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Objective To analyze the clinical features of autonomic nerve dysfunction and sympathetic skin response (SSR) in patients with gout. Methods A total of 25 patients with gout diagnosed from March 2017 to January 2018 were enrolled, including 10 patients with tophus and 8 patients with autonomic nerve dysfunction (symptomatic). EMG was used to detect SSR. Results The main symptoms of autonomic nervous dysfunction in the gout group were abnormal sweat glands. Compared with the normal control group, the lower extremity latency period of patients in the gout group was prolonged (Z = -2.136, P = 0.033) and the amplitude was reduced (Z = -2.959, P = 0.003). Lower extremity amplitude of the symptomatic group was lower than that of the normal control group (Z = -3.426, P = 0.001) and the asymptomatic group (Z = -3.308, P = 0.001). The lower extremity amplitude of patients in tophout group was lower than that in the control group (Z = -3.176, P = 0.001) and the non-tophout group (Z = -2.301, P = 0.021), while the lower extremity latency period of patients without tophout was prolonged (Z = -2.518, P = 0.120) and the amplitude was reduced (Z = -2.327, P = 0.020), which were statistically significant different from the control group. Conclusions Abnormal autonomic nerve function exists in gout patients, mainly in lower limb injury, especially in patients with tophus or symptoms of autonomic nerve dysfunction. SSR can objectively evaluate the autonomic nerve function state. [ABSTRACT FROM AUTHOR]

Objective: To explore the effects of the mu-opioid receptor (MOR) in the paraventricular nucleus (PVN) on the ejaculatory behaviors of male rats and its potential mechanisms., Methods: Male SD rats with normal ejaculation ability were mated with female ones in hormone-induced estrus. After bilateral PVN microinjection of D-Ala-2-Me-Phe-4-Gly-ol enkephalin (DAGO) or D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) with an inserted catheter, the male animals were observed for mount latency (ML), mount frequency (MF), intromission latency (IL), intromission frequency (IF), ejaculation latency (EL), ejaculation frequency (EF), post-ejaculation interval (PEI), and intromission ratio (IR). The lumbar sympathetic nerve activity (LSNA) of the rats was recorded using the PowerLab data acquisition hardware device, and the levels of norepinephrine (NE) in the peripheral plasma were measured by ELISA following microinjection of saline or different doses of DAGO or CTAP., Results: Neither CTAP nor DGAO significantly affected the ML of the male rats (P > 0.05). DGAO remarkably increased IF (P < 0.01) and MF (P < 0.01), prolonged IL (P < 0.01), EL (P < 0.01) and PEI (P < 0.01), and reduced EF (P <0.01) and IR (P < 0.05). On the contrary, CTAP markedly decreased IF (P < 0.01) and MF (P < 0.01), shortened IL (P < 0.01), EL (P < 0.01) and PFI (P < 0.01), and elevated EF (P < 0.01) and IR (P < 0.01). Additionally, DAGO decreased LSNA in a dose-dependent manner and reduced the NE level in the peripheral plasma. CTAP, however, not only offset the effects of DAGO on LSNA, but also significantly increased LSNA., Conclusions: MOR in PVN inhibits ejaculatory behaviors in male rats by weakening LSNA, which has provided some theoretical evidence for the use of highly selective opioids in the treatment of premature ejaculation.

Objective: To elucidate the association between large conductance calcium-activated potassium channels (BK Ca ) in the paraventricular hypothalamic nucleus (PVN) and sympathetic outflow in rats with chronic heart failure (CHF) . Methods: Male Wistar rats (6-7 weeks old) were randomized to sham operated group and CHF group (coronary artery ligation) . Two weeks after operation, BK Ca inhibitor Iberiotoxin (IBTX) was infused into PVN by osmotic minipumps, rats were divided into following groups: sham+aCSF, CHF+aCSF, sham+low dose IBTX (0.125 nmol/nl) , CHF+low dose IBTX, sham+moderate dose IBTX (1.25 nmol/nl) , CHF+moderate dose IBTX, sham+ high dose IBTX (12.5 nmol/nl) , and CHF+high dose IBTX ( n= 6 each) . Additional rats were grouped as follows: sham+vehicle, sham+KCNMB4 knockdown (by rAAV2-KCNMB4 shRNA virus injection in PVN) , CHF+vehicle, CHF+ KCNMB4 knockdown group ( n= 6 each) . The cardiac function was determined by echocardiography, left ventricular hemodynamics were measured invasively, renal sympathetic nerve activity (RSNA) was recorded at 6 weeks after coronary artery ligation or sham operation. The contents of norepinephrine (NE) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in plasma were determined by enzyme-linked immunosorbent assay. The protein and mRNA expression of KCNMB4 in PVN were measured by immunofluorescence staining, Western blot, and real-time PCR, mRNA expression of BK Ca in PVN was detected by real-time PCR. Results: Compared with the sham operation group, the cardiac function of the heart failure group was significantly reduced ( P< 0.05) , and the plasma NE and the serum NT-proBNP were significantly elevated ( P< 0.05) . The protein and mRNA expression of KCNMB4 in PVN were obviously down-regulated in CHF rats ( P< 0.05) . After perfusion of IBTX or KCNMB4 knockdown by microinjection of rAAV2-KCNMB4 shRNA virus,right ventricular weight/body weight and lung weight/body weight ratio as well as left ventricular end-diastolic diameter were increased and left ventricular ejection fraction was decreased (all P< 0.05) , the sympathetic driving indexes was increased in sham rats, changes of these parameters further aggravated in CHF rats ( P< 0.05) . KCNMB4 knockdown further downregulated protein expression in PVN of CHF rats. Conclusion: Downregulation and blunted function of BK Ca in PVN may contribute to sympathoexcitation and deterioration of cardiac function in rats with chronic heart failure.

