[Modulatory effects of capsaicin-sensitive nerve fiber on cardiovascular activity].
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Animals↗
Biomedical subjects
R R He
Publications and source records attributed to R R He.
[Inhibitory effects of nitric oxide on glutamate-induced neuronal activity of CA1 area in rat hippocampal slices].
Using extracellular recording technique, the effects of L-arginine (L-arg), SIN-1 and N-nitro-L-arginine (L-NNA) on glutamate-induced discharge of neurons in CA1 area of hippocampal slices were examined to define the role of L-arg:NO pathway in glutamate-induced discharge of hippocampal neurons and its possible underlying mechanism. The results obtained are as follows. (1) In response to the application of glutamate (0.5 mmol/L) into the superfusate for 1 min, the discharge rate of 12 neurons was increased markedly in an epileptiform pattern. (2) The increased discharge induced by glutamate (0.5 mmol/L) in 10 neurons was suppressed significantly by application of L-arg (10 mmol/L) into the superfusate for 2 min. (3) The glutamate-induced increase of discharge in 12 neurons was decreased markedly by superfusing the brain slice with NO donor SIN-1 (5 mmol/L) for 1 min. (4) As the discharge rate of 12 neurons was increased by pretreatment with glutamate (0.5 mmol/L), application of L-NNA (0.15 mmol/L) into superfusate for 2 min might further augment the discharge intensively and in some case eventually led to abrupt suppression of the discharge. Taken together, it is likely that glutamate binding with NMDA receptors in hippocampal neurons not only induces an increase in discharge, but also activates the L-arg: NO pathway to generate NO responsible for neuroprotection via negative feedback mechanisms.
Action Potentials↗
[Modulatory effects of endothelin on carotid baroreflex in anesthetized rats].
Modulatory effects of endothelin (ET) on carotid baroreflex were examined in 27 anesthetized rats with isolated carotid sinus perfusion. The results obtained were as follows: (1) By perfusing with 1 nmol/L ET-1, the functional curve of carotid baroreflex (FCCB) was shifted to the left and downward with an increase in its peak slope (PS) from 0.40 +/- 0.02 to 0.51 +/- 0.02 kPa/kPa (P < 0.01), while the reflex decrease of mean arterial pressure (RD) was increased from 5.66 +/- 0.23 to 6.76 +/- 0.22 kPa (P < 0.01). The above results indicated that this dose of ET-1 facilitated the carotid baroreflex. (2) On the contrary, by perfusing with 10 nmol/L of ET-1, FCCB was shifted to the right and upward with a decrease of PS to 0.28 +/- 0.01 kPa/kPa (P < 0.01), while RD was decreased to 4.16 +/- 0.19 kPa (P < 0.01). In response to perfusion with 100 nmol/L ET-1, FCCB was further shifted to the right and upward with a marked decrease of PS to 0.19 +/- 0.03 kPa/kPa (P < 0.001), and RD was conspicuously decreased to 3.33 +/- 0.38 kPa (P < 0.001). These results showed that ET-1 at the doses of 10 or 100 nmol/L exerted an inhibitory action on baroreflex. (3) Selective ETA receptor blocker BQ123 (0.15 mumol/L) might abolish the effects of ET-1 (10 nmol/L) on baroreflex. (4) Preperfusing with KATP channel antagonist glibenclamide (10 mumol/L) could also eliminated the effects of ET-1. Taken together, it is suggested that ET-1 exerts a dual effects on baroreflex, being facilitatory at lower dose and inhibitory at higher dose. The latter effect is mediated by ETA receptor, in which KATP channels may be involved.
Animals↗
[Adenosine facilitates carotid baroreflex in rats].
