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Biomedical subjects

S Morimoto

Publications and source records attributed to S Morimoto.

At least 523 records · Page 29Linked to original sources
PubMed1988

Increase of (Ca2++Mg2+)-ATPase activity of renal basolateral membrane by parathyroid hormone via cyclic AMP-dependent membrane phosphorylation.

Studies were made on the mechanism of the effect of parathyroid hormone (PTH) on the activity of (Ca2++Mg2+)-ATPase, a membrane bound Ca2+-extrusion pump enzyme from the basolateral membranes (BLM) of canine kidney (Km for free Ca2+ = 1.3 X 10(-7) M, Vmax = 200 nmol Pi/mg/min). At 1 X 10(-7) M free Ca2+, both PTH (10(-7)-10(-6) M) and cAMP (10(-6)-10(-4) M) stimulated (Ca2++Mg2+)-ATPase activity dose-dependent and their stimulatory effects were inhibited completely by 5 microM H-8, an inhibitor of cAMP-dependent protein kinase. PTH (10(-7) M) also caused 40% increase in 32P incorporation into the BLM and 5 microM H-8 inhibited this increase too. PTH (10(-7) M) was found to stimulate phosphorylation of a protein of Mr 9000 by cAMP dependent protein kinase and 5 microM H-8 was found to block this stimulation also. From these results, it is proposed that PTH stimulates (Ca2++Mg2+)-ATPase activity by enhancing its affinity for free Ca2+ via cAMP-dependent phosphorylation of a BLM protein of Mr 9000.

Animals↗
PubMed1988

Existence of endogenous substrate proteins for Ca2+/calmodulin-dependent and Ca2+/phospholipid-dependent protein kinases in rat adrenal glomerulosa cells.

In rat adrenal glomerulosa cells, endogenous substrate proteins for Ca2+/calmodulin (CaM)-dependent protein kinase (glomerulosa CaM kinase) and Ca2+/phospholipid-dependent protein kinase (protein kinase C) were investigated. In a 105,000 g-supernatant fraction (cytosol), the Mr 100,000 protein was phosphorylated in the presence of calcium (calculated free Ca2+ concentration, 460 microM) alone or calcium and CaM, and the phosphorylation of this protein was completely inhibited by the CaM antagonists pimozide (500 microM) and melittin (5 microM) in the presence of calcium alone, respectively. These results indicate that the Mr 100,000 protein is a major substrate for glomerulosa CaM kinase, and considerable amounts of endogenous CaM might be present in the cytosol. In the presence of phospholipids (the micelles of 8 micrograms of phosphatidyl serine and 1 microgram of diacylglycerol), at least twelve proteins of Mr 127,000, 80,000, 70,000, 36,000, 35,000, 33,000, 32,000, 30,000, 27,000, 22,000, 19,000 and 17,000 were phosphorylated, and the phosphorylation of these proteins was enhanced by the addition of calcium, indicating that these proteins are substrates for protein kinase C. No endogenous protein phosphorylation was found in a 105,000 g-particulate fraction. Thus, these findings demonstrate that adrenal glomerulosa cells have specific substrate proteins for glomerulosa CaM kinase and protein kinase C, respectively.

Adrenal Glands↗
PubMed1988

1,25-Dihydroxyvitamin D3 binds specifically to rat vascular smooth muscle cells and stimulates their proliferation in vitro.

Cultured vascular smooth muscle cells (VSMC) derived from rat aorta were found to contain a specific receptor for 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Its Kd (5.0 x 10(-11) M) and capacity (22.9 fmol/mg of cytosol protein) for 1,25-(OH)2D3, its sedimentation coefficient on a sucrose density gradient (3.2 S), its relative affinities for various vitamin D3 metabolites [1,25-(OH)2D3 greater than 25-hydroxyvitamin D3 greater than 24,25-dihydroxyvitamin D3 greater than vitamin D3] and its affinity for DNA-cellulose were similar to those reported for the 1,25-(OH)2D3 receptor in other tissues. 1,25-(OH)2D3 at concentrations of more than 10(-10) M caused dose-dependent enhancement of the proliferation of VSMC in DMEM with 10% FCS. 25-Hydroxyvitamin D3 stimulated the proliferation of VSMC only at its highest concentration tested (10(-6) M). These data show that 1,25-(OH)2D3 stimulates the proliferation of VSMC after its binding to a cytoplasmic receptor of the cells in vitro, and support the possibility that VSMC are target cells of the hormone.

