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Biomedical subjects

H Hosomi

Publications and source records attributed to H Hosomi.

At least 37 records · Page 2Linked to original sources
PubMed1998

Suppression of renal sympathetic nerve activity during portal vein infusion of hypertonic saline.

Sodium ions absorbed from the intestine are postulated to act on the liver to reflexly suppress renal sympathetic nerve activity (RSNA), resulting in inhibition of sodium reabsorption in the kidney. To test the hypothesis that the renal sympathoinhibitory response to portal venous NaCl infusion involves an action of arginine vasopressin (AVP) at the area postrema, we examined the effects of portal venous infusion of hypertonic NaCl on RSNA before and after lesioning of the area postrema (APL) or after pretreatment with an AVP V1 receptor antagonist (AVPX). Rabbits were chronically instrumented with portal and femoral venous catheters, femoral arterial catheters, and renal nerve electrodes. Portal venous infusion of 9.0% NaCl (0.02, 0.05, 0.10, and 0.15 ml.kg-1.min-1 of 9.0% NaCl for 10 min) produced a dose-dependent suppression of RSNA (-12 +/- 3, -34 +/- 3, -62 +/- 5, and 80 +/- 2%, respectively) that was greater than that produced by femoral vein infusion of 9.0% NaCl (2 +/- 3, -3 +/- 2, -12 +/- 4, and -33 +/- 3%, respectively). The suppression of RSNA produced by portal vein infusion of 9.0% NaCl was partially reversed by pretreatment with AVPX (-9 +/- 3, -20 +/- 3, -41 +/- 4, and -55 +/- 4%, respectively) and by APL (-11 +/- 2, -25 +/- 2, -49 +/- 3, and -59 +/- 6%, respectively). There were no significant differences between the effects of AVPX and APL, and the effect of APL was not augmented by AVPX. These results indicate that the suppression of RSNA due to portal venous infusion of 9.0% NaCl involves an action of AVP via the area postrema.

Animals↗
PubMed1997

Calcium release from intracellular stores evoked by extracellular ATP in a Xenopus renal epithelial cell line.

1. The signal transduction mechanism mediating extracellular adenosine 5'-triphosphate (ATP)-induced calcium release in a renal epithelial cell line (A6) was investigated using the whole-cell voltage-clamp technique and fura-2 fluorescence measurement. 2. ATP (10 microM) activated calcium-dependent non-selective cation channels in cells held under voltage clamp. 3. Guanosine 5'-O-(2-thiodiphosphate) (GDP beta S; 0.1-1.0 mM) in the pipette inhibited the ATP-activated calcium-dependent currents. With guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S; 0.1-1.0 mM) in the pipette, the currents were spontaneously elicited without application of ATP. Pretreatment with pertussis toxin (PTX) affected neither the ATP-activated currents nor the increase in intracellular free calcium concentration ([Ca2+]i) evoked by ATP. 4. Intracellular application of neomycin or heparin inhibited the ATP-activated currents. Inositol 1,4,5-trisphosphate (IP3; 0.1-100 microM) in the internal solution produced currents similar to those due to ATP activation. 5. These results suggest that a PTX-insensitive guanosine 5'-triphosphate (GTP)-binding regulatory protein (G. protein) is involved in extracellular. ATP-induced phosphoinositide turnover and subsequent calcium release from IP3-sensitive stores, which subsequently activates the calcium-dependent channels in A6 cells.

Adenosine Triphosphate↗
PubMed1997

Fos induction in rat brain neurons after stimulation of the hepatoportal Na-sensitive mechanism.

Responses of hepatic afferent nerves to intraportal bolus injection of hypertonic solutions were examined in anesthetized rats. Hepatic afferent nerve activity increased in response to an intraportal injection of 0.75 M NaCl or NaHCO3 but did not respond to a similar injection of 1.5 M mannitol, 0.75 M LiCl, or 0.15 M NaCl, implying that nerves in the hepatoportal area are sensitive to increases in Na concentrations and that this leads to stimulation of hepatic afferent nerve activity. To study central activation in response to stimulation of the hepatic Na-sensitive mechanism, c-fos induction was monitored. After electrical stimulation of hepatic afferent nerves, neurons containing Fos-like immunoreactivity (Fos-li) were found in the area postrema, nucleus of the solitary tract, paraventricular hypothalamic nucleus, and supraoptic nucleus at 90 min after stimulation. Induction of Fos-li was also studied after simultaneous infusion of 0.45 M NaCl into the portal vein and distilled water into the inferior vena cava in conscious rats so as to keep the total amount of solution introduced into the systemic circulation isotonic, thus avoiding changes in mean arterial pressure, plasma osmolality, and plasma NaCl concentrations. Fos-li-containing neurons were found in the same regions in which they were found after electrical stimulation. However, few, if any, Fos-li-containing cells were found if the rats were hepatically denervated or if they received an intraportal infusion of hypertonic LiCl or mannitol. These data provide evidence for involvement of the brain stem and forebrain structures in NaCl regulatory functions induced by stimulation of the hepatoportal Na-sensitive mechanism. However, stimulation of the hepatoportal osmosensitive mechanism does not activate these central structures.

