Effect of AVP V1-receptor antagonist on normal body temperature in rats under light-dark cycle

AIM: To assess if endogenous arginine vasopressin is involved in normal thermoregulatory processes. METHODS: Core temperature was monitored in undisturbed rats using radiotelemetry. Effect of AVP V₁ antagonist on normal body temperature were observed in rats under a 12:12 light-dark cycle. RESULTS: Intraperitoneal injection of AVP V₁-receptor antagonist in rats induced a increase in normal body temperature. Under normal light (light on at 6:00 AM-6:00 PM), AVP V₁ antagonist induced a increase in body temperature persisting for about 6 hour, but male rats had higher hyperthermia than female. Under normal dark exposure (light off at 6:00 PM-6:00 AM), AVP V₁-receptor antagonist caused a increase in body temperature persisting for about 2 hour at the start of the dark phase, but no difference was found between sexes. CONCLUSION: Intraperitoneal injection of AVP V₁-receptor antagonist caused a increase in normal body temperature. The data indicated that endogenous vasopressin could be involved in tonic thermoregulatory process.     

Role of endogenous arginine vasopressin in soman-induced hypothermia in rats

AIM: This study was designed to examine whether endogenous arginine vasopressin (AVP) is involved in soman-induced hypothermic process. METHODS: Core temperature was measured at 60 min intervals with digital thermometer. Effect of AVP V₁ receptor antagonist (30 μg/kg, ip) on soman-induced hypothermia was observed in rats, and plasma AVP concentration was measured at 2 h after administration of soman(60 μg/kg, sc). RESULTS: Administration of soman led to a marked hypothermia. Core temperature recovered to basal levels at 7 h after soman treatment. Plasma AVP concentration increased markedly at 2 h after soman treatment, and administration of AVP V₁ receptor antagonist markedly blocked the hypothermic effect of soman. CONCLUSION: The data indicate that AVP is involved in soman-induced hypothermia in the rat.     

Effect of different ambient temperatures on arginine vasopressin-induced hypothermia in rats and its relationship with heat loss from the tail

AIM：To determine the effect of different ambient temperatures on arginine vasopressin (AVP)-induced hypothermia in rats and its relationship with the change of heat loss from the tail, and to assess if peripheral AVP administration increases heat loss from the tail. METHODS：The core temperature and tail skin temperature in adult male Sprague-Dawley rats at three different ambient temperatures (12 ℃, 22 ℃ and 32 ℃) were monitored by wireless telemetry. The rats were intraperitoneally injected with AVP (10 μg/kg) or vasopressin V1a receptor antagonist (30 μg/kg) at 10:00 AM. The diameters of microvessels in the spinotrapezius muscle and the grooming behavior in the rats were also observed after treatment with AVP or vasopressin V1a receptor antagonist. RESULTS：AVP-induced hypothermia in the rats at three ambient temperatures was accompanied by a decrease in tail skin temperature. V1a receptor antagonist attenuated the hypothermia and the decrease in tail skin temperature induced by AVP (10 μg/kg). AVP induced significant constriction of the microvessels in the spinotrapezius muscle. AVP also enhanced the grooming behavior (salivary grooming) in the rats and this effect was inhibited by peripheral administration of vasopressin V1a receptor antagonist. Endogenous AVP did not mediate the heat loss from the tail in normal rats. CONCLUSION：Peripheral AVP induces hypothermia in rats. It does not lower the set point of body temperature, and its hypothermic effect may attribute to the suppression of thermoregulatory heat production and the increase in salivary grooming (saliva spreading for evaporative heat loss).     