The present study was aimed to investigate the roles of renal sympathetic nerve and oxidative stress in the development of foot shock-induced hypertension. Ninety rats were divided into 6 groups (the number of each group was 15): control group, foot shock group, denervation of renal sympathetic nerve group, denervation of renal sympathetic nerve + foot shock group, Tempol treatment + foot shock group, denervation of renal sympathetic nerve + Tempol treatment + foot shock group. Rats were received electrical foot shock for 14 days (2-4 mA, 75 V, shocks of 50-100 ms every 30 s, for 4 h each session through an electrified grid floor every day). Renal sympathetic ablation was used to remove bilateral renal sympathetic nerve in rats (rats were allowed to recover for one week before the beginning of the foot shock procedure). The antioxidant Tempol was injected intraperitoneally at 1 h before foot shock. Systolic blood pressure was measured at 1 h after foot shock on day 0, 3, 7, 10 and 14. Contents of thiobarbituric acid reactive substance (TBARS), renin, angiotensin II (AngII) and glutathione peroxidase (GSH-Px) in plasma were measured by ELISA after 14-day foot shock. The results showed that systolic blood pressure of foot shock group was significantly increased (P < 0.05) compared with that of control group from day 7 to day 14 of foot shock. Denervation of renal sympathetic nerve and/or Tempol treatment significantly reduced the increase of systolic blood pressure induced by foot shock. Levels of TBARS, renin and AngII in plasma were increased significantly in foot shock group compared with that of control group (P < 0.05). Plasma GSH-Px concentration was decreased in foot shock group rats compared with that of control group (P < 0.05). Denervation of renal sympathetic nerve and/or tempol treatment significantly reduced the increase in TBARS, renin, AngII levels induced by foot shock in comparison with that of foot shock group (P < 0.05), but had no effects on the reduction of GSH-Px concentration. The results suggest that renal sympathetic nerve may play an important role in the development of foot shock-induced hypertension, and renal sympathetic nerve may influence oxidative stress and directly or indirectly activate renin-angiotensin-aldosterone system, so the foot shock-induced high blood pressure may be maintained and hypertension may therefore be produced.

Objective: To investigate the effects of obesity on the lipid and glucose metabolism in female rats., Methods: The litter size was adjusted to 4 pups per litter for the small litter (SL, treatment group) and 12 neonates per dam in the normal litter (NL, controls) at postnatal day 0. Body weights were measured weekly. At the age of 6 weeks, bilateral ovariectomy was performed. The blood levels of free fat acid, triglyceride, total cholesterol, free blood glucose and free insulin were evaluated. The muscular expression of AMP-activated protein kinase was detected by immune staining., Results: As compared to normal litters, the levels of fat acid, triglyceride, total cholesterol, free blood glucose and free insulin significantly increased. The muscular activity of AMP-activated protein kinase decreased. All difference were statistically significant (P < 0.05)., Conclusion: Obesity in early life has obvious effects on the lipid and glucose metabolism in female rats.

Objective: To investigate the role of renal sympathetic nerves in renal sodium transport in ouabain-hypertensive rats (OHR)., Methods: Sixteen male SD rats with sham renal denervation (Sham-RDNX) and 16 with renal denervation (RDNX) were randomly into normal control group and ouabain group to receive intraperitoneal injection of normal saline (1 ml/kg) and ouabain (27.8 µg/kg) once a day, respectively. Systolic blood pressure (SBP), heart rate and body weight were recorded weekly. Food consumption of the rats was determined twice a week. After a 4-week treatment, blood and 24 h urine samples were collected to measure the serum and urinary concentration of sodium, trace lithium and creatinine. Endogenous creatinine clearance rate (Ccr), fractional excretions of sodium (FENa), fractional excretions of lithium (FELi) and fractional reabsorption of sodium in the postproximal tubules (FDRNa) were calculated. Plasma renin activity was determined by radioimmunoassay. Norepinephrine was extracted from the renal tissue and assayed for norepinephrine content by HPLC., Results: The body weight, food intake and heart rate showed no significant difference among the 4 groups (P > 0.05). After 4 weeks, the SBP of control RDNX group (CDNX) was significantly lower than that of the control Sham-DNX group (Csham)(P < 0.05); the SBP of ouabain RDNX group (ODNX) was also significantly lower than that of ouabain Sham-DNX group (Osham) (P < 0.05); RNDX lowered SBP by about 10 mmHg in both ouabain groups and control groups. The SBP was significantly higher in Osham and ODNX groups than in the corresponding control groups (P < 0.01), also significantly higher in ODNX group than in Csham group (P < 0.01). Ccr showed no significant difference among the 4 groups(P > 0.05). FENa, FELi and FDRNa were significantly lower in ouabain groups than in the corresponding control groups (P < 0.05, P < 0.01, P < 0.05), but FENa, FELi and FDRNa of ODNX group were similar with those of Osham group (P > 0.05); FENa , FELi and FDRNa were similar between CDNX and Csham groups (P > 0.05). The plasma renin activity was comparable between the 4 groups (P > 0.05). Renal norepinephrine level was markedly reduced in RDNX group compared with that in Sham-RDNX group in both ouabain and control groups (P < 0.01)., Conclusion: The increase of proximal tubule sodium reabsorption in OHR is not dependent on the renal sympathetic nerve.

Objective: To test the hypothesis that regional sympathetic innervation in the atria and pulmonary veins are correlated with atrial fibrillation (AF)., Methods: Sixteen adult mongrel dogs underwent thoracotomy under general anesthesia. Bilateral cervical vagal trunks were decentralized. Multipolar catheters were placed into right atrial appendage (RAA), left atrial appendage (LAA), left atrium (LA), left superior pulmonary vein (LSPV), left inferior pulmonary vein (LIPV), right superior pulmonary vein (RSPV), and left inferior pulmonary vein (LIPV). The bilateral sympathovagal trunks were stimulated, S1S1 burst stimulation and S1S2 stimulation procedure were performed on different points of RAA, LAA, LA, LSPV, LIPV, RSPV, and LIPV. The TF thus induced was monitored. After that, the dogs were killed with their hearts and lungs were taken out. Immunocytochemical staining of cardiac nerves was performed using anti-tyrosine hydroxylase (TH) antibodies. The nerve fiber density was counted manually for each case and expressed as the mean number per slice., Results: Two dogs died during the experiment and the whole procedure was completed on 14 dogs. There was no significant difference in the AF induction rate among the most points, however, the AF induction rate of the RIPV was significantly lower than those of the other points (all P < 0.05). The levels of density of TH-positive nerves in the atria and atrial appendages were significantly higher than those in the pulmonary veins (P = 0.02). The density of TH-positive nerves in the dogs with AF was significantly higher than that in the dog without AF (P < 0.05). The innervation of sympathetic nerves in atria and pulmonary veins was highly correlated to the induction of atrial fibrillation (r = 0.83)., Conclusion: Regional sympathetic hyperinnervation plays an important role in atrial fibrillation induction.