Afferent Pathways↗
PubMed1997

Long-term effects of AVP-induced neurohumoral interaction via area postrema on body fluid and blood pressure.

Arginine vasopressin (AVP) has been known to interact with the central nervous system via the area postrema (AP), resulting in suppression of renal sympathetic outflow in short-term studies. We hypothesize that if this sympathoinhibitory effect lasts long, then the neurohumoral interaction would enhance urinary output because of the suppression of neurogenic reuptake of sodium (Na+) and water. Intact (Int) and AP-lesioned (APX) rabbits were chronically catheterized and housed in metabolic cages. AVP was intravenously infused (0.1 mU.kg-1.min-1) for 5 consecutive days. Urine volume and urinary Na+ excretion rates in Int rabbits were lower than those in APX rabbits during AVP infusion. This smaller urinary output in Int rabbits was reconfirmed either from the daily balance of water and Na+ or from the body weight, plasma Na+ concentration, and plasma osmolality data. This result contradicted the hypothesis. Mean arterial pressure was not altered in either group of rabbits while heart rate was suppressed in the Int rabbits. These data suggest that AP-mediated long-term action of AVP augments water retention and sustains bradycardia.

Animals↗
PubMed1997

GABA-activated conductance in cultured rat inferior colliculus neurons.

With the use of a whole cell voltage-clamp technique and fura-2 fluorescence measurements, the actions of gamma-aminobutyric acid (GABA) on cultured neurons from rat inferior colliculus were investigated. GABA (10-1,000 microM) induced currents in neurons held under voltage clamp that were inhibited by bicuculline (20 microM). Muscimol (100 microM) also evoked the currents, whereas baclofen (100 microM) affected neither the holding currents nor K+ conductance due to depolarizing pulses. The current density-voltage relation of GABA-induced currents, with equal concentrations of Cl- in the internal and external solutions, reversed near 0 mV. Reduction of the internal Cl- concentration shifted the-reversal potential in the negative direction as predicted from the Cl- equilibrium potential. Baclofen did not affect Ca2+ conductance due to depolarizing pulses. The extracellular application of 150 mM.KCl or 1.0 mM glutamate increased the intracellular Ca2+ concentration ([Ca2+]i) of cultured inferior colliculus neurons only when neurons were bathed in a Ca(2+)-containing external solution. However, GABA (1.0 mM) failed to increase [Ca2+]i at all concentrations of external Ca2+ used, indicating that GABA neither depolarized the cultured inferior colliculus neurons sufficiently to activate the voltage-dependent Ca2+ conductances nor evoked Ca2+ release from intracellular stores. These results suggest that in cultured rat inferior colliculus neurons, GABAA receptor channels may be predominantly responsible for the membrane conductance evoked by GABA and subsequent hyperpolarization of the neurons.

Animals↗
PubMed1996

Intravenously-injected naloxone reverses the decrease in renal sympathetic nerve activity seen during hypotensive hemorrhage in conscious rabbits by acting through central mechanisms.

The response of renal sympathetic nerve activity (RNA) to hemorrhage was examined in chronically-instrumented conscious rabbits. Hemorrhage was induced at a rate of 5 ml/kg per min until the mean arterial pressure fell below 40 mmHg. The mean arterial pressure then remained at around 80 mmHg until 10 ml/kg of hemorrhage (normotensive hemorrhage) before falling to below the pre-hemorrhagic control level (hypotensive hemorrhage). The RNA response showed a biphasic pattern, i.e., it increased during normotensive hemorrhage, then fell below the control level during hypotensive hemorrhage. To examine the mechanism involved in this decrease in RNA, naloxone (7.5 mumol/kg), an opioidergic receptor antagonist, was intravenously injected 1 min after the end of hemorrhage. Intravenous injection of naloxone caused an increase in mean arterial pressure and RNA to the level seen during normotensive hemorrhage. These results indicate that the decrease in RNA induced by hypotensive hemorrhage is mediated by opioidergic receptors. To determine whether the effects of naloxone are mediated via central or peripheral opioidergic receptors, naloxone was replaced by an equimolar solution of methylnaloxone, a form unable to cross the blood-brain barrier. Neither the mean arterial pressure nor RNA was significantly altered by administration of methyl naloxone. These results suggest that the effects of naloxone on both the RNA and the mean arterial pressure are mediated via central opioidergic receptors, i.e., the sympathoinhibition induced by hypotensive hemorrhage is mediated via the stimulation of central opioidergic receptors.

