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Biomedical subjects

T Horio

Publications and source records attributed to T Horio.

At least 145 records · Page 8Linked to original sources
PubMed1993

Stimulation of brain natriuretic peptide release from the heart by thyroid hormone.

This study was designed to examine the involvement of thyroid hormone in the release of brain natriuretic peptide (BNP) from the heart. We measured plasma immunoreactive BNP (ir-BNP) concentrations in patients with untreated hyperthyroidism. We also measured BNP values in experimental rats with hyperthyroidism induced by thyroxine (T4) and in rats with hypothyroidism induced by propylthiouracil (PTU). The in vitro effects of triiodothyronine (T3) and T4 on the release of BNP were examined in newborn rat atrial and ventricular myocytes in primary culture. Plasma BNP levels were increased in hyperthyroid patients compared with normal control subjects. Plasma BNP levels were increased in hyperthyroid rats and decreased in hypothyroid rats compared with euthyroid rats. Plasma BNP level was correlated with serum T4 level in hyperthyroid patients and hyperthyroid rats. A major component of ir-BNP in plasma from hyperthyroid patients was human BNP-32 and that in plasma from hyperthyroid rats was rat BNP-45. T4 and T3 stimulated release of ir-BNP from both cultured atrial and ventricular myocytes in a dose-dependent manner. Plasma BNP concentration is frequently increased in hyperthyroidism, and thyroid hormone may regulate BNP release from both atrial and ventricular myocytes.

Adult↗
PubMed1993

Cosecretion of atrial and brain natriuretic peptides stimulated by endothelin-1 from cultured rat atrial and ventricular cardiocytes.

We examined the secretion of immunoreactive (ir) atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in primary cultures of atrial and ventricular cardiocytes from neonatal rats, and also investigated the stimulatory effect of endothelin-1 (ET-1) on ir-ANP and ir-BNP release from these cells. After 2 days of culture, rat atrial and ventricular cardiocytes secreted both ir-ANP and ir-BNP into serum-free medium in a time-dependent manner. The amount of ir-BNP released per 10(5) ventricular cells was approximately 60% to 70% (1.8 +/- 0.5 pg/h, 2.5 +/- 0.4 pg/2 h, 2.6 +/- 0.4 pg/4 h) of that released from atrial cells (2.8 +/- 0.4 pg/h, 3.5 +/- 0.6 pg/2 h, 4.6 +/- 0.6 pg/4 h), although ir-ANP was secreted almost entirely from atrial cells. ET-1 clearly stimulated secretion of both ir-ANP and ir-BNP in atrial and ventricular cardiocytes. These observations indicate that ir-BNP is cosecreted with ir-ANP not only from atrial cardiocytes, but also from ventricular cardiocytes in the rat, and that ET-1 stimulates the secretion of these natriuretic peptides by a direct mechanism, not through a hemodynamic change.

Animals↗
PubMed1993

Effect of heparin on endothelin-1 production by cultured human endothelial cells.

Heparin shows a blood pressure-lowering effect in various hypertensive rat models. This study was designed to examine the effect of heparin on vasoconstrictor endothelin-1 (ET-1) production by cultured human umbilical vein endothelial cells (HUVECs). ET-1 and cyclic GMP levels in the medium were determined by radioimmunoassay. ET-1 mRNA was quantified by densitometric Northern blot analysis. ET-1 was released into the medium in a time-dependent manner, and its release was augmented by thrombin (10 U/ml). Heparin suppressed both basal and thrombin-stimulated ET-1 secretion and its mRNA expression in a dose-dependent manner. Heparin suppressed ET-1 mRNA expression in a time-dependent fashion. Heparin did not suppress both basal and thrombin-stimulated ET-1 production in the presence of NG-monomethyl-L-arginine (L-NMMA) (10(-5) M). The production of cGMP stimulated by thrombin was significantly enhanced by heparin, but not in the presence of L-NMMA (10(-5) M). Heparin may suppress vasoconstrictor ET-1 production mediated by the enhancement of endothelium-derived nitric oxide in HUVECs.

Blotting, Northern↗
PubMed1993

The effect of ultraviolet (UVB and PUVA) radiation on the expression of epidermal keratins.