Objective: To introduce studies about the effect of different needling manipulation methods on the body surface temperature in recent years, and to probe the mechanism., Methods: It is reviewed from clinical studies and experimental studies, and other aspects., Conclusion: The functions and therapeutic effects of acupuncture are changed with temperature changes induced by different needling manipulations. Reinforcing method of acupuncture can increase body temperature, and the reducing manipulation can decrease it. The temperature of body surface is decided by blood circulation, excitement extent of the sympathetic nerve, and metabolic state of the tissues, and other aspects, which are related with the changes of skin temperature induced by different needling manipulation methods.

To evaluate the effect of aerobic and anaerobic endurance training the regulating the function of autonomic nervous system, in order to provide scientific basis for optimizing the project of physical fitness training. Fourty-one healthy young men were randomly divided into aerobic and anaerobic endurance training groups. The training period was 8 weeks. Pre-exercise, 4 weeks and 8 weeks after trained, HRV were measured compared with pre-exercise. The autonomic balance in aerobic endurance group had an increasing parasympathetic activity (HF, HFnu, RMSSD, PNN50, all P was < 0.05) and relatively decreasing sympathetic activity (LFnu). This group showed a parasympathetic predominance (LF/HF) and increase of HRV. While in the anaerobic group there was a relative stabilization with the function of autonomic nervous system. The present study shows that the effect of aerobic and anaerobic endurance training on the autonomic nervous system depends on its intensity. Proper intensity of anaerobic endurance training may be beneficial to improve the adaptability of human body for circumstances as aerobic endurance training.

Objective: To study the responses of injured dorsal root ganglion (DRG) neurons to sympathetic nerve stimulation with different time sequences., Method: In chronically compressed DRG model, the spontaneous activity of the single fiber from injured DRG neurons was recorded, and the responses of DRG neurons to chaotic and periodic electric stimulation of the lumbar sympathetic trunk compared., Results: Sympathetic-sensory coupling was present in chronically compressed DRG neurons, and the response of DRG neurons increased gradually as the sympathetic stimulating frequency increased from 5 to 20 Hz (P<0.01). The chaotic stimulation evoked much greater response than periodic stimulation, even though the stimulating frequency was similar (P<0.01)., Conclusions: Besides the stimulating frequency, the time sequence of the stimulation is one of the important factors that influence the response of DRG neurons to sympathetic stimulation. Chaotic sympathetic stimulation causes greater response than periodic stimulation does, and the chaotic activity of presynaptic neuron evokes greater postsynaptic response than periodic activity. The chaotic activity of the neurons might be one of the effective ways for information transmission through the nerves.

The effects of paraventricular nucleus (PVN) stimulation and vasopressin on gastric ischemia-reperfusion injury (GI-RI) were investigated in male SD rats of which the celiac artery was clamped for 30 min and reperfused for 1 h by removal of the clamp. The results were as follows. Both electrical and chemical stimulation of the PVN obviously attenuated the GI-RI. Bilateral electrolytic lesion of the nucleus tractus solitarius (NTS) or microinjection of AVP-V(1) receptor antagonist into the NTS could eliminate the protective effect of electrical stimulation of the PVN on GI-RI. Hypophysectomy did not influence the effect of electrical stimulation of the PVN. Both vagotomy and sympathectomy could increase the effect of stimulating PVN on GI-RI. Microinjection of arginine-vasopressin (AVP) into the PVN also attenuated the effect on GI-RI. These results suggest that the PVN and AVP participate in the regulation of GI-RI and play an important role in protection against GI-RI. This protective effect of PVN on GI-RI might be mediated by activation of AVP-ergic neurons in the PVN, which release AVP from the descending projection fibers and activate the AVP-V(1) receptors on the NTS neurons. The vagus and sympathetic nerves are involved in the efferent pathway exerting their effects on GI-RI. Hypophysis does not seem to be involved in the protective effect of PVN stimulation.

Effect of acetylcholine (ACh) on presympathetic neurons of the rostral ventrolateral medulla (RVLM) was studied by extracellular recording technique and microiontophoresis in urethane-anaesthetized rats. Spontaneous discharges of 35 presympathetic neurons of RVLM were recorded. All the neurons showed increased discharge by microiontophoresis of ACh dose- dependently with the increase of iontophoretic current. In 22 units microiontophoresis of atropine decreased the baseline discharge rate and completely blocked the excitatory effect of ACh on these neurons, while in the remaining 7 and 6 neurons microiontophoresis of d-tubocurarine (d-TC) and hexamethonium (C(6)) respectively had no effect and did not block the action of ACh. The above finding suggests that presympathetic neurons of RVLM receive a tonic excitatory cholinergic input mediated by M receptors.

To investigate cardiovascular effects of changed GABAergic tonic activation in periventricular forebrain, arterial pressure (AP), heart rate (HR) and renal sympathetic nerve discharge (RSND) were recorded in anesthetized rats when L-securinine (L-Sec) was administered into the lateral intracerebroventricle. L-Sec elicited dose-dependent increases in RSND, AP and HR, which were much weaker than those of bicuculline. L-Sec antagonized the sympatho-inhibitory and depressor effects evoked by both muscimol and baclofen. These results indicate that GABAergic inhibition originating from periventricular forebrain may suppress tonically sympathetic outflow to cardiovascular system which is disinhibited by L-Sec, and L-Sec is likely an unselective GABA receptor antagonist.