The effects of adenosine (Ado) on the carotid baroreflex were studied in 27 anesthetized rats with isolated carotid sinus perfusion. The results obtained were as follows: (1) By perfusing the isolated carotid sinus with adenosine (125 mumol/L), the functional curve of baroreflex was shifted to the left and downward, with the peak slope (PS) increased from 0.37 +/- 0.02 to 0.55 +/- 0.02 kPa/kPa (P < 0.001) and the reflex decrease in mean arterial pressure (RD) enhanced from 5.53 +/- 0.12 to 7.76 +/- 0.36 kPa (P < 0.001). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly decreased from 8.60 +/- 0.27 to 5.63 +/- 0.11 kPa (P < 0.001), 12.53 +/- 0.30 to 10.89 +/- 0.29 kPa (P < 0.01) and 23.69 +/- 0.15 to 20.18 +/- 0.55 kPa (P < 0.001), respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS and TP induced by Ado were dose-dependent. (2) By pretreatment with (8-cyclopentyl-1, 3-dipropylxanthine, 0.134 mmol/L), a selective adenosine A1-receptor antagonist, the above effects of Ado on carotid baroreflex were abolished. (3) The Ado-induced changes of baroreflex were also eliminated as the carotid sinus was pretreated with KATP channel blocker glibenclamide (10 mumol/L). The results strongly suggest that the carotid baroreflex could be facilitated by Ado. It is proposed that the facilitatory action of Ado on carotid baroreflex may be resulted from the opening of KATP channels mediated by Ado A1-receptors.
Adenosine↗
Effect of intracarotid injection of adenosine on the activity of RVLM neurons in barodenervated rats.
To observe the effect of intracarotid administration of adenosine on neurons in the rostral ventrolateral medulla (RVLM) region, 72 spontaneous active units were extracellularly recorded from 28 Sprague-Dawley rats with sino-aortic denervation. The results obtained are as follows: (1) intracarotid administration of Ado (25 micrograms/kg) reduced the discharge rate from (23.5 +/- 3.0) to (16.5 +/- 2.6) spikes/s (P < 0.001) in 31 out of 36 RVLM neurons, while the blood pressure and heart rate had no significant change (P > 0.05); (2) 8-phenyltheophylline (8-PT, 15 micrograms/kg), a nonselective adenosine receptor antagonist, and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 50 micrograms/kg), a selective A1 adenosine receptor antagonist, completely blocked the inhibitory effects of Ado in 24 units; and (3) in 12 units, glibenclamide (500 micrograms/kg), a blocker of ATP-sensitive potassium channel, abolished the effect of Ado. These results indicate that Ado can induce an inhibition of spontaneous electrical activity of RVLM neurons, an effect which is mediated by adenosine A1-receptor with the involvement of ATP-sensitive potassium channels.
Adenosine↗
[Adenosine facilitates carotid baroreceptor activity in rats].
The effects of adenosine (Ado) on the carotid baroreceptor were studied in 36 anesthetized rats with isolated carotid sinus perfusion by recording the sinus nerve afferent activity. The results obtained were as follows: (1) By perfusing the isolated carotid sinus with 75 mumol/L Ado, the functional curve for intrasinus pressure(ISP)-integral of sinus nerve activity (ISNA) relation was shifted to the left and upward with peak slope (PS) increased from (18.75 +/- 0.12)%/kPa to (22.21 +/- 0.11)%/kPa (P < 0.001) and the peak integral value (PIV) enhanced from (209.83 +/- 2.57)% to (239.17 +/- 1.75)% (P < 0.001), while the threshold pressure (TP) and saturation pressure (SP) were significantly decreased from 8.57 +/- 0.24 to 7.15 +/- 0.23 kPa (P < 0.001) and from 22.99 +/- 0.34 to 21.21 +/- 0.43 kPa (P < 0.01). By perfusing with high concentrations of Ado (125 and 175 mumol/L), the curves for ISP-ISNA relation were shifted to the left and upward further and the changes of the functional parameters such as PS, TP and SP were dose-dependent. (2) By pretreatment with 8-cyclopentyl-1,3-dipropylxanthine (0.134 mmol/L), a selective adenosine A1-receptor antagonist, the above mentioned effects of Ado on carotid baroreceptor activity were abolished. (3) The Ado-induced increase in sinus nerve afferent activity could be eliminated by pretreatment with KATP channel blocker glibenclamide (10 mumol/L). The above results suggest that Ado exerts a facilitatory action on the isolated carotid baroreceptor and such an action of Ado may be attributed to the opening of KATP channels, which is mediated by A1-receptors.