Effects of arginine vasopressin on subunit phosphorylation of GABAA receptors in rat preoptic area

AIM: To investigate the effects of arginine vasopressin (AVP) on the expression and phosphorylation of γ-aminobutyric acid (GABA) subtype A receptor (GABA_A receptor) subunits in the preoptic area (POA) of rats. METHODS: The rats were divided into AVP group (n=10), AVP+V1a receptor blocker group (n=10), V1a receptor blocker group (n=10) and control group (n=10). After intraperitoneal injection of AVP or V1a receptor antagonist for 0.5 h, the changes of the expression and phosphorylation of POA GABA_A receptor subunits (α, β and γ2) were analyzed by RT-qPCR and Western blot. RESULTS: Compared with control group, no significant change of GABA_A receptor subunit expression in the rats injected with AVP or V1a receptor antagonist was observed. AVP up-regulated the phosphorylation level of POA GABA_A receptor γ2 subunit (P<0.05), and significantly increased the expression and phosphorylation of protein kinase C (PKC) and calcium/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ). CONCLUSION: Exogenous AVP has no effect on expression of POA GABA_A receptor subunits (α, β and γ2) and is involved in modulation of GABAergic synaptic transmission in the POA by activation of PKC and CaMKⅡ and phosphorylation of γ2 subunit via V1a receptor.     

The central role of corticotropin-releasing hormone in stress-induced hyperthermia and LPS-induced fever in rats

AIM:To further investigate the role of central corticotropin-releasing hormone in stress-induced hyperthermia and lipopolysaccharide (LPS)-induced fever in the rat.METHODS:Test substances were administered intracerebroventricularly (icv) via a third ventricle cannula. Body temperature responses were monitored at 30 min intervals using colonic thermistor probes. Arginine vasopressin (AVP) level in the ventral septal area (VSA) determined by radioimmunoassay. RESULTS:In normal saline controls,rats were handled to take the colonic temperature,their body temperature significantly increased with a peak of(0.88±0.31)℃.The injection(icv)of α-helical CRH(9-41),a CRH-41 receptor antagonists,markedly attenuated the stress-induced hyperthermia within 90 min after injection of normal saline.LPS(300 ng,icv)stimulated a biphasic rise in the colonic temperature,the 3.5 h thermal response index(TRI_3.5)and AVP levels in the VSA of LPS-treated rats were higher than those of control rats.The AVP responses to LPS were inhibited significantly by blockade of central CRH actions using α-helical CRH(9-41)(5μg,icv)administered 10 min prior to LPS,whileα-helical CRH(9-41)(5μg,icv)resulted in exacerbated febrile responses to LPS(300 ng,icv). CONCLUSION:Central CRH plays an important role in stress-induced hyperthermia. The injection (icv) of α-helical CRH(9-41) enhances markedly LPS-induced fever in rats. CRH is a dual action molecule in LPS-induced fever, which itself mediates LPS-induced fever, at the same time, and limits the rise in body temperature during fever through actions of AVP in the VSA and glucocoticoids.     

Effects of angiotensin II and losartan on collagen synthesis in rat hepatic stellate cells

AIM: To investigate the effects of angiotensin II (Ang II) and AT_1a receptor antagonist (losartan) collagen synthesis in rat hepatic stellate cells (HSCs). METHODS: ① Rat HSCs were isolated, cultured and identified. ② Rat HSCs were incubated in the medium with different concentrations of AngII or losartan, then the quantity of collagen was examined by -proline release assay. RESULTS: ① The yield of HSCs was 2×10⁷-3×10⁷/per rat, their viability and purity was more than 95% and 90%, respectively. ② The yield of collagen in HSCs significantly got a rise in a concentration-dependent manner when HSCs were incubated with AngII (10^－6mol/L-10^－10 mol/L) (P<0.05). While HSCs were influenced by the antagonist of AT_1a (10^－6 mol/L-10^－9 mol/L), the quantity of collagen dropped greatly (P<0.05). CONCLUSIONS: Ang II stimulates HSCs to produce more collagen. Losartan inhibits the cell to synthesize collagen via AT_1a receptor (P<0.05). The results indicate that Ang II may play an important role in the development of hepatic fibrosis, and using AT_1a antagonist may offer a new strategy to prevent hepatic fibrosis.     