Experiments were performed on rabbits anaesthetized with urethane and chloralose. The electrocardiogram (ECG), heart rate (HR), and blood pressure (BP) were recorded and the power spectrum density (PSD) of R-R interval was analysed by a computer. The low frequency component (LF) was higher during the respective stimulation of the nucleus ambiguous, depressor nerve, and the peripheral end of right vagus with a low frequency fluctuant style than with a monotonous style (P < 0.05). Intravenous infusion of phenylephrine resulted in increases of total variance of RRI (TV), very low frequency components (VLF), LF, high frequency components (HF) and LF/HF during the first 256 RRI only (P < 0.05-0.01). In order to observe the influence of different activities of sympathetic nerves on heart rate variability (HRV), DL-homocysteine (DLH) was microinjected into the vicinity of N. Paraventricularis of hypothalamus. This injection caused increases of the TV, LF, LF/HF and VLF during the rising phase of BP and HR, but no significant change occurred at the plateau period of high BP and HR. These results suggest that heart rate variability mainly reflects the fluctuation of vagal and sympathetic tone.

The effect of spinal alpha adrenoceptor blockage on the inhibition of renal sympathetic nerve activity (RSNA) and natriuresis induced by blood volume expansion was investigated in anesthetized and bilateral sinoaortic denervated rabbits. In the groups of rabbits with intrathecal injection of alpha-adrenoceptor blocker phentolamine or artificial cerebrospinal fluid the inhibition of RSNA induced by blood volume expansion were (-25.4 +/- 5.4)% and (-42.5 +/- 5.2)% respectively (P < 0.05). In the groups of rabbits with intrathecal injection of alpha 1 adtenoceptor blocker prazosin or artificial cerebrospinal fluid the inhibition of RSNA induced by blood volume expansion were (-29.3 +/- 6.1)% and (-42.5 +/- 5.2)% respectively (P < 0.05). These results suggested that both spinal alpha and alpha 1 adrenceptor blockage with attenuated the inhibition of RSNA induced by blood volume expansion. The spinal alpha 1 adrenceptor blockage with intrathecal injection of prazosin also attenuated signiticantly the natriuresis and diuresis induced by blood volume expansion (P < 0.05).

The effects of intraventricular injection and epicardial application of adenosine on spontaneous electrical activity of nucleus paragigantocellularis lateralis (PGL) neurons in rostral ventrolateral medulla (RVLM) were examined in 35 anesthetized rats with sinoaortic denervation and vagotomy. The results obtained were as follows: (1) The spontaneous discharge of 121 PGL neurons (mean discharge rate: 22.5 +/- 1.9 spikes/s) were recorded in 35 rats. (2) In response to intraventricular injection of adenosine (0.5 mumol/kg), mean arterial pressure (MAP) was initially increased by 1.7 +/- 0.2 kPa(P < 0.001) and subsequently decreased by 4.6 +/- 0.5 kPa(P < 0.001), while the heart rate (HR) was decreased by 126.5 +/- 12.3 bpm (P < 0.001). Of 35 PGL spontaneous discharge units responsive to intraventricular injection of adenosine, 30 showed an average increase from 21.9 +/- 2.6 to 29.2 +/- 3.4 spikes/s (P < 0.001), 3 with no change, while 2 with a decrease. (3) Following epicardial application of 20 mmol/L adenosine, the BP and HR were not significantly changed, while the spontaneous discharge of 22 PGL neurons were increased from 18.8 +/- 1.9 to 26.9 +/- 2.8 spikes/s (P < 0.001), and that of 3 neurons was not changed. (4) The excitatory response of PGL neurons to intraventricular injection or epicardial application of adenosine was completely inhibited by pretreatment with selective adenosine A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX, 500 micrograms/kg). (5) Following epicardial application of phenol or bilateral stellate ganglionectomy, adenosine failed to affect the activity of PGL neurons. The results obtained indicate that adenosine may stimulate cardiac sympathetic afferents through adenosine A1-receptor, thereby resulting in the activation of PGL neurons.

Experiments were performed on 36 anesthetized rabbits. By cervical vagal afferent stimulation (VAS) with lower electric frequency (5-8 Hz) and higher electric frequency (50-100 Hz), the depressor and pressor responses were established. Both of these responses accompanied by decreasing in renal sympathetic activity (RSA). With the parameters of vagal-pressure reflex and vagal-sympathetic stimulation reflex, effects of stimulation of the locus coeruleus on these were investigated. The vagal-pressure and sympathetic reflexes were significantly inhibited by electric and chemical (glutamate) stimulation of the locus coeruleus. Meanwhile both the electric and chemical stimulation of the locus coeruleus per se elicited the elevation of BP and RSA. These results together with the recently hypothesized global function of the locus coeruleus were discussed.

Experiments were performed on urethane anesthetized and artificially ventilated rabbits. The results were as follows. Application of substance P (SP) to the pressor area of ventral surface of medulla oblongata (VSMp) elicited a dose-dependent increase in blood pressure (BP), but no significant change in heart rate. The pressor response of SP was blocked by pretreatment with SP receptor antagonist (DSP) in VSMp. Application of DSP alone to VSMp elicited a significant decrease in BP. The pressor response of SP was attenuated when VSMp was pretreated with phentolamine or prazosine, whereas pretreatment with yohimbin or propranolol was without effect. Application of SP to VSMp elicited an increase in renal sympathetic nerve discharge (RSND) in association with pressor response; both these responses were blocked by pretreatment with DSP in VSMp. Application of DSP alone to VSMp elicited a significant decrease in RSND and BP. The above results indicate that SP has a pressor effect in VSMp due to activation of SP receptor mediated by alpha 1-receptor. The pressor effect of SP may be mainly due to an increase of peripheral vascular resistance induced by the augmented sympathetic nerve activity. In summary, it appears that endogenous SP in VSMp plays an important role in maintaining sympathetic tone and BP level.

