PubMed Health⌕ Search

Biomedical subjects

R R He

Publications and source records attributed to R R He.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Adenosine inhibits spontaneous and glutamate induced discharges of hippocampal CA1 neurons].

Effects of adenosine (Ado) on spontaneous and glutamate induced discharges of neurons in CA1 area of hippocampal slices were examined using extracelluar recording technique. The results are as follows. (1) In response to the application of Ado (0.01 0.1 micromol/L, n=20) into the superfusate, spontaneous discharge rates (SDR) of 20 neurons decreased significantly in a dose dependent manner. (2) Both Ado non selective receptor antagonist 8 phenyltheophylline (8-PT, 0.5 mmol/L) and Ado selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 50 nmol/L), completely blocked the inhibitory effects of Ado in 22 CA1 units. (3) In 10 units, ATP sensitive K(+) channel blocker glibenclamide (Gli, 15 mmol/L) also abolished the effect of Ado. (4) Application of glutamate (Glu, 0.2 mmol/L) into the superfusate for 2 min led to a marked increase in the discharge rate of 15 neurons in an epileptiform pattern; the epileptiform discharges induced by glutamate (Glu, 0.2 mmol/L) in 15 neurons were suppressed significantly by application of Ado (10 micromol/L) into the superfusate. (5) 8-PT (2 mmol/L), DPCPX (200 nmol/L) and Gli (7 mmol/L) were all capable of abolishing the inhibiting effect of Ado on the action of glutamate. Taken together, it is suggested that Ado can bind with adenosine A1-receptors on CA1 neurons, resulting in an activation of K(ATP) channels and inhibition of neuronal activity. The inhibitory effect of Ado on glutamate induced epileptiform activities in rat hippocampal neurons is also mediated by adenosine A1-receptor with involvement of ATP-sensitive potassium channels.

Adenosine↗
PubMed2000

Effects of microinjection of adenosine into area postrema on heart rate, blood pressure and renal sympathetic nerve activity in rats.

The effects of microinjection of adenosine (Ado) into area postrema (AP) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were examined in 53 anesthetized Sprague Dawley rats. The results obtained are as follows. (1) Following microinjection of Ado (1 ng/60 nl) into AP, MAP, HR and RSNA were decreased from 13.76+/-0.46 kPa, 356.28+/-4.25 bpm and 100+/-0% to 11.23+/-0.49 kPa (P<0.001), 336.91+/-5.23 bpm (P<0.01) and 70.95+/-5.19% (P<0.001), respectively; (2) 8-phenyltheophylline (150 microgram/kg, 0.2 ml,iv), a nonselective adenosine receptor antagonist, and 8-cyclopentyl-1,3-dipropylxanthine (500 microgram/kg, 0.2 ml, iv), a selective A(1) adenosine receptor antagonist, blocked the inhibitory effect of Ado completely; and (3) glibenclamide (5 mg/kg, 0.2 ml, iv), a blocker of ATP-sensitive potassium channel, also abolished the effect of Ado. The above results indicate that microinjection of Ado into AP induces inhibitory effects on MAP, HR and RSNA, which may be related to activation of ATP-sensitive potassium channels mediated by A(1) receptors.

Adenosine↗
PubMed2000

[Ischemic preconditioning reduces cardiomyocytic apoptosis in rabbit heart in vivo].

The effects of ischemia-reperfusion (IR) and ischemic preconditioning (IP) on hemodynamics, epicardial electrography, myocardial infarct size, cardiomyocytic apoptosis and gene proteins involving apoptosis (Fas, Bcl-2 and Bax) were observed in aneasthetized rabbit myocardium. The results are as follows. (1) During ischemia-reperfusion, heart rate, arterial blood pressure and myocardial oxygen consumption were reduced progressively. The epicardial electrographic ST-segment was elevated significantly during ischemia (P<0.001)and recovered to the baseline during reperfusion. (2) The infarct size occupied 57.7+/-2.0% of the ischemic myocardium in IR group while IP reduced the infarct size to 27.7+/-1.5% (P<0.01). (3) DNA ladder pattern of ischemic myocardium was revealed by agrose gel electrophoresis in IR group while it was not found in IP group. Apoptotic cardiomyocytes were sparse within the ischemic myocardium at risk in IP as compared with those in IR heart. Apoptosis rate of the ischemic myocardium from IR and IP groups detected by flow cytometry was 11.2+/-0.4% and 6.35+/-0.2% (P<0.01), respectively. (4) Fas and Bax protein expression in the ischemic myocardium of IR and IP groups was elevated as compared with those in non-ischemic myocardium group (P<0.05). The Fas protein expression of IR group was higher than that of IP group (P<0.05). Bcl-2/Bax ratio of IR group was lower than that in non-ischemic myocardium (P<0.01). From the results, it is suggested that IP decreases cardiomyocytic apoptosis induced by IR and this action is mediated by the reduction of Fas protein expression.