Microinjection of AT1 and AT2 receptor antagonists into PVN affects renal sympathetic nerve activity in chronic heart failure rats

AIM: To examine the renal sympathoexcitation affected by microinjection of angiotensin Ⅱ type 1 (AT₁) receptor antagonist L-158809 and angiotensin Ⅱ type 2 (AT₂) receptor antagonist PD123319 into paraventricular nucleus (PVN) in heart failure rats.METHODS: Left anterior descending coronary artery ligation was used to induce rat heart failure (HF) . Four weeks after operation, the left ventricular end-diastolic pressure (LVEDP), the ratios of heart weight/body weight and lung weight/body weight, and the ratio of infarct area of the left ventricle were observed. Under anesthesia, SD rats were fixed into the brain stereo controller to locate PVN for microinjection and the artificial cerebrospinal fluid (ACSF) was used for control. The left kidney was exposed by retroperitoneal approach and the renal sympathetic nerve was separated under surgical microscope. The heart rate, blood pressure and the activity of renal sympathetic nerve discharge (RSNA) were recorded by POWERLAB 8/30 system. RESULTS: Microinjection of AT₁ receptor antagonist into PVN induced a decrease in RSNA in both HF rats and sham rats. The RSNA responses to L-158809 in the HF rats were significantly greater (P<0.05) than those in the sham rats. However, microinjection of AT₂ receptor antagonist and ACSF into PVN induced no change of RSNA in both HF and sham rats. CONCLUSION: There are some differences of sympathetic nerve outputs between using AT₁ receptor antagonist and AT₂ receptor antagonist on PVN, indicating the up-regulation of AT₁ receptors in PVN during HF. The central renin-angiotensin-aldosterone system(RAAS) may be affected by AT₁ receptor, not by AT₂ receptor.     

起爆剂和微生物菌剂对蔬菜废弃物堆肥效果的影响

以玉米秸秆为辅料，葡萄糖为起爆剂，设置了V₀（蔬菜废弃物+ 玉米秸秆）、V₁（V₀+ 微生物菌剂）、V₂（V₀+ 微生 物菌剂+ 起爆剂）、V₃（V₀+ 起爆剂）4 个处理，所有处理的初始C/N 都调节为25，含水率调节为60% 左右，通过测定堆体温度、 含水率、C/N、pH 值、电导率（EC）、发芽指数（GI）等指标，研究起爆剂和微生物菌剂对蔬菜废弃物堆肥效果的影响。结 果表明：同时添加起爆剂和微生物菌剂的处理在堆体升温速率、最高温度、高温天数、含水率降幅、降低C/N、提高发芽指 数方面均优于其他处理，且能缩短堆肥周期，提高堆肥产品品质。总体堆肥效果表现为：V₂ ＞ V₁ ＞ V₃ ＞ V₀。     

Effects of propylthiouracil on body temperature in rats during cold exposure

AIM: To investigate the effect of cold exposure on the thermoregulatory function in hypothyroid rats. METHODS: Hypothyroid model was established by administration of antithyroid drug propylthiouracil(PTU) in rats. Colonic temperature was measured using digital thermometer. Plasma T₃ and T₄ concentrations were determined by radioimmunoassay. The effect of cold exposure on body temperature was observed after 2 weeks of PTU treatment. RESULTS: Plasma T₃ and T₄ concentrations were reduced markedly 2 weeks after PTU treatment, and colonic temperature was also decreased markedly; Hyperthermic response was not different between PTU group and control group during cold exposure. CONCLUSION: This study suggests that PTU-induced hypothyroid rat possesses a robust thermogenic response to short bouts of cold exposure.     