The effects of intraventricular injection of adenosine and its analogues on renal sympathetic nerve activity (RSNA) were examined in sinoaortic denervated and vagotomized anesthetized rats. In response to intraventricular bolus injection of adenosine, RSNA was increased by 41.9 +/- 6.08% (P < 0.001), mean arterial pressure (MAP) was initially increased by 1.39 +/- 0.19 kPa (P < 0.001) and subsequently decreased by 3.74 +/- 0.64 kPa (P < 0.001), and heart rate (HR) was reduced by 95 +/- 14 bpm (P < 0.001). To determine the adenosine-receptor subtype which mediates the response of RSNA to adenosine, we used selective A1-receptor agonist (R-PIA) and A2-receptor agonist (NECA) and found that MAP and HR were reduced by R-PIA and NECA. The effects lasted significantly longer than those of adenosine. R-PIA induced an increase in RSNA by 31.6 +/- 5.21% (P < 0.001), while NECA showed no effect on RSNA. The renal sympathoexcitatory response to intraventricular injection of adenosine was completely inhibited by pretreatment with a selective A1-receptor antagonist (DPCPX). Following the bilateral stellate ganglionectomy, intraventricular injection of adenosine failed to induce the increase in RSNA. The results indicate that adenosine may activate cardiac sympathetic afferents through A1-receptor, resulting in a reflex augmentation of RSNA.

The effect of central administration of interleukin-2 (IL-2) on the splenic sympathetic nerve activity was studied. Intracerebro ventricular infusion of recombinant human IL-2 (300 U/rat) elicited marked long term (> 120 min) decrease in the electrical activity of the splenic nerve without altering blood pressure and body temperature. This splenic effect could be blocked by prior or post treatment with an opioid antagonist naloxone (1 mg/kg, iv). Naloxone alone injected intravenously had no effect on the splenic nerve activity. These results imply that the inhibitory effect of intracerebral IL-2 on splenic sympathetic nerve activity is mediated by opioid receptors.

Experiments were performed on 63 rabbits anesthetized with pentobarbital, paralyzed with gallamine triethiodide and ventiled artifically. Ipsilateral renal sympathetic nerve discharge (RSND), unit discharges of rostral ventrolateral medulla (RVL), caudal ventrolateral medulla (CVL) and blood pressure (BP) were recorded. The sympatho-inhibitory response were evoked by stimulation of the central end of vagal nerve (CVN) (731/788 exp.). The inhibitory duration is 3.6 +/- 0.185 s. The responses vary with the functional state of the CNS. The RSND inhibitory duration could be shortened or prolonged, depending on the excitatory background of RSND or the basal sympathetic tonic activity. The results indicate that CVN-induced inhibitory of RSND may be mediated, at least partly, by excitation of NTS and CVL, which results, in turn, in depressing RVL and final reduction of sympathetic efferent activity.

Objective: To study the effects of PEEP 0.98 kPa (1 kPa = 10.2 cmH2O) on the sympathetic nerve activities of visceral organs in anesthetized dogs with intact neuraxis or with vagotomy., Methods: Renal (RNA), cardiac (CNA), hepatic (HNA) and adrenal gland (AdNA) sympathetic nerve activities were recorded. Mean blood pressure (MBP), central venous pressure (CVP), left atrial pressure (LAP) and airway pressure (AWP) were also measured., Results: AdNA significantly decreased, but RNA, CNA and HNA had a tendency toward decrease during PEEP loading in the intact dogs. However, vagotomy reversed the changes in all nerve activities in the intact dogs. CVP, LAP and AWP significantly increased, while MBP significantly decreased during PEEP loading., Conclusion: The results indicated that PEEP loading caused sympathoinhibition in the adrenal gland, kidney, heart and liver, which were mediated by activation of cardiopulmonary baroreceptor.

Experiments were performed on 86 cats anesthetized with chloralose, paralyzed with gallamine triethiodide and ventilated artificially. Autospectral and coherence analysis revealed that the frontal-parietal cortex activity (EEG) and cardiac sympathetic nerve discharge (SND) were remarkably correlated in 33/44 cats. SND lagged EEG by 50 +/- 20 ms with a cross-correlation value of 0.4 +/- 0.1. Coherence value was 0.25 +/- 0.05, indicating a statistically significant relationship between the two signals. Midbrain transection at stereotaxic plane A3 preferentially decreased SND power at frequencies 3-4.2 Hz, accompanied by a fall in mean blood pressure (5.47 +/- 0.13 kPa). The coherence of SND to EEG was eliminated after decerebration. However, the total power in EEG was not significantly affected. The SND rhythm and blood pressure returned nearly to control level within 1 h after decerebration. The effects of midbrain transection were significantly attenuated by prior minor lesions of the lateral hypothalamus or medial thalamus. These results suggest that the forebrain is responsible significantly for a component of sympathetic tone in anesthetic cats. The integrity of diencephalon is required for the participation of forebrain in setting the level of basal SND. Reduction in SND following decerebration was due in part to interruption of the descending influence from diencephalon and brain stem sympathetic rhythm generators are involved in compensating for the loss of the forebrain dependent component of SND.

The effect of electrical stimulation of afferent renal nerve (ARN) on cardiovascular response, the synthesis and release of vasopressin were studied in rabbits. During the course of the experiment, the pathway of ARN to central nerve system was also analyzed. The results showed that electrical stimulation of ARN elicited significantly decrease of mean arteral blood pressure and heart rate as well as inhibition of cervical sympathetic nerve activity. In the event of the above physiological changes, the AVP concentration in supraoptic nucleus (SON), paraventricular nucleus (PVN) and plasma was increased, but that in hypophysis was decreased. Injection of sodium nitropruside (SNP) or AVPa indicated that increase of AVP release was due directly to stimulation of ARN. Nodose ganglionectomy or transversal section of spinal cord at different levels suggested that the main afferent pathway of ARN to higher level of central nerve system entered into spinal cord at T5-L2.

This is the first time to report the existence of new presynaptic inhibitory autoreceptors--histamine H3-receptors in guinea pig myocardium. We found that (R)-alpha-methylhistamine (alpha-MeHA), a selective histamine H3-receptor agonist, attenuates the sympathetic inotropic response of isolated guinea pig atria elicited by electrical field stimulation. This inhibition was associated with a marked reduction in endogenous norepinephrine release. The above phenomenon was antagonised by selective histamine H3-receptor antagonists, and inhibited by pretreatment with N ethylmeleimide. The cardiac sympathetic response could be attenuated or facilitated by increase or decrease of endogenous histamine. Our findings indicate that the endogenous histamine might be involved in the modulation of cardiac sympathetic neurotransmission by interacting with histamine H3-receptors and the receptors are probably coupled to a G(o)/Gi protein.