Adenosine↗
[Effects of endothelin on carotid baroreceptor activity in anesthetized rats].
The effects of endothelin (ET-1) on carotid baroreceptor activity were examined in 33 anesthetized rats with perfused isolated carotid sinus by recording sinus nerve afferent discharge. The results obtained were as follows: (1) By perfusing with 1 nmol/L ET-1, the functional curve of carotid baroreceptor (FCCB) was shifted to the left and upward with increase of peak slope (PS), while the peak integral value of carotid sinus nerve discharge (PIV) was increased, indicating that the carotid baroreceptor activity was facilitated. (2) On the contrary, by perfusing with 10 nmol/L ET-1, FCCB was shifted to the right and downward with a decrease of PS and PIV. In response to perfusion with 100 nmol/L ET-1, FCCB was further shifted to the right and downward with a marked decrease of PS and PIV. These results showed that ET-1 at 10 or 100 nmol/L exerted an inhibitory action on the baroreceptor activity. (3) Selective ETA receptor blocker-BQ-123 (0.15 mumol/L) could abolish the inhibitory effects of ET-1 (10 nmol/L) on baroreceptor. (4) Preperfusing with KATP channel antagonist-glibenclamide (10 mumol/L) could also eliminated the effects of ET-1. All the above results suggested that ET-1 exerts the dual effects on baroreceptor, facilitation at low doses and inhibition at high doses. The later effect may be mediated by ETA through KATP channels.
Animals↗
[Research progresses on agmatine].
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Agmatine↗
Effects of moxonidine injected into rostral ventrolateral medulla on blood pressure, heart rate, and renal sympathetic nerve activity in rats.
AIM: To examine the effects of moxonidine (Mox) injected into the rostral ventrolateral medulla (RVLM) on blood pressure (BP), heart rate (HR), and the renal sympathetic nerve activity (RSNA) in anesthetized normotensive rats. METHODS: BP, HR, and RSNA were simultaneously recorded after 1 microL Mox 1, 10, and 100 mumol.L-1 was injected into RVLM. RESULTS: Mox 1, 10, and 100 mumol.L-1 reduced BP from 13.9 +/- 1.0 kPa to 13.0 +/- 1.7 kPa (P < 0.05), 13.8 +/- 1.8 kPa to 11.4 +/- 1.5 kPa (P < 0.01), and 13.9 +/- 1.9 kPa to 9.4 +/- 1.7 kPa (P < 0.01), respectively. Mox did not influence HR. RSNA varied with the doses: Mox 1 mumol.L-1 increased RSNA by 50% (P < 0.05), 10 mumol.L-1 insignificantly influenced RSNA (P > 0.05), and 100 mumol.L-1 reduced RSNA by 23% (P < 0.05). In sinoaortic barodenervated rats, Mox 10 mumol.L-1 inhibited RSNA by 50% (P < 0.05), which substantially differed from that in buffer nerve intact rats (P < 0.01). CONCLUSION: Mox injected into RVLM decreased BP, but did not influence HR. The changes of RSNA did not parallel with the depressor effect of Mox.
Animals↗
[Effects of intraventricular injection of adenosine on renal sympathetic nerve activity].
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.
Adenosine↗
[Role of KATP channels in the cardioprotection provided by ischemic preconditioning in anesthetized rabbits].