Clonal expansion and specific cytotoxicity of autologous or allogeneic T cells induced by M2a cells

AIM: To investigate clonal expansion and specific cytotoxicity of TCR Vβ subfamily T cells from acute myelogenous leukemia M_2a subtype (AML-M_2a)patients and normal individuals induced by AML-M_2a cells, respectively. METHODS: Complementarity determining region 3(CDR3) of TCR β with variable region genes was amplified in autologous or allogeneic T cells from mixed lymphocyte and tumor culture (MLTC) using RT-PCR. The positive products were further analyzed to identify the clonality of T cells by genescan. The specific cytotoxicity of T cells was analyzed by MTT. RESULTS: T cells from both M_2a patients and normal individuals after MLTC showed high response to M_2a cells with 4-17 TCR Vβ subfamily dominant utilization, one or two clonal expansion of T cells were identified in some predominant TCR Vβ subfamilies. Difference of distribution and clonal expansion of TCR Vβ subfamily T cells were related to source of T cells and the phase during MLTC. Compared with LAK cell, most of T cells from MLTC were CD3⁺CD8⁺T cells with higher and more specific cytoxicity to the induced cells, M_2a cells, but not HL60 or K562 cell line. CONCLUSION: Clonal expansion of TCR Vβ subfamily T cells stimulated selectively by M_2a cells may be a specific immune response of autologous and allogeneic T cells to M_2a cells associated antigen. The T cells induced by M_2a cells have the ability of specific cytoxicity to the AML-M_2a cells.     

Effect of Nao-re-qing oral liquid on cAMP content in hypothalamus and CSF,and AVP content in ventral septal area of endotoxin-induced febrile rabbits

AIM: To explore the mechanism of Nao-re-qing oral liquid (NRQ) decreasing endotoxin (ET)-induced fever in rabbits. METHODS: (1) The ET-induced fever model was established in rabbits. Febrile response of rabbits was observed. (2) The arginine vasopressin (AVP) content in the ventral septal area (VSA), and cAMP content in hypothalarmus (HP) and CSF were determined by radioimmunoassay.RESULTS: (1) In ET group, the maximal increment in body temperature (ΔT) [(1.80±0.16) ℃], 6 h thermal respone index (TRI₆)(11.31±0.20), the cAMP content in the HP [(1.35±0.21)nmol/g], the cAMP content in CSF [(66.69±1.82) nmol/L] and AVP content in the VSA [(30.80±9.59)ng/g ] were significantly higher than those in NRQ+ET group[ΔT(0.82±0.08) ℃, TRI₆(5.73±0.09), HP: cAMP(0.70±0.50)nmol/g, CSF: cAMP(56.86±1.34), AVP:(11.91±3.47)ng/g]( P<0.01). (2) The AVP content in VSA, and cAMP content in HP and CSF were separately paralleled with the fluctuation of body temperature (AVP: r=0.972, P<0.01; HP: cAMP r=0.899, P<0.05; CSF: cAMP r=0.991, P<0.01). CONCLUSION: The antipyretic action of NRQ may be due to inhibiting the increase in cAMP in HP and meanwhile promoting the release of AVP in VSA.     

Effect of Qing-Kai-Ling Injecta on cAMP content of hypothalamus and AVP content in ventral septal area of endotoxin-induced febrile rabbits

AIM:To investigate the mechanism of Qing-Kai-Ling(QKL) Injecta suppressing endotoxin(ET)-induced fever in rabbits.METHODS:①The ET-induced fever model was established in rabbits. QKL injecta was administered intravenously, and the febrile response of rabbits was observed. The cAMP content in the hypothalamus (HP) and arginine vasopressin (AVP) content in the ventral septal area (VSA) were determined by radioimmunoassay.RESULTS:①The maximal increment in body temperature (△T) ,6 h thermal response index (TRI₆)(29.59±10.39), cAMP content in the HP and AVP content in the VSA in the ET group were significantly higher than those in the normal saline (NS) group and the QKL+ET group .②The positive correlation was observed between the cAMP content in the HP and the fluctuation of body temperature (r=0.904,P＜0.01).CONCLUSION:The antipyretic mechanisms of QKL were probably due to inhibiting the increase in cAMP content in HP, and meanwhile stimulating the release of AVP in VSA.     