1. In normal control mice (only injected SRBC) after EA the lymphocyte transformation test (LTT, P < 0.05) and interlukin-2 (IL-2) activity (P < 0.05) were significantly increased, but the serum lysozyme (IZM, P < 0.01) was apparantly decreased. 2. After injection of 6-OHDA in mice, the spleen weight, spleen index, thymus weight, thymusindex, spleen lymphocyte population and serum IZM, igG contents were markedly decreased, whereas LTT, IL-2 and plaque forming cell (PFC) were umchanged, In contrast, the thymus lymphocyte population was markedly increased. 3. After EA of mice axotomized sympathetic nerve with 6-OHDA the above mentioned immune parameters deceased by 6-OHDA could be returned to normal or nearing normal levels. However, the unchanged LTT, IL-2 and the increased thymus lymphocyte population could be enhanced further, especially IL-2. These results suggest that peripheral sympathetic nerve may be participation in the EA-mediating immunological responses.

In urethane-anesthetized, tubocurarine-immobilized and artificially ventilated rats, microinjection of L-glutamate (Glu) into the insular cortex (INS) caused a rise in blood pressure and heart rate. Bilateral injection of either phentolamine, propranolol or atropine into the rostral ventrolateral medulla (RVL) all could decrease the INS-pressor response. The latter could also be attenuated by phentolamine (i.v.), but not by propranolol or methyl atropine. These results indicate that the INS-pressor response is mediated by RVL (alpha-, beta- and M-receptors) -sympathetic vasoconstrictor nerve system.

In anesthetized and bilateral sinoaortic denervated rabbits with either intact or ascorbic acid injected paraventricular nucleus (PVN), the inhibition of renal sympathetic nerve activity (RSNA) induced by blood volume expansion (VE) all decreased by approximately 48%. However, 3-4 h and 3-4 d after kainic acid lesion of PVN, the inhibition of RSNA was attenuated respectively to -28.0 +/- 4.5% and -25.7 +/- 4.1% (P < 0.05) with considerably shortened time course (P < 0.01). Also such inhibition could be significantly attenuated (P < 0.05) by intrathecal injection of vasop ressinergic V1 receptor antagonist in spinal T10-T12 segments. There was no significant difference with the slight and brief increase of mean arterial pressure induced by VE in the control and the experimental group. Thus it can be concluded that the inhibition of RSNA induced by VE is partly mediated by a vagal afferent triggered PVN-spinal pathway.

This paper reported our observation of the action of acupuncture on the change of gastric function induced by the excitation of the lateral hypothalamus area (LHA, the feeding center), and research on the mechanism of the acupuncture to inhibiting excessive appetite and reducing hunger in obese people. Electroacupuncture at Zusanli (ST 36) or Neiting (ST 44) could inhibit the hyperactivity of the stomach induced by stimulation of LHA (P < 0.05, P < 0.01). The electroacupuncture effect on LHA remained statistically significant (P < 0.05, P < 0.01) 0.5-2.5 hours after acupuncturing. The alpha-receptor blocking agent phentolamine (1mg/kg) was not distinctly affected (P > 0.05) on the inhibition of electroacupuncturing Zusanli (ST 36) to restrain the hyperactivity of the stomach induced by stimulation on LHA; But beta-receptor blocking agent propranolol (0.3mg/kg) could obviously inhibit the effect of electroacupuncturing Zusanli (ST 36) to restrain hyperactivity of stomach triggered by excitation of the LHA. The result shows that electroacupuncture obviously inhibits gastric hyperfunction caused by excitation of the LHA, for as long as over 3 hours, thus indicating the participation of the humoral factors. Since the electroacupuncture at Zusanli (ST 36) only inhibits gastric hyperfunction caused by excitation of the LHA, it is suggested that the electroacupuncture has an anticholinergic effect through the gastric beta receptor, therefore it inhibits the appetite, relieves hunger and reduces body weight in obese people.

Experiment were performed on 40 urethane anesthetized Wistar rats. After preinjection of 6-hydroxydopamine (6-OHDA) into subarachnoid cavity at inferior thoracic part. Enhancement of renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) induced by electrical stimulation of pressor area of ventral surface of medulla (VSMp) were attenuated; but intrathecal phenylephrine had no effects. The results suggest that the alpha 1-adrenoceptors mediating descending excitatory effects of VSMp are located postsynaptically on the sympathetic preganglionic neurons.

In order to elucidate the relationship between several structures of CNS and the vestibulo-sympathetic response (VSR) in rat, the technique of spike triggering average (STA) was used. The spike of the neuron which responded to the pendular rotation (pendular positive unit, PPU) was used to trigger the onset of averaged activities of the splanchnic nerve (SN). Making use of the spike of PPU of nucleus vestibularis medialis (NVM) as an indicator, the SN-STA had a latency of 33.28 +/- 3.1 ms. SN-STA triggered by PPU of reticular formation (RF) of caudal brain stem, a positive response with a latency of 11.13 +/- 0.91 ms was observed. SN-STA triggered by PPU of vestibulocerebellum, a positive response with a latency of 21.86 +/- 1.73 ms was observed. Our results suggest that the nearest supraspinal relay may be the nuclei of medical RF in caudal brain stem and the descending flow of VSR was probably transmitted by the slow conducted fibers of reticulo-spinal tract. According to the latency of SN-STA by PPU of vestibulo-cerebellum, the vestibulcerebellum possibly executed a polysynaptic mission between the transmission of VSR outflow from NVM to RF nuclei of caudal brain stem.