Using a panel of monoclonal antibodies directed against keratins (PKK2, CK8.12 and KL1), the effects of ultraviolet B (UVB) and psoralen plus ultraviolet A (PUVA) irradiation on keratin expression in guinea-pig skin were examined immunohistochemically. Following irradiation, whether by UVB or PUVA, rapid alterations in the distribution pattern of keratins were observed in the epidermis. The alterations included the induction of basal cell-type keratins (PKK2 and CK8.12 staining) in the suprabasal layers, with concomitant reduction of the suprabasal-type keratins (KL1 staining). These alterations in keratin expression were observed during the period when DNA synthesis appears to be accelerated by ultraviolet light exposure (5 h-5 days after UVB, and 2-10 days after PUVA irradiation). Therefore, these changes are probably reflections of a proliferative or regenerative state of keratinocytes. This explanation was supported by the result of an experiment involving tape stripping of the epidermal horny layers, which also accelerates DNA synthesis by keratinocytes. Immunohistochemistry appears to be a useful and sensitive method of detecting the effect of ultraviolet light on keratinization.

Animals↗
PubMed1993

Interaction of PDGF and natriuretic peptides on mesangial cell proliferation and endothelin secretion.

The present study examined the possible interaction of platelet-derived growth factor (PDGF) and atrial or brain natriuretic peptides (ANP and BNP, respectively) on cellular proliferation and secretion of endothelin-1 in cultured rat mesangial cells. PDGF increased cellular proliferation and endothelin-1 secretion. The protein kinase C (PKC) inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, staurosporine, and PKC inhibitor peptide, inhibited such stimulation. Rat ANP-(1-28) and rat BNP-45 exhibited clearly dose-related inhibition of PDGF-stimulated cellular proliferation and endothelin-1 secretion. This inhibition by ANP and BNP was paralleled by an increase in the cellular level of guanosine 3',5'-cyclic monophosphate (cGMP). Results indicate that PDGF stimulates cellular proliferation and endothelin-1 secretion in cultured rat mesangial cells by a mechanism probably involving activation of PKC and that ANP and BNP inhibit such stimulation through a cGMP-dependent process.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Interaction between a phorbol ester and dopamine DA1 receptors on vascular smooth muscle.

The interaction between dopamine DA1 receptors and a phorbol ester was studied to elucidate the role of protein kinase C in the response of this receptor. The in vitro binding of [3H]Sch 23390 to DA1 receptor sites on vascular smooth muscle cells was saturable. The extent of [3H]Sch 23390 binding to phorbol ester-treated cells was increased without any change in the dissociation constant. The production of adenosine 3',5'-cyclic monophosphate (cAMP) in response to DA1 receptor stimulation was enhanced by preincubation of vascular smooth muscle cells with the phorbol ester for 4 h. However, no enhancement was observed when the medium used for preincubation was supplemented with a protein kinase C inhibitor. Direct stimulation of stimulatory guanine nucleotide-binding regulatory protein with 5-guanylylimidodiphosphate and direct stimulation of adenylate cyclase with forskolin produced no significant differences in cyclase levels between phorbol ester-treated and untreated cells. These results suggest that activation of protein kinase C triggers an increase in the membrane expression of DA1 receptors, thereby enhancing receptor-coupled cAMP generation.

Adenylyl Cyclases↗
PubMed1993

Natriuretic peptides inhibit mesangial cell production of endothelin induced by arginine vasopressin.

The present study examined the effects of atrial, brain, and C-type natriuretic peptides (ANP, BNP, and CNP, respectively) on endothelin-1 (ET-1) secretion after stimulation with arginine vasopressin (AVP), using cultured rat glomerular mesangial cells. AVP stimulated immunoreactive (ir) ET-1 secretion in a concentration-dependent manner via a receptor-mediated process. Rat ANP-(1-28) and rat BNP-45 potently inhibited this stimulated secretion in a concentration-dependent manner. Inhibition by ANP and BNP of AVP-stimulated ET-1 secretion was paralleled by an increase in the medium level of guanosine 3',5'-cyclic monophosphate (cGMP). The addition of a cGMP analogue, 8-bromo-cGMP, reduced the stimulated ET-1 secretion. CNP was much less effective than rat ANP-(1-28) or rat BNP-45 with respect to inhibiting irET-1 secretion and increasing cGMP levels. High-performance liquid chromatography indicated that the major component of irET-1 in the culture medium corresponds to ET-1-(1-21). These findings indicate that AVP stimulates ET-1 secretion in cultured rat mesangial cells and that rat ANP and BNP inhibit this stimulated secretion, probably through a cGMP-dependent process.

