) pg/ml, Group C: 42.7 +/- 8.8 (SD) pg/ml----69.3 +/- 10.0 (SD) pg/ml; each p less than 0.01). Gel filtration profiles showed that the increased form of plasma ANP in the three groups was alpha-ANP. These results suggest that alpha-ANP may be a main molecular form in plasma from dogs stimulated by the stretch of pulmonary arterial wall and right atrial wall, and atrial pacing.

Animals↗
PubMed1989

[A patient with olivopontocerebellar atrophy combined with sleep apnea syndrome].

A 52-year-old man with olivopontocerebellar atrophy was admitted to Ehime University Hospital for examination of sleep apnea. Overnight polysomnographic study revealed that his sleep apnea was predominantly the central type. With progress of the disease, the dominance of apnea pattern changed from the central type to the obstructive type. After tracheostomy, the apnea index decreased from 15 per hour to 12.4 per hour. However, the apnea index of the central type increased from 1.5 per hour to 12.4 per hour. These findings suggest that the effect of tracheostomy is not always beneficial in sleep apnea, and that the frequency and the pattern of apnea are not always indicators of tracheostomy.

Humans↗
PubMed1989

Kidney renin gene expression in spontaneously hypertensive rats.

We studied the expression of kidney renin gene in hypertensive animals by measuring the kidney renin messenger (m) RNA. The kidney renin mRNA was quantified by densitometric Northern blot analysis using a 32P-labelled rat renin genomic DNA fragment as a hybridization probe. Spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats (WKY) were treated with a low-sodium diet plus furosemide, captopril or propranolol for a week. Plasma renin activity (PRA) in SHR and WKY was increased similarly by sodium depletion and by treatment with captopril. PRA in both strains was not decreased significantly by treatment with propranolol. Both sodium depletion and captopril treatment caused significant increases in the kidney renin mRNA in SHR and WKY. However, the increases in the kidney renin mRNA of SHR were greater than those in the corresponding WKY (SHR, 10.0- and 22.1-fold increases; WKY, 6.2- and 7.8-fold increases, respectively). Propranolol had no effect on the kidney renin gene expression in either WKY or SHR. These results indicate that SHR show an enhanced expression of the renin gene in the kidney compared with WKY in response to stimuli that increase renin release.

Animals↗
PubMed1988

A novel troponin T-like protein (calponin) in vascular smooth muscle: interaction with tropomyosin paracrystals.

Calponin is a smooth muscle tropomyosin-binding protein which is antigenically related to troponin T. The fine localization of calponin and troponin T on the polar paracrystals of smooth muscle tropomyosin were studied by electron microscopy. Both calponin and troponin T bound to the filamentous tropomyosin at a site about 17 nm away from the C-terminal end of tropomyosin molecule. This calponin-binding site corresponds to the domain which is highly conserved in the amino-acid sequences among the tropomyosin isoforms from skeletal muscle and smooth muscle. The result suggests that calponin, in collaboration with tropomyosin, may play an important role in regulating contractile apparatus.

Animals↗
PubMed1988

Vascular smooth muscle calponin. A novel troponin T-like protein.

In a search for additional Ca2+ regulatory components in vascular smooth muscle, a novel troponin T-like protein was purified from bovine aorta smooth muscle. The isolated protein was separated into several isoforms on isoelectric focusing. The major isoelectric variants were focused in the pH region of 8.4 to 9.1. The protein had slightly different molecular masses in the Mr range of 35,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Its molar ratio relative to tropomyosin in the muscle extract was estimated to be 0.9:1.0. The novel protein bound to the immobilized calmodulin and exhibited a number of common physicochemical properties with gizzard (Mr = 34,000) calmodulin-binding and F-actin-binding protein. The aorta and gizzard proteins were immunologically cross-reactive. Both proteins shared a common antigenic determinant with COOH-terminal segments of rabbit skeletal and bovine cardiac troponin T and bound to the immobilized smooth muscle tropomyosin. Both proteins interacted with rabbit skeletal troponin C in the presence and absence of Ca2+, but they did not interact with troponin I. These results suggest that the novel protein, which is designated calponin, may be a specialized component of smooth muscle thin filament involved in the regulation of contractile apparatus.

Animals↗
PubMed1988

A highly potent and long-acting oral inhibitor of human renin.

An orally active renin inhibitor, ES 6864 (N-[(2R)-3-morpholinocarbonyl-2-(1-naphthylmethyl)propionyl]-(4- thiazolyl)-L-alanyl-cyclostatine-(2-morpholinoethyl)amide), was synthesized. ES 6864 was found to be a highly potent inhibitor of human renin with a Ki value of 7.3 x 10(-9) M. The compound competitively inhibited human renin. The inhibitor was also potent against monkey renin but was less effective against renins from pig, goat, dog, rabbit, and rat. ES 6864 did not inhibit cathepsin D, pepsin, trypsin, chymotrypsin, angiotensin converting enzyme, and urinary kallikrein at a concentration of 10(-5) M. ES 6864 was resistant to proteolytic actions of the enzymes in rat tissue homogenates (liver, kidney, pancreas, and small intestine). Oral administration of ES 6864 at 30 mg/kg to conscious, sodium-depleted marmosets produced a significant blood pressure reduction and almost complete inhibition of plasma renin activity, which persisted for 5 hours. Oral administration of ES 6864 also produced dose-related decreases of blood pressure in hog renin-infused rats, but the duration of action was much shorter than that in conscious marmosets. The parent compound in the blood following oral administration of ES 6864 to marmosets was confirmed directly by measuring the plasma concentration of ES 6864. These results enhance the possibility of developing renin inhibitors that can be used clinically.

Administration, Oral↗
PubMed1988

Cerebral and myocardial infarction induced by nonbacterial thrombotic endocarditis in a patient with ovarian cancer: report of a case.

A 40-year-old woman was admitted to our hospital because of left hemiplegia. She was affected with myocardial infarction and cerebral infarction. Echocardiogram revealed that the aortic and mitral valves had thick and uneven echoes suggesting vegetations. Judging from the finding that repeated blood cultures were negative, we had considered in her lifetime that myocardial and cerebral infarctions were due to embolization associated with nonbacterial thrombotic endocarditis (NBTE). At autopsy, histological diagnosis was made as ovarian cancer with disseminated intravascular coagulation. From the clinical course and the histological findings, we diagnosed this patient as NBTE.

Adult↗