Electrical stimulation of the pressor area of the ventral surface of medulla oblongata (VSMp) of rat elicited an enhancement of renal sympathetic nerve activities (RSNA) and an increase of MAP, pressure of kidney (PPK), which depended on the integrity of renal sympathetic nerve (RSN). The effect of VSMp on PPK could be blocked by alpha 2-adrenoceptor antagonist yohimbine, but not by alpha 1-adrenoceptor antagonist prazosine when VSMp was stimulated. alpha 2-adrenoceptor agonist clonidine perfused renal vessels induced PPK increase similar to that due to stimulation of VSMp. The results indicate that the effect of VSMp on PPK are mediated by RSN of alpha 2 type sympathetic transmitter in the tonic control renal vascularture.

68 urethan-anesthetized rabbits were prepared for registration of changes of respiration, arterial blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) due to stimulation of area postrema (AP) by rectangular pulse trains each lasting for 4 s for every 30 s. During 40 min of such a stimulation paradigm the venous blood samples were collected for radioimmunoassay of plasma renin activity (PRA) (both pre- and post-stimulation), RSNA registered and processed by a computer. Animals were divided into three groups: (1) with AP stimulation only (n = 47); (2) AP stimulation after bilateral renal denervation (n = 13); (3) AP stimulation after propranolol injection (n = 8). In Group I, a 91% increase in PRA, an augmentation of RSNA, a rise of BP and a decrease of HR were observed, while respiration did not show obvious change. In Group II, hemodynamic and RSNA response was similar to that in Group I, but PRA was not changed significantly. In Group III, the effects on BP, HR, respiration and RSNA showed no remarkable changes compared with Group I, but significant inhibition of the response of PRA [from 0.65 +/- 0.07 ng/(ml.h-1) to 0.72 +/- 0.10 ng/(ml.h-1), P > 0.05] was observed. The results mentioned above suggested that electrical stimulation of AP may induce an increase in renin release and renal sympathetic nerve activity and hemodynamic changes in rabbits.

The effects of four various Qigong breathing pattern on variability of heart rate have been observed by R-R interval spectral analysis in 26 healthy volunteers. The differences in the shape of peaks in spectra were found to be correlated with the Qigong breathing pattern. The amplitude of peak in high-frequency area increased with a reduction of the low-frequency 2/high-frequency (LF2/HF) ratio during the Qigong breathing pattern A, B, and C, indicating the vagal activity increased during above-mentioned three Qigong breathing pattern. However, the amplitude of peak decreased and LF2/HF ratio increased during the Qigong breathing pattern D, it reflected the increase of sympathetic activities. Thus, the results suggested that the Qigong could indirectly regulate the function of viscera after controlling the direct breathing pattern.

In the present study, co-release of noradrenaline and neuropeptide y (NPY) evoked by electrical stimulation of the left stellate ganglion, was investigated in the in situ perfused guinea pig heart with intact sympathetic innervation, a model modified from Legendorff technique. Endogenous noradrenaline was measured by HPLC and endogenous NPY was determined by RIA. Electrical stimulation of the left stellate ganglion (4, 8, 12 and 50 Hz) evoked a calcium-dependent and frequency-related overflow of noradrenaline and NPY. The release of both transmitters was positively correlated (r = 0.83, p less than 0.001). When two subsequent stimulations were performed in the same heart, adding exogenous noradrenaline before the second stimulation reduced NPY overflow on the contrary, and NPY decreased the overflow of noradrenaline. The stimulated release of noradrenaline and NPY was increased by the alpha 2-adrenergic receptor antagonist yohimbine, and attenuated by the alpha 2-adrenergic receptor agonist B-HT 920, respectively. The adenosine analogue cyclohexyladenosine significantly reduced co-release of noradrenaline and NPY. Blocking the uptake of NA with despramine or Nisoxetine significantly increased noradrenaline overflow, however, NPY release was markedly reduced. We concluded that electrical stimulation can induce calcium-dependent co-release of noradrenaline and NPY, and this co-release of both transmitters is modulated by presynaptic alpha 2-adrenoceptors.

Experiments were performed on 40 urethane-anesthetized rabbits. The aortic nerves, carotid sinus nerves and vagus nerves were cut, mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were recorded. The conditional stimulation (0.02 ms, 50 Hz, 4-6 V, 5 min) of central cut end of aortic nerve was used to evoke the afferent A-fibers and to mimic the response of low threshold baroreflex to holding pressure, so as to induce the central process of acute resetting. It was observed that after conditional stimulation ceased 1 min, the MAP and RSNA for response to stimulation of myelinated aortic afferent was attenuated at 41.8 +/- 7.6% (P less than 0.01, n = 11) and 19.31 +/- 2.6% (P less than 0.05, n = 11), but both MAP and RSNA were not significantly changed for non-myelinated fibers. The result suggests that the characteristics of central resetting were dependent on the component of baroreflex afferent fibers. The central resetting of low threshold myelinated afferent activities was attenuated only on the baroreflex produced by myelinated afferent fibers.

Experiments were performed on rats anesthetized with alpha-chloralose and urethane. The sympathetic response evoked by stimulation of the vestibular nerve root at its entrance to brain-stem was recorded from the ipsi-splanchnic nerve. Electrical stimulation of the vestibular nerve elecited a distinct averaged response in the ipsilateral splanchnic nerve. The mean latency of response was 45.8 +/- 6.98 ms with a duration of 55.21 +/- 5.35 ms. With increasing the strength of stimulation, the amplitude of response was increased, but the latency was unchanged. By monitoring the lamellar field potentials in NVM and choosing the locus of phase-reversal of field potential as the stimulating site, an averaged response in ipsi-splanchnic nerve with a latency of 32 ms was obtained, while the recorded splanchnic nerve response had a latency of 43 ms, when the vestibular nerve was stimulated. After electrolytic lesion of the rostral part of ipsi-NVM, the vestibulo-sympathetic response was significantly reduced. When a second lesion was placed in the caudal NVM, the response disappeared. Lesion in Deiters' nucleus had no effect on the vestibulo-sympathetic response. The results suggest that NVM is a critical relay station in vestibulo-sympathetic response recorded in the splanchnic nerve.