Animals↗
PubMed1992

Purification and partial characterization of two types of growth-inhibitory protein latently present in rabbit serum.

Normal rabbit serum contained two kinds of growth-inhibitory protein, GI-I and GI-II, in latent forms. These latent inhibitors were activated by incubation at 37 degrees C for 12 h, and their activation was lowered by inhibitors for serine, cysteine and metalloproteinases. Both growth inhibitors were highly purified in active forms by successive column chromatographies. GI-I showed a major protein band with an Mr of 18,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, while GI-II showed a major protein band with an Mr of 36,000. GI-I and GI-II half-inhibited the growth of rat tumorigenic cell line (RSV-BRL) at concentrations of 0.5 ng/ml and 10 ng/ml, excess concentrations. Of the 15 cell lines tested, GI-I specifically inhibited the growth of rodent and lagomorph cells, whereas GI-II nonspecifically inhibited the growth of all cell lines tested. Specificities for cell type and malignancy were not observed with either inhibitor. These growth inhibitors were stable to a reducing reagent and proteinase inhibitors, but labile to urea, acid, organic solvents, trypsin, plasmin and heating at 95 degrees C for 5 min. These properties suggested that both growth inhibitors might be distinct from known growth-inhibitory factors.

Animals↗
PubMed1992

Infrared radiation suppresses ultraviolet B-induced sunburn-cell formation.

Sunburn cell (SC) formation, a quantifiable measure of epidermal cell injury induced in mouse ear skin by ultraviolet-B (UVB) radiation (290-320 nm), was significantly decreased by pre-exposure to infrared radiation (IR), which elevated the surface temperature of ear lobes to 37-42 degrees C. An autoradiographic study demonstrated that the basal cell labelling indices were significantly reduced in a surface temperature-dependent manner by pre-exposure to IR. Taken together with our previous findings that SC formation depends upon the ratio of cycling to non-cycling cells, the present findings suggest that IR retards the cell cycle and, as a result, decreases SC formation. SC counts were not altered by post-UVB exposure to IR. The effect of IR or the IR-induced increase in surface temperature should be considered when studying cutaneous damage by UVB and sunlight.

Animals↗
PubMed1992

Brain natriuretic peptide as a cardiac hormone in essential hypertension.

PURPOSE: A natriuretic peptide, brain natriuretic peptide (BNP), has been isolated from porcine hearts. We performed this study to determine if BNP is secreted from the heart and to identify changes, if any, in the plasma BNP concentration in essential hypertension. PATIENTS AND METHODS: We measured the immunoreactive (ir) BNP concentration at intracardiac sites including the coronary sinus of five patients with heart disease during cardiac catheterization. We examined plasma ir-BNP in 48 hypertensive patients, 15 borderline hypertensive patients, and 25 normotensive subjects. RESULTS: Plasma ir-BNP in the coronary sinus was greater than at other cardiac sites. The concentration was significantly higher in hypertensive subjects than in borderline hypertensive or normotensive subjects. Hypertensive patients with left ventricular hypertrophy (LVH) established by echocardiography had higher plasma ir-BNP levels than those without LVH. In the hypertensive group, plasma ir-BNP was closely correlated with the LV mass index. In these patients, BNP levels were correlated with mean arterial pressure and inversely correlated with the LV ejection fraction, although these correlations were weak. Reverse-phase high-pressure liquid chromatography showed that the major component of circulating ir-BNP in the hypertensive and normotensive subjects corresponded to authentic human BNP-32. CONCLUSIONS: Human BNP-32 was secreted through the coronary sinus from the heart and may act as a cardiac hormone. Plasma BNP was increased in many of the hypertensive subjects with LVH. The increase in BNP seemed to be related to LVH or the cardiac overload associated with LVH.

