Search PubMed⌕ Search

Biomedical subjects

H Jin

Publications and source records attributed to H Jin.

At least 235 records · Page 13Linked to original sources

Ganglion atrial natriuretic peptide in NaCl sensitive spontaneously hypertensive rats.

Reports from other laboratories have shown that atrial natriuretic peptide (ANP) stores in sympathetic ganglia are increased during dietary NaCl supplementation in normotensive rats. We have previously demonstrated that dietary NaCl supplementation in NaCl sensitive spontaneously hypertensive rats (SHR-S) exacerbates hypertension and enhances peripheral sympathetic nervous system activity, while NaCl resistant Wistar-Kyoto (WKY) rats show neither response. Since endogenous ANP may inhibit ganglion transmission, an inability of SHR-S to increase ganglion ANP appropriately in response to high NaCl feeding could contribute to the NaCl induced increase in sympathetic nervous system activity and blood pressure in this model, while an increase in ganglion ANP in NaCl supplemented WKY would tend to prevent sympathetic activity and blood pressure from rising. The current study tested the hypothesis that ganglion ANP levels increase in WKY but not in SHR-S during dietary NaCl supplementation. Male SHR-S and WKY rats were placed on 1% or 8% NaCl diets at 7 weeks of age. The rats were decapitated without prior anesthesia 3 weeks later, and the superior cervical and celiac ganglia were removed for the measurement of ANP by radioimmunoassay. Dietary NaCl supplementation produced significant increases in blood pressure in SHR-S, but not in WKY rats; the high NaCl diet was associated with significant increases in the ANP content of superior cervical and celiac ganglia in WKY rats, but not in SHR-S.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of acute and chronic blockade of neutral endopeptidase with Sch 34826 on NaCl-sensitive hypertension in spontaneously hypertensive rats.

We have previously demonstrated that dietary NaCl supplementation is associated with increased circulating atrial natriuretic peptide (ANP) levels in Wistar-Kyoto (WKY) rats but not in spontaneously hypertensive rats (SHR), and that replacement with exogenous ANP prevents NaCl-sensitive hypertension in NaCl-sensitive SHR (SHR-S). The current study tested the hypothesis that chronic administration of the neutral endopeptidase (NEP) inhibitor Sch 34826 prevents NaCl sensitive hypertension in SHR-S by increasing endogenous ANP. Male SHR-S received Sch 34826 (90 mg/kg/day) or vehicle by gavage for 4 weeks beginning immediately before the initiation of 1% or 8% NaCl diets at age 7 weeks. Sch 34826 prevented the increase in arterial pressure in response to 8% NaCl in SHR-S, but had no effect on blood pressure in 1% NaCl fed SHR-S; plasma ANP levels were increased by 63 and 68% in the 1% and 8% NaCl groups, respectively, in response to Sch 34826. To examine the mechanism(s) of the antihypertensive effect of Sch 34826 in NaCl-supplemented SHR-S, a single dose (90 mg/kg) of Sch 34826 or vehicle was administered by gavage to SHR-S that had consumed 1% or 8% NaCl diets for 3 weeks. Sch 34826 abolished the NaCl-induced increase in blood pressure 3 h after treatment in 8% NaCl fed SHR-S, but had no effect in SHR-S fed the 1% NaCl diet. This effect was associated with increased urine volume and urinary sodium, ANP, and cyclic GMP in 8% NaCl fed SHR-S.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Cicletanine blunts the pulmonary pressor response to acute hypoxia in rats.