Changes of mean arterial pressure (MAP), heart rate (HR), respiration and renal sympathetic nerve activity (RSNA) induced by close-arterial administration of adenosine to carotid body (CB) were observed in 33 anesthetized rabbits. The results were as follows: (1) In response to intracarotid injections of adenosine, MAP decreased in a dose-dependent manner, while the frequency of respiration increases with little change in depth. Following carotid sinus denervation, intracarotid injection of adenosine still resulted in a decrease of MAP but with no changes in respiration. (2) By adding adenosine to perfusate of the isolated carotid sinus, both MAP and HR decreased, but these effects could be abolished by inactivation of carotid body. (3) MAP decreased and RSNA enhanced during perfusing adenosine into carotid sinus. These effects could be abolished by the section of sinus nerve or inactivation of CB. From the results obtained, it is considered that adenosine is capable of activating CB, decreasing MAP and heart rate but with a concomitant increases in respiration and RSNA.

Experiments were performed on 64 cats anesthetized with chloralose-urethane, paralyzed and artificially ventilated. Electrical stimulation of locus coeruleus (LC) elicited increases in BP, HR, LVSP, dP/dt max and RNA. Buffer nerve section had no effect on the increase of these parameters, but could prolong the time of rise of BP and recovery phases. Injection of L-glutamate into LC, on the other hand, could decrease BP, HR, LVSP and dP/dt max. Intra-LC injection of kainic acid could also decrease BP. When the LC neurons showed degeneration or depolarization block after kainic acid injection, electrical stimulation of the LC could still elicit marked pressor response. The results suggest that the pressor response induced by electrical stimulation of LC might be mediated by the fibers passing through LC, while activation of LC neurons themselves would result in the depressor response.

The effects of atriopeptin III (AP III) on the arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in anesthetized rats. The results were as follows: (1) In intact rats (n = 12), following intravenous injection of AP III (50 micrograms/kg), systolic arterial pressure (SAP) decreased by 23.0 +/- 1.66 mmHg (M +/- SE, P less than 0.001), HR decreased by 9 +/- 3.5 beats/min (P less than 0.05), and RSNA decreased by 4.89 +/- 2.95% (P greater than 0.05). After vagotomy, the decrease in SAP following iv. AP III showed no significant difference with that of intact rats. HR showed no change, while there was a small increase in RSNA (P greater than 0.05); (2) In the intact vagi but sinoaortic denervated rats (n = 7), intravenous AP III decreased SAP by 27.4 +/- 3.25 mmHg (P less than 0.001), HR by 13 +/- 3.1 beats/min (P less than 0.01), and RSNA by 11.67 +/- 1.95% (P less than 0.001). After vagotomy, the decrease in SAP following i.v. AP III was attenuated, HR showed no significant change, but there was a small but significant increase in RSNA (P less than 0.05); (3) Following intravenous injection of nitroprusside, SAP decreased significantly. Such a hypotensive effect was associated with an increase in RSNA in either the intact or the vagotomized rats. The results indicate that (1) the hypotensive effect of AP III was mediated partly by vagi; (2) in the sinoaortic denervated rats AP III could reflexly inhibit RSNA by activation of vagal afferent fibers.

Experiments were carried out on 47 urethane-chloralose anesthetized and flaxedil immobilized rabbits under artificial respiration. Intracerebroventricular injection (ICV) of neostigmine (100 micrograms/200 microliters) caused a marked increase in blood pressure (BP), left ventricular pressure (LVP) and renal sympathetic nerve discharge (RND), while femoral blood flow (FBF) and conductance (COND), were decreased and the heart rate (HR) was initially reduced and then slightly increased. Microinjection of atropine (0.25 micrograms/site) into the rostral ventrolateral medulla (rVLM) caused a decrease in BP, HR, RND and LVP and a increase in FBF and COND. Pretreatment of atropine injection into rVLM before ICV of neostigmine blocked the pressor response of neostigmine. These results indicate that rVLM is important for the pressor response to ICV neostigmine, which may be mediated via cholinergic muscarinic receptors in rVLM.

The electrical stimulation of the habenula (4 V, 100 Hz, 9 s) raised the arterial blood pressure (P less than 0.01) and quickened the heart rate of rats (P less than 0.05). Also, splanchnic nerve discharges were increased (P less than 0.01), the pupils dilated and the ear arteries constricted. The pressor effect was obviously weakened by phentolamine iv (P less than 0.01) and strengthened by bilateral vagotomy (P less than 0.05). The pressor effect disappeared after spinal cord transected at C1. Morphine iv elevated pain threshold (P less than 0.01) and eliminated the pain threshold change caused by exciting habenula. The pressor response of habenula was not influenced by elevating the pain threshold. The results suggest that the pressor effect of habenula occurs via the sympathetic vasoconstrictor fibers, vagus nerve exerts inhibition on the effect and the pressor effect of habenula is not a pain response caused by exciting habenula itself.

Experiments were performed on rabbits anesthetized with chloralose-urethane mixture, paralyzed with gallamine triethiodide, and ventilated artificially. Bilateral vagi, aortic and carotid sinus nerves were severed. Renal sympathetic efferent discharge (RSED) and its histogram were recorded, while the blood pressure (BP) of the femoral artery was monitored. When PVH was strongly stimulated, a transient increase of RSED was observed, which was followed by an inhibition of RSED. The inhibition of RSED was divided into two phases: the initial inhibitory phase without change in BP and the late inhibitory phase with an increase of BP. It was found that both the duration of total inhibition and the late, but not initial, inhibitory phase were positively correlated with the alterations of BP. When PVH was weakly stimulated, no change in BP was observed, but the inhibition of RSED still appeared. The inhibition duration was shortened remarkably following cutting of baroreceptor nerves. In some experiments, the RSED inhibition was not accompanied by a definite excitatory response. The present results indicate that 1) an inhibitory mechanism of PVH-renal sympathetic efferent system is present in the central nervous system; 2) the initial inhibitory phase of RSED originates from central mechanisms, while the late inhibitory phase is associated with the baroreceptor reflex and a direct action of the central nervous system; 3) the inhibition of RSED seems not to be a post-excitation depression, but an active inhibition exerted by the PVH on the spinal sympathetic preganglionic neurons.