Effects of A2a adenosine receptor on hypoxic pulmonary hypertension in rats treated with salidroside

AIM: To study the protective effect of A_2a adenosine receptor (A_2aAR) on hypoxic pulmonary hypertension in the rats treated with salidroside. METHODS: Sprague-Dawley rats were randomly divided into 6 groups: normal control group, hypoxia group, hypoxia+salidroside (low dose) group, hypoxia+salidroside (median dose) group, hypoxia+salidroside (high dose) group, and hypoxia+CGS-21680 (a selective agonist of A_2aAR) group. Pulmonary hypertension in the rats was produced for 4 weeks. Mean pulmonary artery pressure (mPAP), mean carotid arterial pressure (mCAP) and the weight ratio of right ventricle/(left ventricle+septum)［RV/(LV+S)］ were measured. The expression of A_2aAR in the pulmonary arterioles was determined by immunohistochemistry and in situ hybridization. The mRNA expression of A2aAR in the lung tissues was detected by real-time RT-PCR. The protein level of A_2aAR in the lung tissues was analyzed by Western blotting. RESULTS: The mPAP in hypoxia group was significantly higher than that in normal control group. The mPAP in hypoxia+salidroside (high dose) group and CGS-21680 group was significantly lower than that in hypoxia group. RV/(LV+S) in hypoxia group were significantly higher than that in normal control group. RV/(LV+S) in hypoxia+salidroside (median dose) group, hypoxia+salidroside (high dose) group and CGS-21680 group were lower than that in hypoxia group. The ratio of vessel wall area/vessel total area (WA/TA) in hypoxia group was significantly higher than that in normal control group. WA/TA in hypoxia+salidroside (low dose) group, hypoxia+salidroside (median dose) group, hypoxia+salidroside (high dose) group and CGS21680 group were obviously lower than that in hypoxia group. The expression of A_2aAR was significantly higher in hypoxia group than that in normal control group. The expression of A_2aAR in hypoxia+salidroside (high dose) group and CGS-21680 group was obviously higher than that in hypoxia group. CONCLUSION: The A_2aAR attenuates pulmonary vessel remodeling and pulmonary hypertension induced by hypoxia. Salidroside protects the pulmonary vessel from remodeling and inhibits the development of hypoxia-induced pulmonary hypertension by up-regulation of A_2aAR expression.     

Role of PKC-α and δ isoforms in AVP improved contractile response of VSMC after hypoxia and its relations to MLC20 phosphorylation

AIM:The present study was to investigate the roles of protein kinase C α and δ isoforms (PKC-α, δ) in arginine vasopressin (AVP) improved contractile response of vascular smooth muscle cells (VSMC) to norepinephrine (NE) after hypoxia and its relations to myosin light chain (MLC₂₀) phosphorylation, myosin light chain phosphatase (MLCP) and myosin light chain kinase (MLCK) activity.METHODS: Primary cultures of VSMC were obtained from the superior mesenteric artery (SMA) of rats by explanting technique and the cells in third to fifth passage were used in the study. The effects of PKC-α and δ antagonists on AVP induced contractile response of VSMC to NE after 1.5 h hypoxia were observed by measuring the ratio of accumulative infiltration of fluorescent isothiocyanate-conjugated bovine serum albumin with transwell, and their effect on the activity of MLCP/MLCK in VSMC was assayed by enzymatic catalysis. At the same time, with the SMA from hemorrhagic shock rats (30 mmHg for 2 h), the effects of PKC α and δ isoforms in the regulation of AVP on MLC₂₀ phosphorylation of SMA after shock were observed by Western blotting.RESULTS: G 6976 (5×10^-6 mol/L, PKC-α isoform inhibitor) significantly antagonized AVP (5×10^-10 mol/L)-induced increase in the contractile response of VSMC to NE after hypoxia, and rottlerin (10^-5 mol/L, PKC-δ isoform inhibitor) also partly inhibited this effect. Hypoxia resulted in a significant increase in MLCP activity, with a decrease in MLCK activity of VSMC, and at the same time, the MLC₂₀ phosphorylation of SMA following hemorrhagic shock was significantly decreased. AVP inhibited the activity of MLCP and increased the phosphorylation of MLC₂₀, which was inhibited by G 6976, while rottlerin treatment only showed a slightly inhibitory effect. AVP and PKC-α, δ inhibitor had no significant influence on MLCK activity.CONCLUSION:AVP up-regulates vascular reactivity and calcium sensitivity of VSMC possibly through inhibiting the activity of MLCP and increasing the phosphorylation of MLC₂₀ by PKC-α isoform.     