Animals↗
PubMed1988

Stimulatory effects of neuronally released norepinephrine on renin release from rat kidney cortical slices.

Stimulatory effects of extracellular high K+ in the presence of nifedipine (NIF) on renin release (RR) from kidney cortical slices were investigated. The stimulation was suppressed either by propranolol or by metoprolol but not by prazosin. High K+ plus NIF-induced increase in RR was attenuated by renal denervation. The enhancing effect was not observed when the slices were incubated in Ca2+-free buffer or in medium containing divalent cations such as Cd2+, Co2+ and Mn2+. These alterations in RR correlated with 3H-efflux from the slices preloaded with 3H-norepinephrine. We conclude that the high K+ plus NIF-induced increase in RR from the slices is mediated by norepinephrine (NE) derived from renal sympathetic nerves and that this neuronally released NE stimulates RR via the activation of beta-adrenoceptors.

Animals↗
PubMed1988

Effect of substitution of troponin C in cardiac myofibrils with skeletal troponin C or calmodulin on the Ca2+- and Sr2+-sensitive ATPase activity.

Troponin C was removed almost completely from the porcine cardiac myofibrils by the same extraction procedure using CDTA as that previously reported for the rabbit skeletal myofibrils (Morimoto, S. & Ohtsuki, I. (1987) J. Biochem. 101, 291-301), and the effects of substitution of troponin C in cardiac myofibrils with rabbit skeletal troponin C or bovine brain calmodulin were examined. While the ATPase activity of intact cardiac myofibrils or cardiac troponin C-reconstituted cardiac myofibrils was activated at only a little higher concentration of Sr2+ than Ca2+, the skeletal troponin C-substituted cardiac myofibrils, as well as intact rabbit skeletal myofibrils, required more than 10 times higher concentration of Sr2+ than Ca2+ for activation of the myofibrillar ATPase activity. However, the concentrations of Ca2+ and Sr2+ required for the activation of the ATPase activity of the skeletal troponin C-substituted cardiac myofibrils were both about 5 times higher than those of intact skeletal myofibrils. The skeletal troponin C-substituted cardiac myofibrils, as well as intact skeletal myofibrils, also showed higher cooperativity in the Ca2+-activation of the ATPase activity than intact or cardiac troponin C-reconstituted cardiac myofibrils. The ATPase activity of calmodulin-substituted cardiac myofibrils was activated at a several times lower concentration of Ca2+ or Sr2+ than that of calmodulin-substituted skeletal myofibrils, while the ratios of the concentration of Sr2+ to Ca2+ required for activation were almost the same in both cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Restoration of Ca2+-activated tension of CDTA-treated single skeletal muscle fibers by troponin C.

Single fibers from glycerinated rabbit psoas muscle were treated with a solution containing CDTA, a strong chelator of metal ions. The CDTA-treated fibers lost all of the troponin C and showed no Ca2+-activated tension development. The addition of troponin C restored the Ca2+-activated tension of CDTA-treated fibers. The tension-pCa relationship in the case of the CDTA-treated fibers reconstituted with troponin C was almost the same as that in the case of the same fibers before the CDTA treatment. These results are consistent with those of the previous study on the Ca2+-activated ATPase of CDTA-treated rabbit skeletal myofibrils.

Animals↗
PubMed1988

Calmodulin-independent stimulation of renin release by exposure of rat kidney cortical slices to calcium.

1. Effects of calcium-interacting agents on the calcium-induced stimulation of renin release from kidney cortical slices pretreated with calcium-free medium were examined. 2. The exposure of calcium to the slices pretreated with calcium-free medium enhanced the release of renin, followed by a decreased response in the release. The amount of lactate dehydrogenase released from the slices did not correlate with that of renin. 3. High potassium depolarization significantly potentiated the decreased response of renin release, with no influence on the stimulation of the release by exposure to calcium. 4. The decrease in renin release was attenuated by calcium-interacting agents, such as nifedipine, TMB-8 and W-7, but these agents were without effect on the stimulation of the release by exposure to calcium. 5. Thus, the calcium-calmodulin system apparently is not involved in the increased response of renin release following exposure to calcium.

Angiotensin I↗
PubMed1988

Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit.