Cicletanine (CIC) recently has been shown to lower systemic arterial pressure in hypertensive animals and man by a mechanism that may involve potentiation of the vasodilator effect of atrial natriuretic peptide (ANP). We previously have shown that ANP prevents acute hypoxia-induced pulmonary vasoconstriction and modulates the severity of chronic hypoxic pulmonary hypertension. The current study tested the hypothesis that CIC inhibits the pulmonary pressor response to acute hypoxia by a cyclic guanosine monophosphate (cGMP)-dependent mechanism. Catheters were placed in the pulmonary arteries of Sprague-Dawley rats through the right jugular vein using a closed chest technique, and in the aorta through the right femoral artery. After a 24 hour recovery, CIC (600 mg/kg) or vehicle was administered orally by gavage to conscious rats 4 hours prior to exposure to 10% oxygen at ambient pressure or to room air. Mean pulmonary arterial pressure (MPAP) and mean systemic arterial pressure (MSAP) and heart rate (HR) were monitored for 3 hours. CIC attenuated the acute pulmonary pressor response to hypoxia (MPAP = 24.5 +/- 1.0 mm Hg in the "hypoxic+CIC" group vs. 29.9 +/- 1.0 mm Hg in the "hypoxic+vehicle" group; p less than 0.05 at 3 hours of hypoxic exposure), but had no significant effect on MSAP or HR. CIC had no effect on MPAP, MSAP, or HR in air control rats. Acute hypoxia caused significant increases in plasma ANP and cGMP and in kidney cGMP content, but CIC administration did not alter these parameters further. This is the first demonstration that acute administration of CIC attenuates the pulmonary pressor response to acute hypoxia in conscious rats.

Animals↗

Mutagenesis of the L protein encoded by Bunyamwera virus and production of monospecific antibodies.

Bacterial fusion proteins containing portions of the Bunyamwera virus L protein were used as immunogens to prepare antisera in rabbits. Of five fusion proteins injected into rabbits, three yielded sera that reacted with the Bunyamwera virus L protein, detected by Western blotting or immunoprecipitation. Two of these antisera were specific for either the amino- or carboxy-terminal regions of the L protein. The specificity of these antisera was confirmed by their pattern of reactivity with full-length and truncated forms of the L protein. Plasmids containing the L gene cDNA under control of a bacteriophage T7 promoter were transfected into CV-1 cells which had previously been infected with a recombinant vaccinia virus, vTF7-3, that expresses T7 RNA polymerase. Antigenically authentic L protein was expressed. Using a nucleocapsid transfection assay developed previously, we showed that the transiently expressed L protein had RNA synthesis activity. Site-specific mutations were made in the L cDNA-containing plasmid to change certain amino acids in the putative polymerase domain of the L protein. The effects of these amino acid substitutions on the RNA synthesis activity of the L protein were monitored using the nucleocapsid transfection assay. These experiments showed that residues strictly conserved between the L proteins of different viruses in the family Bunyaviridae were obligatorily required for activity, whereas non-conserved residues could be substituted without abolishing RNA synthesis capability. Our results provide direct evidence for the functional significance of particular amino acids in the polymerase domain of a negative-strand virus RNA polymerase.

Amino Acid Sequence↗

Spontaneously hypertensive rat: lymphoid depression is age dependent and mediated via a mononuclear cell subpopulation.

Immune dysfunction has been reported in spontaneously hypertensive rats (SHR), particularly in mature animals with established hypertension. The current study examined the time course of development of immune dysfunction and defined its cellular basis in male SHR and control normotensive Wistar-Kyoto rats (WKY). Mitogen-induced proliferative responses in lymphoid cells obtained from induced proliferative responses in lymphoid cells obtained from SHR thymus and spleen before (age 4 wk) and during the development of (ages 8 and 12 wk) hypertension and in age-matched normotensive WKY were monitored. A 50% reduction in concanavalin A (Con A)-induced proliferative responses was seen in SHR thymocytes compared with those of WKY at 12 wk only, suggesting differences in immature T-cell populations. Con A-induced T-cell proliferative responses in splenocytes also differed between strains: greatest (as much as 8-fold) decreases were found in 12-wk-old SHR. Similar findings were obtained in splenocytes stimulated with lipopolysaccharide (LPS), indicating differences in B-cell function. Mononuclear cells depleted of their adherent cell population were prepared from SHR and WKY at 12+ wk of age and assayed for their proliferative responses to LPS and Con A. The remaining nonadherent mononuclear cells of SHR had proliferative responses equal to or greater than those of WKY. Further, when SHR splenic mononuclear cells were allowed to adhere to plastic, and the adherent fraction was co-cultured with either SHR G-10 nonadherent or unfractionated SHR splenic mononuclear cells, proliferative responses were suppressed by as much as 88%.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Normobaric hypoxia stimulates endothelin-1 gene expression in the rat.