Effects of angiotensin II receptor antagonist on remodeling of renal arterioles in hypertension

AIM: To investigate the effects of angiotensin II receptor antagonist on remodeling of renal arterioles in hypertension. METHODS: Eighteen 4 weeks old male rats were divided into three groups: Wistar-Kyoto rats (WKY) for normotensive group, and spontaneously hypertensive rats (SHR) for hypertensive group, and SHR treated with losartan orally (15 mg·kg^-1·d^-1). The rats were raised to 16 weeks old. The morphometric parameters of the renal arterioles, and the widths of vascular smooth muscle cells (VSMC) and intercellular space were studied on kidney slices by light microscope and electromicroscope respectively, combined with computer-assistant image analysis system. The minimal renal vascular resistance (RVR_min) was studied by isolated kidney perfusion system. RESULTS: The systolic blood pressure of the tail artery, wall thickness, wall area, ratio of wall thickness to inner diameter, width of VSMC of renal arterioles and RVR_min were all smaller or lower in losartan group than those of SHR.     

Nucleus tractus solitarius participates in regulation of paraventricular nucleus vasopressinergic neurons on gastric ischemia-reperfusion injury in rats

AIM: To investigate the role of the nucleus tractus solitarius (NTS) in the regulation of paraventricular nucleus (PVN) AVP-ergic neurons on gastric ischemia- reperfusion injury (GI-RI). METHODS: Male SD rats were used in experiments. The celiac artery were clamped for 30 min and reperfused 1 h by removal of the clamp to obtain the ischemia-reperfusion state. The mechanism was analysed with nucleus electrical stimulation, electrolytic lesion and nucleus microinjection technique. RESULTS: Microinjection of arginine-vasopressin (AVP) into PVN obviously attenuated the GI-RI and dose-dependent effects were observed (r=-0.477, P<0.05) ; NTS lesion or microinjection of AVP antagonist into NTS both eliminated the attenuate effect of electrical stimulation of PVN on GI-RI. The effect of microinjection of AVP into NTS was similar to microinjection of AVP into PVN. CONCLUSION: The NTS participates in regulation of PVN AVP-ergic on GI-RI, which is mediated by the AVP receptor in the NTS.     

Effect of L-arginine on function and structure of mitochondria in ischemia-reperfusion myocardial cells in rabbits