1. Nicotine produced a transient contraction of rabbit isolated iris sphincter muscle, a parasympathetic ganglion-free tissue. The response to nicotine was antagonized by hexamethonium, but was insensitive to tetrodotoxin (TTX). While single treatments with atropine, capsaicin or [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-substance P (rpwwL-SP) partially blocked the response, combined treatment abolished it. 2. Chronic treatment of animals with nicotine added to the drinking water (about 12 mg kg-1 per day) had no effect on the responsiveness to nicotine or the pharmacological properties of nicotine-induced contraction. 3. These results suggest that acetylcholine and tachykinin(s) released via sodium channel-independent mechanisms from nerve terminals of parasympathetic and primary sensory nerves, respectively, are involved in the nicotine-induced contractile response.

Animals↗
PubMed1988

Diffuse panbronchiolitis: evaluation with high-resolution CT.

High-resolution computed tomography (CT) was performed in 20 patients with diffuse panbronchiolitis. Images of abnormal peripheral lung were classified into four types: small nodules around the end of bronchovascular branchings (CT type I), small nodules in the centrilobular area connected with small branching linear opacities (CT type II), nodules accompanied by ring-shaped or small ductal opacities connected to proximal bronchovascular bundles (CT type III), large cystic opacities accompanied by dilated proximal bronchi (CT type IV). CT classifications were compared with radiographic classifications and clinical stages of the disease. The comparison revealed that the classification based on CT findings reflected the clinical stages and pathologic process of diffuse panbronchiolitis. The authors conclude that high-resolution CT is useful in the evaluation of both the location and severity of the lesions.

Adult↗
PubMed1988

Primary thyroid lymphoma: evaluation with CT.

The appearance of primary thyroid lymphoma on computed tomographic (CT) scans and clinical data for 15 patients were analyzed. The CT appearances were classified into three types: 12 patients (80%) had a solitary nodule (type 1), two (13%) had multiple nodules (type 2), and one (7%) had a diffuse goiter (type 3). In 47% of cases, both lobes were involved. The tumors had a strong tendency to compress (80%) or infiltrate (53%) the surrounding structures. The frequency of calcification (7%) or necrosis (7%) was low. Most patients (87%) had a rapidly enlarging thyroid mass, and six (40%) complained of symptoms from obstruction. All patients had coexistent Hashimoto thyroiditis. In 13 of 15 patients (87%), a highly probable diagnosis of thyroid lymphomas was determined with CT and clinical findings. A staging workup with CT and clinical findings confirmed at biopsy will allow appropriate therapy and may lead to improved prognosis for patients with this condition.

Aged↗
PubMed1988

Stimulatory effects of neuronally released norepinephrine on renin release in vitro.

Extracellular high potassium inhibits renin release in vitro by increasing calcium concentrations in the juxtaglomerular cells. We found that the decreased response of renin release from rat kidney cortical slices in high potassium solution (20-80 mM) changed to a strikingly increased one in the presence of nifedipine at doses over 10(-6) M. We then examined the stimulatory effect of extracellular high potassium in the presence of nifedipine on renin release. The enhancement of release was significantly suppressed either by propranolol or by metoprolol but not by prazosin. High potassium plus nifedipine-induced increase in renin release was markedly attenuated by renal denervation. The enhancing effect was not observed when the slices were incubated in calcium-free medium. Divalent cations such as Cd2+, Co2+, and Mn2+ (0.1-3.0 mM) blocked this enhancement in a concentration-dependent manner. High potassium elicited an increase in 3H efflux from the slices preloaded with [3H]norepinephrine. The increasing effect was not influenced by nifedipine but was abolished by the removal of extracellular calcium or by the addition of divalent cations. These observations suggest to us that the high potassium plus nifedipine-induced increase in renin release from the slices is mediated by norepinephrine derived from renal sympathetic nerves and that this neuronally released norepinephrine stimulates renin release via activation of beta-adrenoceptors.

Animals↗
PubMed1988

Effect of sodium intake on urinary renin excretion in rats.