The current study tested the hypothesis that exposure to hypoxia enhances endothelin-1 (ET-1) gene expression and elevates circulating ET-1 levels in the rat. Rats were exposed to normobaric hypoxia (10% O2) or room air for 24 or 48 h. ET-1 in arterial blood was measured by radioimmunoassay. ET-1 gene transcript levels were measured by the slot blot technique on total RNA isolated from lung, right and left atria, right and left ventricles, kidney, spleen, liver, brain, main trunk of pulmonary artery, and thoracic aorta. Blots were probed with a 0.5 kb rat prepro ET-1 cDNA that does not cross-hybridize with mRNA for ET-2 or ET-3. Plasma ET-1 levels were increased significantly at 24 (10.03 +/- 2.33 pg/ml) and 48 h (14.02 +/- 3.44 pg/ml) of hypoxia compared with air controls (4.14 +/- 0.66 pg/ml). ET-1 mRNA levels were increased significantly (2-fold) in lung and right atrium after 48 h of hypoxia; no change was seen in organs perfused by the systemic vascular bed. These findings suggest that the hypoxia-induced increase in circulating ET-1 levels is mainly of pulmonary origin. A paracrine effect of ET-1 produced by lung endothelial cells could account for hypoxic pulmonary hypertension.

Animals↗

Depressor effect of blocking angiotensin subtype 1 receptors in anterior hypothalamus.

Previous studies have shown that the anterior hypothalamic area participates in the centrally mediated pressor response to exogenous angiotensin II. The current study was designed to test the hypothesis that endogenous anterior hypothalamic angiotensin II plays a significant role in blood pressure control. Type 1 angiotensin II receptors in the anterior hypothalamic area were blocked by local microinjection of DuP 753 (2-n-butyl-4-chloro-5-(hydroxymethyl)-1-[(2'-(1H-tetrazol-5-yl) biphenyl-4-yl)methyl]imidazole, potassium salt), a highly selective nonpeptide antagonist. DuP 753 (20 or 40 micrograms; in 100 nl artificial cerebrospinal fluid) or vehicle alone was microinjected into the anterior hypothalamic area of conscious NaCl-sensitive spontaneously hypertensive rats and Wistar-Kyoto controls. DuP 753 caused significant dose-related decreases in mean arterial pressure (maximal decrease, 22.5 +/- 1.8 mm Hg) with unchanged heart rate in NaCl-sensitive spontaneously hypertensive rats but effected no change in Wistar-Kyoto rats. Injections of equal volumes of artificial cerebrospinal fluid into the anterior hypothalamic area had no effect in either strain. Further, microinjection of DuP 753 into the posterior hypothalamic area produced no significant effect on blood pressure or heart rate in NaCl-sensitive spontaneously hypertensive rats. Microinjection into the anterior hypothalamic area of the selective type 2 angiotensin II receptor antagonist PD 123319 did not affect blood pressure or heart rate in NaCl-sensitive spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

Salt supplementation does not alter the pressor effect of blocking atrial natriuretic peptide in nucleus tractus solitarii.