Animals↗
PubMed1996

Response of renal nerve activity to high NaCl food intake in dogs with chronic bile duct ligation.

Hepatic sensory systems are thought to play an important role in the response of renal nerve activity and natriuresis to oral NaCl load. In this study, responses of renal nerve activity and urinary Na+ and Cl- excretions to a high-NaCl food intake (20 g/kg boiled rice containing 0.4 g/kg NaCl) were examined in sham-operated dogs (n = 12) and dogs with chronic bile duct ligation (CBDL; n = 10). In sham-operated dogs, renal nerve activity gradually decreased and reached minimal value (50% +/- 7% of the control value) at 100 minutes after the high-NaCl food intake and remained depressed until 4 hours after the food intake. Of the orally administered sodium and chloride, 27% +/- 5% and 23% +/- 6% were excreted over the following 4 hours, respectively. In CBDL dogs, the decrease in renal nerve activity induced by the high-NaCl food was completely abolished and only 4% +/- 1% of the loaded Na+ and 3% +/- 2% of the loaded Cl- were excreted. Furthermore, liver tissue norepinephrine concentration in CBDL dogs decreased to 21% of that of sham-operated dogs. These results suggest that (1) In CBDL dogs, the decrease in renal nerve activity induced by a high-NaCl food is completely abolished, probably because of the impairment of hepatic neural regulation. (2) The lack of renal nerve response may contribute, at least in part, to the abnormalities in body fluid homeostasis in cirrhosis.

Animals↗
PubMed1996

Soybean protein suppresses hepatic lipogenic enzyme gene expression in Wistar fatty rats.

The effects of dietary soybean protein on lipogenic enzyme gene expression in livers of genetically fatty rats (Wistar fatty) have been investigated. When Wistar fatty rats and their lean littermates (7-8-wk old) were fed a casein or soybean protein isolate diet containing hydrogenated fat (4% hydrogenated fat plus 1% corn oil) or corn oil (5%) for 3 wk, the hepatic messenger RNA concentrations and activities of lipogenic enzymes were significantly lower in rats fed soybean protein than in those fed casein, regardless of genotype or dietary fat. The conversion rates of thyroxine to triiodothyronine by liver microsomes and plasma triiodothyronine concentrations were lower in the fatty rats than in the lean rats and were significantly greater in rats fed soybean protein than in those fed casein. Conversely, plasma and liver triacylglycerol concentrations were lower in soybean protein-fed fatty and lean rats than in those fed casein. The body weight was less in the fatty rats fed soybean protein than in those fed casein after 3 wk of feeding. Moreover, dietary polyunsaturated fatty acids suppressed lipogenic enzyme gene expression in the lean rats but did not in the fatty rats. Dietary soybean protein appeared to be useful for the reduction of obesity.

ATP Citrate (pro-S)-Lyase↗
PubMed1995

Long-term potentiation of neurotransmission in the inferior colliculus of the rat.

Postsynaptic field potential was elicited in the central nucleus of the rat inferior colliculus after electrical stimulation to the lateral lemniscus. The inhibitory action of locally applied GABA on the potential was blocked by the systemic administration of picrotoxin, a GABAA antagonist (2.5 mg/kg, i.p.). After the administration of picrotoxin, the tetanic stimulation of 50 Hz for 20 s increased the amplitude of the field potential to over 120% of the original level in 10 min; this was maintained for 40 min, and formed the long-term potentiation (LTP). The tetanic stimulation alone, however, failed to enhance the amplitude. Thus, LTP was induced in the inferior colliculus only when GABAergic action was depressed.

Animals↗
PubMed1995

Role of hepatic nerves in long-term control of NaCl homeostasis in Wistar-Kyoto rats.