The present study was carried out to investigate the effect of sodium intake on urinary renin excretion in rats. Renin activity was measured before and after acidification, by radioimmunoassay of angiotensin I generated by incubation with partially purified homologous renin substrate. The molecular weight of renin was determined by gel filtration. Low sodium intake for 4 weeks resulted in a 16-fold increase in urinary renin excretion and led to a 15-fold increase in plasma renin activity. A 2.5-fold increase in renal renin content was simultaneously observed. In contrast, high sodium intake for 4 weeks decreased urinary renin excretion, plasma renin activity and renal renin content to about 20%, 25% and 35% of the control level, respectively. No significant change in renin activity after acidification was observed in all the urine samples. The molecular weight of renin in the urine from rats on low or high sodium intake was 40,000, the value being identical with that from control rats. These results indicate that urinary renin excretion is well correlated with plasma renin activity, and that only active renin with a molecular weight of 40,000 is excreted in the urine of rats, even under conditions of altered sodium intake.

Animals↗
PubMed1988

Plaque rupture possibly induced by coronary spasm--an autopsy case of acute myocardial infarction.

The histological picture of sites of coronary spasms has not yet been made sufficiently clear. A histopathological examination was performed on the coronary artery of a patient who died of acute myocardial infarction after a refractory coronary spasm was identified by coronary arteriography. In the site of the coronary spasm, intimal bleeding as well as infiltration by lymphocytes and plasma cells in the adventitia were seen. In the same region, fracture of intimal collagen fibers and rupture of atheromatous plaque were observed. Although it is very difficult to prove in individual cases of acute myocardial infarction that spasms played a part, some cases involving spasms may possibly exist among the cases of acute myocardial infarction showing atheromatous plaque rupture--thrombus formation.

Coronary Angiography↗
PubMed1988

Effect of estrogens on renal responsiveness to parathyroid hormone in elderly female subjects.

The effect of estrogens on the renal responsiveness to parathyroid hormone (PTH) was examined by PTH loading tests with synthetic human-PTH (1-34) in 8 normal elderly females (mean +/- SD age, 81.0 +/- 7.1 yr) before and after administration of estrogen (Premarin 1.25 mg/day for 4 weeks). Basal urinary adenosine cyclic 3', 5'-monophosphate (cAMP) excretion showed a tendency to increase after estrogen administration (5.47 +/- 1.68 vs 6.60 +/- 2.67 nmol/100 ml GFR) and the theoretical renal phosphorous threshold showed a tendency to decrease from 3.22 +/- 0.98 to 2.73 +/- 0.56 mg/dl. The blood ionized calcium concentration did not change after estrogen administration (4.44 +/- 0.16 vs 4.32 +/- 0.20 mg/dl) and serum phosphorous (P) decreased significantly (3.65 +/- 0.47 vs 3.01 +/- 0.42 mg/dl, p less than 0.05). There was no increase in mean serum immunoreactive PTH (0.34 +/- 0.10 vs 0.34 +/- 0.05 ngeq/ml). The urinary excretions of cAMP in response to PTH loading [100 U of human-PTH (1-34), intravenously] significantly (p less than 0.05) increased (94.8 +/- 57.0 vs 196.7 +/- 118.3 nmol/100 ml GFR/h) after estrogen administration. Moreover the changes in urinary excretion of cAMP (r = 0.698, p less than 0.01) and P (r = 0.555, p less than 0.05) induced by the PTH loading were positively correlated with serum estradiol in elderly females, assessed as groups before and after estrogen administration. These results suggest that estrogens may enhance the renal responsiveness to exogenous PTH administration.

Adult↗
PubMed1988

A patient with hypogonadotropic hypogonadism successfully treated by long-term pulsatile administration of luteinizing hormone-releasing hormone.

A male patient with hypogonadotropic hypogonadism has been treated by pulsatile administration lf luteinizing hormone-releasing hormone (LHRH) (20-25 micrograms, every 2 hours, sc) for 4 years 6 months. His plasma testosterone (T) concentration began to increase after 4 weeks of treatment and reached the normal range in week 5. He showed complete secondary sexual development after 1 year of treatment. His sperm count was normalized after 1 year of treatment. He was married after 29 months of therapy, and has a healthy male child. Blood type tests showed his paternity of the child. During the long duration of pulsatile LHRH therapy, his gonadotropin secretion has been stimulated by LHRH and his T level has been maintained with no observable side effects. There are no other reports of patients treated by pulsatile LHRH injection for such a long duration, but finding in this patient indicated that long-term pulsatile LHRH therapy is a useful and safe method for treatment of hypothalamic hypogonadotropic hypogonadism.

Adult↗