We have previously shown that microinjection of monoclonal antibody to atrial natriuretic peptide (ANP) into the caudal nucleus tractus solitarii causes a pressor response in salt-sensitive spontaneously hypertensive rats (SHR) fed a basal (1%) salt diet, suggesting that endogenous ANP in this region may be involved in the centrally mediated regulation of blood pressure in this model. The present study tested the hypothesis that the pressor effect of blocking endogenous ANP in caudal nucleus tractus solitarii is enhanced by dietary salt supplementation in salt-sensitive SHR. Monoclonal antibody to ANP (0.55 micrograms) in 50 nl artificial cerebrospinal fluid or control immunoglobulin G was microinjected into the caudal nucleus tractus solitarii of conscious salt-sensitive SHR, salt-resistant SHR, and Wistar-Kyoto rats fed 1% or 8% salt diets for 3 weeks. Microinjection of the monoclonal antibody into the caudal nucleus tractus solitarii evoked similar increases in mean arterial pressure in salt-sensitive SHR on both 1% and 8% salt diets and in salt-resistant SHR on a 1% salt diet but had no effect in Wistar-Kyoto rats. In contrast, microinjection of control immunoglobulin G into this brain area did not alter mean arterial pressure or heart rate in any experimental group. Thus, endogenous ANP in caudal nucleus tractus solitarii mediates tonic control of blood pressure in both salt-sensitive and salt-resistant SHR but not in Wistar-Kyoto rats, and this effect is independent of the salt sensitivity of hypertension and of dietary salt intake.

Animals↗

Atrial natriuretic peptide modulates baroreceptor reflex in spontaneously hypertensive rat.

Our previous studies have suggested that atrial natriuretic peptide in the caudal nucleus tractus solitarii is involved in the centrally mediated regulation of blood pressure in the salt-sensitive spontaneously hypertensive rat (SHR). The current study tested the hypothesis that endogenous atrial natriuretic peptide in the caudal nucleus tractus solitarii participates in baroreceptor reflex control of heart rate in this hypertensive model. Salt-sensitive SHR and control Wistar-Kyoto (WKY) rats maintained on basal (1%) salt intake were studied. Arterial baroreceptor reflex-mediated changes in heart rate were recorded in conscious unrestrained rats during phenylephrine (5-40 micrograms.kg-1.min-1 infusion; 30 minutes later, atrial natriuretic peptide (50 ng), monoclonal antibody to atrial natriuretic peptide (0.55 micrograms), purified mouse immunoglobulin G (0.55 micrograms), or artificial cerebrospinal fluid vehicle (50 nl) was microinjected into the caudal nucleus tractus solitarii. Phenylephrine infusion was then repeated and mean arterial pressure and heart rate were monitored as before. The slope of the heart rate/mean arterial pressure relation was significantly less (p less than 0.05) in the salt-sensitive SHR than in the WKY control, indicating that baroreceptor reflex control of heart rate was blunted in this hypertensive model. Microinjection of atrial natriuretic peptide into the caudal nucleus tractus solitarii further blunted (p less than 0.05) baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats. In contrast, microinjection of the monoclonal antibody enhanced the sensitivity of baroreceptor reflex control of heart rate in salt-sensitive SHR but not in WKY rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Blocking hypothalamic AT1 receptors lowers blood pressure in salt-sensitive rats.

Previous studies from our laboratory have shown that microinjection of DuP 753 (2-n-butyl-4-chloro-5-(hydroxymethyl)-1-[[2'-(1H-tetrazol-5-yl) biphenyl-4-yl]methyl]imidazole, potassium salt), a highly selective nonpeptide antagonist of type 1 angiotensin II receptors, into the anterior hypothalamic area produces a dose-related depressor response in salt-sensitive spontaneously hypertensive rats fed a basal (1%) salt diet. The current study tested the hypothesis that the depressor response to anterior hypothalamic type 1 angiotensin II receptor blockade with DuP 753 or its metabolite EXP 3174 is enhanced by high (8%) salt feeding in this model. DuP 753 or EXP 3174 (40 micrograms in 100 nl artificial cerebrospinal fluid vehicle) or vehicle alone was microinjected into the anterior hypothalamic area of conscious salt-sensitive spontaneously hypertensive and Wistar-Kyoto rats that had been fed 1% or 8% salt diets for 3 weeks. Both DuP 753 and EXP 3174 caused significant decreases in mean arterial pressure in spontaneously hypertensive but not in Wistar-Kyoto rats fed either diet. The magnitude and duration of the depressor responses to DuP 753 and EXP 3174 were significantly greater in the 8% salt-fed spontaneously hypertensive rats than in 1% salt-fed rats. Vehicle injections had no effect on blood pressure in either strain-diet group. Microinjection of angiotensin II (2 micrograms in 100 nl artificial cerebrospinal fluid vehicle) into the anterior hypothalamic area caused significant pressor and bradycardiac responses in all strain-diet groups; dietary salt supplementation enhanced these effects in salt-sensitive spontaneously hypertensive rats but not in Wistar-Kyoto rats. These responses were blocked by pretreatment with EXP 3174.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗

Altered synthesis and intracellular transport of proteoglycans by cyst-derived cells from human polycystic kidneys.

Employing in vitro pulse-chase techniques, we investigated the de novo synthesis and the kinetics of intracellular transport and extracellular matrix incorporation of proteoglycans (PG) by normal human renal epithelial cell and by epithelial cells isolated from cysts of autosomal dominant kidneys (ADPKD). Cell monolayers were pulsed either with (3H)leucine for 15 min and chased for seven intervals between 15 and 270 min or with (35S)sulfate for 150 min and chased for a single interval of 120 min. Total proteins and PG were isolated from cell, media, and matrix fractions and characterized by Sepharose CL-6B and DEAE-Sephacel chromatographies. ADPKD and NK cells synthesized comparable amounts of total proteins; however, the de novo synthesis of PG by ADPKD cells was significantly reduced. ADPKD versus NK cells exhibited a substantial delay in the cellular transport and extracellular release of de novo synthesized PG, indicating an impairment at the level of the Golgi complex and/or secretory vacuoles. PG synthesized by ADPKD versus NK cells had decreased charge density characteristics, probably due to a posttranslational defect in the sulfation of the PG glycosaminoglycan chains. ADPKD versus NK cells synthesized PG of higher molecular weight and had an increased proportion of chondroitin sulfate PG versus heparan sulfate PG. Collectively, these findings suggest a defect in the synthesis and intracellular transport of sulfated PG in human ADPKD cells.

Biological Transport, Active↗

Mesenchymal hamartoma of the liver: report of an adult case and review of the literature.

A case of mesenchymal hamartoma of the liver incidentally found to be a hyperechoic mass by abdominal ultrasonography in a 62-year-old male is described. Computed tomography and magnetic resonance imaging of the liver confirmed the presence of a well-demarcated inhomogeneous mass in the left medial segment. Hepatic arteriography revealed the mass to be generally hypovascular. Histopathologic diagnosis of the resected specimen was a solid form of benign mesenchymal hamartoma, a rather rare lesion for the patient's age. Fifteen adult cases of hepatic mesenchymal hamartoma in the literature including the present case are reviewed.

Diagnosis, Differential↗

[Immunohistochemical studies on the guinea pig's vestibular ganglion cell--with reference to the distribution of substance P and neurofilament].

The immunocytochemical distribution and morphological characteristics of substance P and neurofilament in vestibular end organs and the vestibular ganglion of the guinea pig were investigated. The effect of capsaicin on substance P-like immunoreactivity was also evaluated in this study. Substance P-like immunoreactivity was found in the peripheral region of vestibular end organs and in small or medium size vestibular ganglion cells. Approximately 85% of vestibular ganglion cells showed substance P-like immunoreactivity. Although substance P-like immunoreactivity was depleted in the nasal mucosa and trigeminal ganglion by capsaicin treatment, substance P distributed in the primary vestibular neurons was not affected. In contrast to the distribution of substance P, neurofilament was also found in the primary afferent neurons in the central regions of vestibular end organs. Neurofilament immunoreactive cells, which were larger in size than cells without neurofilament-like immunoreactivity comprised about 34% of vestibular ganglion cells. These immunocytochemical findings suggest that vestibular ganglion cells can be classified on the basis of size and immunocytochemical characteristics.