The effects of KATP channel opener cromaklim (Cro) and ischemic preconditioning (IP) on hemodynamics and myocardial infarct size were examined in both urethane and sodium pentobarbital anesthetized rabbit models of myocardial ischemia-reperfusion to determine whether the KATP channel was involved in the cardioprotection provided by IP. The results were as follows: (1) All hemodynamic parameters and myocardial oxygen consumption were decreased progressively during the course of ischemia (30 min)-reperfusion (180 min). (2) In the urethane anesthetized model, the myocardial infarct size of the left ventricle induced by ischemia-reperfusion was (32.3 +/- 0.8)%. Pretreatment with Cro reduced the myocardial infarct size to (23.3 +/- 2.2)%, while IP significantly reduced the infarct size to (21.6 +/- 1.8)%, which was abolished by a potent KATP channel blocker glibenclamide. (3) In the sodium pentobarbital anesthetized model, myocardial infarct size was (32.7 +/- 1.0)%. IP also reduced the myocardial infarct size to (19.7 +/- 1.5)%, which could not be blocked by cardioprotection of IP by glibenclamide. Cro failed to decrease infarct size. Such results indicated that activation of KATP channels exerted a beneficial action on ischemia-reperfused myocardium only in the urethane anesthetized rabbit.
Adenosine Triphosphate↗
[Effects of endothelin on electrophysiological and contractile activity of guinea pig papillary muscles].
Effects of endothelin on electrophysiological activity and contractility were examined in guinea pig papillary muscle using intracellular microelectrode and contractile tension recording technique. The results indicated that ET-1 prolonged APD, especially PPD and increased the contractile tension in a dose-dependent manner. The ET-induced effects were not influenced by K+ channel blocker TEA, but inhibited by L-type Ca2+ channel blocker nifedipine, ETA receptor selective antagonist BQ-123 and atriopeptin III in a concentration-dependent manner. It is suggested that the changes in electrophysiological activity and the positive inotropic effect induced by ET-1 in guinea pig muscles are due to the elevation of intracellular calcium, which may be mediated by ETA receptor.
Animals↗
[Effects of no precursor and donor on neuronal activity of rat hippocampal slices].
Using extracellular recording technique, the effects of L-arginine (L-arg), N-nitro-L-arginine (L-NNA), SIN-1 and methylene blue (MB) on spontaneous discharges of neurons in CA1 area of hippocampal slices were examined to determine the role of L-arg: NO pathway and the possible underlying mechanism. The results were as follows: (1) In response to the application of L-arg (1 mmol/L) into the superfusate for 2 min, spontaneous discharge rate (SDR) of 42/54 (77.8%) neurons was decreased significantly, while that of 12/54 (22.2%) neurons showed no change. Following the application of L-NNA (0.15 mmol/L) into the superfusate for 2 min, SDR of 25/29 (86.2%) neurons was increased markedly and that of 4/29 (13.8%) neurons was not affected. The effect of L-NNA might be reversed by pretreatment with L-arg. (2) With application of NO donor SIN-1 (5 mmol/L), SDR of 25 (100%) neurons was decreased in a dose-dependent manner. (3) After superfusing the brain slice with guanylate cyclase inhibitor, MB (3 mumol/L) for 30 min, SDR of 10 units showed significant increase as compared with control. However, MB failed to abolish the effect of L-arg on hippocampal neurons. Taken together, it is likely that NO is released during the resting state of hippocampal neurons and may inhibit the activity of hippocampus, an effect not mediated by the action of guanylate cyclase.
Action Potentials↗
[Expression of c-fos in spinal cord, medulla oblongata and thalamus following epicardial application of adenosine].
Effects of epicardial application of adenosine on the expression of c-fos proto-oncogene in spinal cord, medulla oblongata and thalamus were examined in 12 sinoaortic denervated and vagotomized anesthetized rats. The results showed that following epicardial application of adenosine the Fos-like protein immunoreactive (FLI) neurons were remarkably increased in the dorsal horn of T3 spinal segment, nucleus paragigantocellularis lateralis (PGL) of medulla oblongata, ventral postero-lateral thalamic nucleus (VPL), posterior thalamic nucleus (Po), parafascicular thalamic nucleus (PF) and centrolateral thalamic nucleus (CL), while the blood pressure and heart rate were not affected. Only a few FLI neurons were found in the vehicle-control rats. The results indicate that epicardial application of adenosine may activate the pain-related neurons in spinal cord, medulla oblongata and thalamus.
Adenosine↗
[Effects of intraventricular and epicardial application of adenosine on electrical activity of medullary PGL neurons].
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.