Adult↗
PubMed1992

Pulmonary arterial brain natriuretic peptide concentration and cardiopulmonary hemodynamics during exercise in patients with essential hypertension.

Brain natriuretic peptide (BNP) is secreted through the coronary sinus of the human heart. The purpose of this study was to determine whether BNP secretion from the heart is stimulated by exercise and to examine the relationship between pulmonary arterial BNP concentrations and hemodynamic measurements, especially cardiopulmonary hemodynamics, during exercise in patients with essential hypertension. The exercise protocol consisted of three fixed workloads (25, 50, 75 W) on a bicycle ergometer in the supine position. The mean pulmonary arterial BNP level at rest was 14.8 +/- 4.1 pg/mL, and BNP values gradually increased with higher stages of exercise. At the maximum exercise stage, the BNP value increased to 40.9 +/- 6.5 pg/mL. Close correlations of pulmonary arterial pressure (PAP) and pulmonary arterial wedge pressure (PAWP) with pulmonary arterial BNP level were observed at four points at rest and during each stage of exercise. In contrast, heart rate, mean blood pressure, cardiac index (CI), and stroke index (SI) were not correlated with BNP values. Results suggest that cardiac secretion of BNP was increased during exercise in essential hypertensive subjects, and the observed increase of BNP may be related to elevated PAP and PAWP. The enhancement of BNP secretion during exercise in these patients may reflect increased redistribution of blood to the cardiopulmonary compartment.

Adult↗
PubMed1992

Angiotensin II stimulates endothelin-1 secretion in cultured rat mesangial cells.

The present study was designed to test two hypotheses: (1) that angiotensin II (Ang II) stimulates endothelin-1 secretion in cultured rat mesangial cells and (2) that atrial and brain natriuretic peptides (ANP and BNP) inhibit the above-mentioned secretion in these cells. Ang II stimulated immunoreactive (ir) endothelin-1 secretion in a concentration-dependent manner between 10(-8) M and 10(-7) M. The protein kinase C (PKC) inhibitors from two chemical classes, H7 and staurosporine, inhibited secretion following such stimulation. The stimulatory effect of Ang II was also abolished in the PKC-depleted cells. Rat ANP(1-28) and rat BNP-45, which are the respective major circulating forms of ANP and BNP in rats, potently inhibited Ang II-stimulated endothelin-1 secretion in a concentration-dependent manner. Inhibition by ANP and BNP of Ang II-stimulated endothelin-1 secretion was paralleled by an increase in the cellular level of cyclic guanosine 5'-monophosphate (GMP). The addition of a cyclic GMP analogue, 8-bromo cyclic GMP, reduced the stimulated endothelin-1 secretion. Rat ANP(5-25) was less effective that rat ANP(1-28) with respect to inhibiting ir-endothelin-1 secretion and increasing cellular cyclic GMP. These findings indicate that Ang II stimulates endothelin-1 secretion in cultured rat mesangial cells by a mechanism probably involving activation of PKC, and that rat ANP and BNP inhibit this stimulated secretion through a cyclic GMP-dependent process.

Angiotensin II↗
PubMed1992

A new animal model for contact dermatitis: the hairless guinea pig.

Allergic and irritant contact reactions were evaluated in the recently identified hairless guinea pig, Crl:IAF(HA)BR, a mutant from the Hartley strain. The cutaneous changes were observed macro- and microscopically. The irritant contact dermatitis was induced by croton oil, 2,4-dinitrochlorobenzene (DNCB), or anthralin. Both hairless and hairy guinea pigs developed similar reactions to these chemicals. The density of the epidermal Langerhans cells (LC) of hairless guinea pigs was significantly higher than that in the hairy strain. Allergic contact sensitization was easily induced with DNCB. Photoallergic contact sensitization was also induced with tetrachlorosalicylanilide (TCSA) but not with tribromosalicylanilide (TBS). However, by administration of cyclophosphamide before sensitization, positive photocontact responses were seen with TBS. These results indicate that hairless guinea pigs can be used as animal models for investigation of immunologic and nonimmunologic contact reactions.

Allergens↗
PubMed1992

Erythema multiforme: pathomechanism of papular erythema and target lesion.