Animals↗

[A preliminary approach to pathological and biochemical changes of the lungs injured by domestic pingyangmycinum].

Two hundred male mice, weighing 18-24g, were randomized into four groups. A model of lung injury was established in mice by intratracheal administration of a single dose of domestic pingyangmycinum (Bleomycin A5). The dose-effect relationship for different doses of pingyangmycinum (0.05, 0.1, 0.2 mg) on the lung injury, and the change of hydroxyprolin (Hyp), ceruloplasmin (CP), angiotensin converting enzyme (ACE), superoxide dismutase (SOD) in mice were investigated. The results showed that the pathological changes of alveolitis and pulmonary interstitial fibrosis were more severe, and mortality of the mice was increased when pingyangmycinum dose was increased. During 2-6 weeks of this experiment, Hyp, CP, ACE and SOD in serum and Hyp in lung tissue were increased in different degrees. However, the activity of SOD in lung tissue was decreased. The possible mechanism of this lung injury is also discussed.

Animals↗

[The relationship between plasma atrial natriuretic peptide (ANP) and glomerular ANP receptors in 5/6 nephrectomized rats].

Chronic renal failure was induced in male Wistar rats with 5/6 nephrectomy (group I) and sham-operation was carried in the controls (group II). The results showed that in group I, plasma ANP levels increased progressively as Scr elevated. The plasma levels of renin and angiotensin raised simultaneously as compared with the controls (P < 0.001). At the 20th week after operation, urine volume and Na decreased significantly (P < 0.05) and the number of glomerular ANP receptors decreased significantly at the 12th week (P < 0.05) and 20th week (P < 0.01). Our data suggest that in 5/6 nephrectomized rats: 1. The elevation of plasma ANP level might be partly caused by damage of glomerular receptors. 2. The elevated plasma ANP could not cause its diuretic, natriuretic, blood pressure depression and R-A inhibition effect due to the damage of kidney ANP receptors.

Aldosterone↗

[Isolation and identification of Leclercia adecarboxylate in clinical isolates in China].

1987, 3 strains of gram-negative straight rods were examined from 3 cases of patients with diarrhea. It's producing yellow pigment, fermentative metabolism of carbohydrates, oxidase test negative and motility with the help of peritrichous flagella. Through systematic biochemical identification, calculation of G+C mol% and homology of DNA/DNA, the species of Leclercia adecarboxylate are identified. While the susceptibility to certain antibiotics and the pathogenicity for white mice are tested, and relation of these microorganisms to clinical diarrhea is discussed.

Animals↗

Human dopamine D5 receptor pseudogenes.

Molecular cloning studies have now identified five structurally homologous genes encoding the biosynthesis of the human dopamine receptors, DRD1, DRD2, DRD3, DRD4, and DRD5. Two of these dopamine receptors (DRD1 and DRD5) are encoded by intronless genes. To ascertain whether there are other intronless genes that share identity with the gene (DRD5) encoding the DRD5 receptor, we used a cloning method based on the polymerase chain reaction (PCR). Human genomic DNA was amplified by PCR with oligodeoxyribonucleotides (oligos) based on the DRD5 nucleotide (nt) sequence. Amplification of nt sequences between these oligos allowed the isolation of two independent intronless genes that share identity with DRD5. The full-length clones have also been isolated by screening human genomic libraries. The deduced amino acid sequences for these genes, PG-1 and PG-2, share 91% and 92% identity to DRD5, respectively. However, each of the genes contains differences in the coding regions that would render these genes incapable of encoding functional receptors. Thus, the human genome contains at least two DRD5 pseudogenes, consistent with in situ human chromosomal hybridization analysis which reveals the presence of two pseudogenes.

Amino Acid Sequence↗