Action Potentials↗
Effects of dipfluzine on cortical somatosensory evoked potentials and amino acid contents in ischemic rat brain.
AIM: To evaluate the effects of dipfluzine ¿1-diphenyl-methyl-4-[3-(4-fluorobenzoyl)]-piperazine, Dip¿ on the intra- and extra-cellular contents of the amino acids in brain and the cortical somatosensory evoked potentials (SEP) in rats with cerebral ischemia. METHODS: Amino acids in micro-dialysates and brain tissue homogenates in female Wistar rats with bilateral carotid artery ligation (BCAL) were measured by HPLC and SEP was measured by the electrophysiological technique. RESULTS: Dip 50 mg.kg-1 i.p. prevented SEP from prolonging of the latency and overactivity of lowered amplitude, markedly lowered the elevation in extracellular level of glutamate (Glu), aspartate (Asp), and glycine (Gly) in intracerebral microdialysates, and alleviated the decrement of intracellular contents of Glu, Asp, Gly, taurine (Tau), and GABA in brain tissue. CONCLUSION: Dip reduced the disturbance of cortical function and the imbalance between excitatory and inhibitory amino acids in ischemic brain, therefore provided a further evidence for its protective effect on ischemic cerebral damage.
Animals↗
[Endothelin and ATP-sensitive potassium channel mediate electrophysiological changes induced by hypoxia in rabbit sinoatrial node].
The role of ET and KATP channel in hypoxia-induced negative chronotropic effect of pacemaker cells in rabbit sinoatrial node was studied with intracellular microelectrode technique. The results obtained were as follows: (1) Hypoxia produced a progressive decrease in the velocity of diastolic depolarization (VDD) of pacemaker cells resulting in a reduced rate of pacemaker firing (RPF), and induced a decrease in APD, especially APD50. (2) KATP channel opener cromakalim markedly induced a negative chronotropic effect in a concentration-dependent manner and significantly shortened APD50. KATP channel blocker glibenclamide alleviated the effects of hypoxia on pacemaker cells, thereby suggesting the involvement of KATP channel in the hypoxia-induced effects. (3) By superfusion of ET-1, the hypoxia-induced decrease in RPF was remarkably potentiated and the occurrence of pacemaker arrest was shifted to an earlier time. The hypoxia-induced effects could be effectively attenuated after pretreatment with BQ-123, implying the role of endogenous ET-1 release in hypoxia-induced effects. It is concluded that the negative chronotropic effect and the decrease in APD induced by hypoxia may be attributed to the activation of KATP channel and the release of endogenous ET.
Adenosine Triphosphate↗
[Effects of L-NNA and NO donors on spontaneous activity of rostral ventrolateral medulla neurons].
The effects of intravenous injection of a NO synthase inhibitor--N-nitro-L-arginine (L-NNA) and NO donors--sodium nitroprusside (SNP) and SIN-1 on blood pressure (BP), heart rate (HR) and spontaneous activity of rostral ventrolateral medulla (RVLM) neurons were examined in 22 anesthetized rats to define the action site of L-arginine: NO pathway in BP regulation. The results obtained were as follows. (1) Following i.v. injection of L-NNA, mean artery pressure (MAP), HR and spontaneous discharge rate of 14 RVLM neurons were all increased, all effects starting at 5 min after administration of L-NNA and lasting for more than 30 min. (2) In response to i.v. injection of SNP, MAP was decreased with concomitant increase in HR and the discharge rate of 23 RVLM neurons decreased in a dose-dependent manner. These effects were rapid in onset and also disappeared promptly. To exclude the effect of cerebral ischemia induced by decreased of BP, the effects of intracarotid injection of SNP were examined. Following i.a. injection, MAP was only slightly decreased and HR showed no significant change, but the discharge rate of 14 RVLM neurons was significantly decreased. (3) During i.v. injection of another NO donor--SIN-I, MAP and the spontaneous discharge rate of 11 RVLM neurons were decreased. The above results indicate that the L-arginine: NO pathway may exert a modulatory action on the blood pressure through rostral ventrolateral medulla.
Animals↗