Skin lesions of erythema multiforme show time-dependent changes from early papular erythema to the late target lesion which consists of a peripheral elevated erythematous area and a central depressed area. We investigated the pathomechanism of erythema multiforme, by examining the papular erythema and target lesion separately. In the early papular erythema, a small number of polymorphonuclear leukocytes and nuclear debris were seen intermingled with mononuclear cells around the slightly swollen blood vessels, on which immunoglobulin and complement components were deposited. Circulating immune complex levels were occasionally elevated. Sera from the patients generated high levels of reactive oxygen species and nitroblue tetrazolium test revealed positive reaction on the infiltrating cells around the blood vessels. These findings suggest that the papular erythema develops via incomplete type III allergic reaction, followed by damage through reactive oxygen species. In the target lesion, the activity of histamine-N-methyltransferase, which is the major histamine-degrading enzyme, was markedly decreased in the peripheral elevated erythematous area and it was recovering in the central clearing area. ICAM-1 and HLA-DR antigens were expressed on the surfaces of the keratinocytes. An increased number of epidermal Langerhans cells and CD4 cell infiltration were observed in the peripheral elevated erythematous area, while a decreased number of epidermal Langerhans cells and CD8 cell infiltration in the central depressed area were observed. These findings suggest that impaired histamine metabolism and cellular allergic reactions play important roles in the development of the target lesion.

Antigen-Antibody Complex↗
PubMed1992

Atrial and brain natriuretic peptides: secretion during exercise in patients with essential hypertension and modulation by acute angiotensin-converting enzyme inhibition.

1. This study examined whether brain and atrial natriuretic peptides (BNP, ANP) are secreted together through the coronary sinus from the heart, and whether plasma concentrations of BNP and ANP were affected by ergometric exercise in patients with essential hypertension. The effects of temocapril, a potent angiotensin-converting enzyme (ACE) inhibitor, on plasma concentrations of these peptides was also examined. 2. The plasma concentrations of immunoreactive (ir) BNP and ir-ANP in the coronary sinus in seven patients with ischaemic heart disease during cardiac catheterization were far greater than values with plasma obtained at the same time from the femoral artery. 3. The plasma concentrations of ir-BNP and ir-ANP increased with exercise and were correlated with each other. Temocapril reduced the blood pressure and slightly (but significantly) decreased the levels of both peptides at rest and during exercise. 4. The results suggest that BNP and ANP were secreted together through the coronary sinus from the heart. The secretion was increased by exercise and suppressed by acute ACE inhibition. The increase in these peptides during exercise may reflect a compensatory mechanism against further elevation of blood pressure.

Aged↗
PubMed1992

Effects of arginine vasopressin, angiotensin II and endothelin-1 on the release of brain natriuretic peptide in vivo and in vitro.

1. The stimulatory effects of the vasoactive peptides arginine vasopressin (AVP), angiotensin II (AII) and endothelin-1 (ET-1) on the release of brain natriuretic peptide (BNP) were investigated in anaesthetized rats and in cultured rat atrial and ventricular cardiocytes. 2. A bolus injection of AVP induced a dose-dependent increase in plasma immunoreactive (ir)-BNP concentration in rats. AII induced a rapid and transient elevation in the ir-BNP level, while the increase produced by ET-1 was long-lasting. The elevation of the plasma ir-BNP concentration after stimulation by these three vasoconstrictors appeared to be paralleled by the elevation in mean blood pressure. 3. In the in vitro study, the rat atrial and ventricular cardiocytes both secreted ir-BNP into the medium in a time-dependent manner. ET-1 clearly stimulated the secretion of ir-BNP in both atrial and ventricular cardiocytes. In contrast, AVP and AII had no stimulatory effect in vitro. 4. Reverse-phase high performance liquid chromatography of the rat plasma and culture medium revealed a single major ir-BNP component that corresponded to synthetic rat BNP-45. 5. These observations indicate that AVP, AII and ET-1 stimulate the release of ir-BNP (probably rat BNP-45) through a change in blood pressure. In addition, ET-1 may also induce ir-BNP release through direct stimulation. As a cardiac hormone secreted from ventricles as well as atria, rat BNP may play a role in the regulation of blood pressure against the pressor effects of AVP, AII and ET-1.

Anesthesia↗