This study was designed to investigate the effects of hepatic denervation (HD) on NaCl balance and arterial blood pressure in conscious Wistar-Kyoto rats maintained on normal or high-NaCl food. When rats were fed normal NaCl food (0.45% NaCl), HD had no significant effect on NaCl balance and arterial pressure. However, when rats were fed high-NaCl food (8% NaCl for 10 days), NaCl balance became more positive in HD rats than in sham rats. Furthermore, mean arterial pressure in HD rats (120 +/- 2 mmHg) was higher than that in sham rats (108 +/- 3 mmHg). These results indicate that the hepatic nerves play a significant role in the long-term control of NaCl balance and arterial pressure during high-NaCl food intake.

Animals↗
PubMed1995

Polyunsaturated fatty acid regulation of lipogenic enzyme gene expression in liver of genetically obese rat.

The polyunsaturated fatty acid regulation of lipogenic enzyme gene expression in genetically obese rats (Wistar fatty, non-insulin-dependent diabetes mellitus) has been investigated. The hepatic mRNA concentrations and activities of lipogenic enzymes in the fatty and lean rat were greatly increased by feeding a hydrogenated fat diet to fasted rats, and also reached similar maximum levels with similar time courses. By feeding a corn oil diet, however, the increases were markedly reduced in the lean rats, but were not significantly reduced in the fatty rats. Consequently, when the animals were fed corn oil, the mRNA concentrations and activities in the fatty rats were higher than those in the lean. Thus, it appeared that the higher gene expression in the fatty rats can be ascribed to the defects of polyunsaturated fatty acid suppression. On the other hand, insulin binding to receptors in the liver was reduced by the corn oil diet in the lean rats but was not reduced in the fatty rats (although the insulin binding level was lower in the Wistar fatty rats than in the lean). Changes in the insulin receptor autophosphorylation and kinase activity toward exogenous substrate were similar to the insulin binding. It is suggested that the polyunsaturated fatty acids may not suppress insulin binding activity to receptors in the livers of the fatty rats, probably due to down regulation by hyperinsulinemia. The defects of polyunsaturated fatty acid suppression of lipogenic enzyme gene expression may be one of the factors of obesity.

Animals↗
PubMed1995

The role of extrinsic nervous system in jejunal absorption during elevation of intraluminal pressure in anesthetized dogs.

The aim of this study was to investigate the role of the extrinsic nervous system in jejunal absorption under elevated intraluminal pressure of the jejunum. Increase in intraluminal pressure from 0 to 70-100 mmHg decreased net absorption of fluid, Na+ and Cl-, from 7.6 +/- 0.5 to 5.6 +/- 0.3 ml/15 min, 1.1 +/- 0.1 to 0.7 +/- 0.1 mEq/15 min, and 1.2 +/- 0.1 to 0.8 +/- 0.1 mEq/15 min, respectively. To examine the role of the extrinsic nervous system in the depressed net jejunal absorption induced by the increase in intraluminal pressure, jejunal afferent and efferent nerve activities were measured in response to the increase in intraluminal pressure. Both afferent and efferent nerve activities increased to 224 +/- 14 and 236 +/- 18% in response to the increase in intraluminal pressure. In the extrinsic denervated jejunal loop, the responses of net absorption to the elevation of intraluminal pressure were quite different from those in innervated jejunum. That is, in the denervated jejunal loop the elevation of intraluminal pressure converted jejunal absorption to jejunal secretion. These results indicate that elevation of intraluminal pressure elicits the jejuno-jejunal reflex, and this mechanism counteracts jejunal secretion.

Anesthetics↗
PubMed1995

Effects of a high-salt diet on tissue noradrenaline concentrations in Dahl salt-resistant and -sensitive rats.

1. We measured systolic arterial pressure (SAP) and tissue noradrenaline concentrations (tNA) of 16 organs (heart, kidney, aorta, brain stem, pancreas, spleen, stomach, jejunum, ileum, colon, lung, muscle, cerebrum, liver, bone, salivary gland) in Dahl salt-resistant (DSR) and -sensitive rats (DSS) fed 0.4 (0.4%) or 8% salt diet (8%) from 5 weeks old until the age of 5, 7, 9 and 11 weeks. 2. SAP increased in DSS with the 8% salt diet. An increased rate of SAP of DSS with the 0.4% salt diet was larger than DSR with the 0.4% diet. In DSR with 0.4%, tNA tended to increase from 5 weeks old except in the bone, which may have been the result of ageing. In DSS with 0.4%, tNA did not increase from 5 weeks old. DSS showed salt-sensitivity even to 0.4%. 3. tNA of the heart and kidney of both DSS and DSR with 8% were lower than 0.4%. These organs are high-salt-sensitive organs. tNA of the aorta, spleen, stomach, jejunum, ileum, and colon of DSS with 8% were lower than 0.4%, but not DSR. These organs are medium salt-sensitive organs. tNA of the pancreas of DSS with 8% was lower than 0.4% which was not different from DSR with 0.4 and 8%. The pancreas is a low salt-sensitive organ. tNA of the lung, muscle, cerebrum, liver, bone and salivary gland did not show any differences between 0.4 and 8% in DSS as well as DSR. These organs are not salt-sensitive organs. 4. There were large organ differences in tNA among organs studied. There were large organ differences in decrease rate of tNA in response to a high-salt diet. The organ function and the period of salt diet influence tNA.