AIM: To study the effect of L-arginine (L-Arg) on function and structure of mitochondria in ischemia-reperfusion (MRI) myocardial cells. METHODS: Thirty rabbits were randomly divided into three groups (n=10 in each), control group, MIR group and MIR+L-Arg group. The mitochondrial respiratory function, Ca²⁺ concentration ([Ca²⁺]m), malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. Meanwhile, the contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), total adenylic acid number (TAN) and energy charge (EC) in the myocardial tissue were respectively measured. Moreover, the ultrastructure changes in myocardial mitochondria were observed during MIR. RESULTS: The mitochondrial respiratory control rate (RCR), velocity 3 (V₃), SOD, surface density (Sv) and specific surface (δ) in MIR+L-Arg group were higher than those in MIR group, velocity 4 (V₄), [Ca²⁺]m, MDA, volume density (Vv), horizental diameter (Hd) were lower than those in MIR group. ATP, ADP, TAN and EC levels of myocardial tissue were higher than those in MIR group. There was no significant difference between MIR+L-Arg and control group in V₃, V₄, SOD, MDA, Vv, Sv, δ, Nv, Vd, AMP and TNA. CONCLUSION: It is suggested that L-Arg improves the function and structure of mitochondria in myocardial cells in the reperfusion injury after myocardial ischemia by decreasing oxygen free radical level and Ca²⁺ overload in the mitochondria.     

Expression of human inducible nitric oxide synthase in fibroblast cell line V79 and effects of H4Bon iNOS activity

AIM: To explore the feasibility of human iNOS transfected into V₇₉ cells by gene transfer and investigate the effects of H₄B on iNOS activity. METHODS: Human iNOS was transfected into V₇₉ cells with the karyocyte expressive vector. The cloned cells were selected by G₄₁₈. The expression of iNOS mRNA was quantified by RT-PCR and iNOS expression was observed by immunofluorescence. NO product in cells was determined by measuring nitrite (NO^-₂) release using the Griess reaction. RESULTS: V₇₉ cells infected human iNOS was proved to have iNOS mRNA at 462 bp by RT-PCR, and iNOS protein in the cytochylema by immunofluorescence. When the cells were incubated without H₄B, the content of NO in pcDNA₃ cells was minimal, with NO^-₂ production (82.32±13.08) just above the normal group (74 38±9 80, P>0.05, n=6) There was no significant difference between pcDNA₃ cells incubated with or without H₄B, (P>0.05, n=6) NO^-₂ production by pcDNA₃-iNOS cells without H₄B was higher (105 58±13 33) (n=6, P<0.01vs the normal cells or pcDNA cells). However, in pcDNA₃-iNOS cells incubated with H₄B, NO^-₂ production was much higher (236 57±3183) (n=6, P<0.01vs the all former groups). CONCLUSION: iNOS activity was increased by adding H₄B in pcDNA₃-iNOS cells, and the fibroblast can be a target cell of iNOS gene transfer.     

Influence of vestibular training on plasma levels of stress-related hormones in rats with motion sickness

AIM: To investigate the relationship between motion sickness and the plasma levels of stress-related hormones in the rats before and after vestibular training.METHODS: Conditioned taste aversion (CTA) was induced in 72 female SD rats after rotatory stimulation. The magnitude of CTA was measured to reflect the susceptibility of rats to motion sickness. The plasma levels of corticosterone, adrenocorticotrophic hormone (ACTH), corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) were analyzed by radioimmunoassay. Hormone levels were determined before and after rotatory stimulation, and after 1 month of vestibular training when the rats obtained habituation to this rotation.RESULTS: CTA to 0.15% saccharin solution in rats after the rotatory stimulation was completely inhibited after vestibular training, suggesting that a habituation of the rats to motion sickness was obtained. The rotatory stimulation induced an elevation in the plasma levels of corticosterone, ACTH and AVP, and this response of corticosterone to rotation was greatly reduced after vestibular training. The plasma levels of all 4 hormones in the rats insusceptible to motion sickness were higher than those in susceptible group, especially the plasma levels of corticosterone and ACTH after rotation, and the basal level of CRH. In addition, after vestibular training, the basal plasma levels of corticosterone, ACTH and CRH in both groups were higher than those before training, and a slight elevation was also observed in the basal level of AVP.CONCLUSION: Vestibular training may induce a habituation to rotatory stimulation in rats, thus inhibiting the development of motion sickness. The difference of the susceptibility of rats to motion sickness may negatively relate to the basal plasma levels of stress-related hormones.