Aging↗
PubMed1995

Depressed sensitivity of the hepatoportal NaCl receptors in rats with carbon tetrachloride-induced liver cirrhosis.

In normal rats, the activity of the hepatoportal NaCl-sensitive afferent nerves is increased by portal injection of hypertonic NaCl. In the present article, we have found this effect to be markedly reduced in rats with CCl4-induced liver cirrhosis (CT rats). Liver tissue norepinephrine content, a marker of tissue innervation, was also decreased in the treated rats. Over the 12 wk CCl4-treatment period, no significant difference in Na balance was found between control and CT rats when both groups were given normal NaCl (0.45%) food. However, when both were given high NaCl (8%) food, the Na balance of CT rats was positive and greater than that of controls. These results indicate that the sensitivity of the hepatoportal NaCl receptors is decreased even when the degree of liver cirrhosis is slight. This mechanism plays an important role in maintaining Na balance during intake of high NaCl food.

Animals↗
PubMed1995

Role of endogenous opioids and central opioid receptors in cerebral cortical blood flow autoregulation.

To examine the role of endogenous opioids in autoregulatory maintenance of cerebral cortical blood flow (CoBF), CoBF was measured continuously by laser-Doppler flowmetry during changes in arterial pressure. Experiments were conducted on pentobarbital sodium-anesthetized adult mongrel dogs. Mean arterial pressure (MAP) was decreased or increased by inflating a perivascular occluder placed around the inferior vena cava or the thoracic descending aorta, respectively. To exclude the influence of the baroreceptor reflex on the autoregulatory maintenance of CoBF, all experiments were conducted on dogs with bilateral carotid sinus denervation plus vagotomy. CoBF was well maintained within its normal range despite large changes in MAP. Intravenous injection of naloxone (2.5 mumol/kg), an opioid receptor antagonist, significantly impaired the autoregulatory maintenance of CoBF during the decrease in MAP. On the other hand, intravenous injection of methyl naloxone (2.5 mumol/kg), which does not cross the blood-brain barrier, did not exert any significant effect on the MAP-CoBF relationship. Furthermore, intracerebroventricular injection of a smaller dose of naloxone (2.5 nmol/kg) significantly impaired the autoregulatory maintenance of CoBF during the decrease in MAP, as the larger dose of intravenous naloxone (2.5 mumol/kg) did. On the other hand, intravenous injection of the smaller dose of naloxone did not exert any significant effect on the MAP-CoBF relationship. These findings suggest that endogenous opioids and central opioid receptors may be partly involved in the CoBF autoregulatory mechanism. The endogenous opioids may modulate the autoregulatory vasodilation of the cerebral cortex during the decrease in MAP.

Animals↗
PubMed1995

[A Japanese family with congenital abnormal plasminogen].

A Japanese family with congenital abnormal plasminogen is reported. The patient was a 44-year-old male with no past history of thrombosis. Since only the plasminogen (PLG) activity was reduced on laboratory tests before surgery for lumbar disc herniation, coagulation and fibrinolysis studies were performed in the patient and his family. The patient underwent resection of the nucleus pulposus and posteriorlateral fixation of the lumbar spine. The PLG activity was 8% in the patient and his sister, 55% in his father, and 53% and 48% in his nephew brothers. The PLG antigen level was normal in all members of his family examined. IEF of PLG antigen showed abnormal patterns in which all bands were shifted slightly to the cathode side in the patient and his sister, but his father and nephew brothers exhibited duplicated bands showing combinations of normal and abnormal patterns. From these results, the proband and his sister were considered to be homozygotes, and his father and nephew brothers to be heterozygotes for congenital abnormal plasminogen. Acute reactant substances (fibrinogen, CRP, CPK, C1IN, alpha 1AT, etc.) and PIC (plasmin, alpha 2-plasmin inhibitor complex) increased after the operation due to the surgical insult, but the surgery did not trigger thrombosis. This patient is considered not to have developed thrombosis although he was a homozygote for congenital abnormal plasminogen, because the anticoagulation process until thrombogenesis was normal.

Adult↗