Animals↗
PubMed2000

[Streptomycin inhibits carotid sinus baroreflex in anesthetized rats].

The effect of streptomycin on the carotid baroreflex was examined in 23 anesthetized rats with isolated carotid sinus perfusion. The results obtained are as follows. (1) By perfusing the isolated carotid sinus with streptomycin (100 micromol/L) the functional curve of baroreflex was shifted to the right and upward with its peak slope (PS) decreasing from 0.40+/-0.01 to 0.33+/-0.01 kPa (P<0.001), and the reflex decrease in the mean arterial pressure (RD) was lowered from 6.22+/-0.13 to 5.02+/-0.11 kPa (P<0.001), while the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly increased from 8.27+/-0.25 to 10.33+/-0.32 kPa (P<0.01), 12.71+/-0.21 to 13.33+/-0.30 kPa (P<0.01) and 24.41+/-0.14 to 26.11+/-0.28 kPa (P<0.01),respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP induced by streptomycin were dose-dependent. (2) By perfusing the isolated carotid sinus with adenosine (125 micromol/L), carotid baroreflex was facilitated. Pretreatment with streptomycin (200 micromol/L) not only eliminated the facilitated effect of ado on carotid baroreflex but also caused a reflex decrease in MAP to a level lower than control. Taken together, it is suggested that streptomycin can markedly inhibit the carotid sinus baroreflex in anesthetized rats.

Animals↗
PubMed2000

[Increased expression of c-fos in the brainstem nuclei involved in cardiova scular regulation by capsaicin].

Effects of intracarotid injected capsaicin on the expression of Fos proto-oncogene in the brainstem nuclei involved in cardiovascular regulation were examined in 16 anesthetized rats with sinoaortic denervation. Only a few Fos-like protein immunoreactivity (FLI) neurons were found in the vehicle-control rats. Following intracarotid injection of capsaicin (10 micromol, 0.1 ml), the FLI neurons were markedly increased in nucleus paragigantocellularis lateralis (PGL), locus coeruleus (LC), area postrema (AP) and nucleus tractus solitarius (NTS), as compared with the results of vehicle-control rats, while the FLI neurons of raphe nuclei (RN) and periaqueductal gray (PAG) were not affected. The excitatory response to intracarotid injection of capsaicin was significantly inhibited by pretreatment with the vanilloid receptor (capsaicin receptor) antagonist ruthenium red (200 mmol, 0.1 ml). The results indicate that capsaicin may activate the neurons of the brainstem nuclei involved in cardiovascular regulation through vanilloid receptors, but does not exert any effects on PAG and RN.

Animals↗
PubMed2000

[K(ATP) channel opener facilitates carotid sinus baroreflex in anesthetized rats].

The effects of cromakalim (Cro), a K(ATP) channel opener, on the carotid baroreflex were studied in 32 anesthetized rats with perfused isolated carotid sinus. The results obtained are as follows. (1) By perfusing the isolated carotid sinus with Cro (10 micromol/L), the functional curve of the baroreflex was shifted to the left and downward, with a peak slope (PS) increasing from 0.36+/-0.01 to 0.48+/-0.01 kPa/kPa (P<0.001), whereas the reflex decrease in mean arterial pressure (RD) was increased from 5.78+/-0.14 to 7.87+/-0.12 kPa (P<0.001). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were all significantly decreased from 8.34+/-0.35 to 6.41+/-0.09 kPa (P<0.01), 12.71+/-0.25 to 11.78+/-0.24 kPa (P<0.01) and 24.89+/-0.25 to 22.56+/-0.16 kPa (P<0.001), respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP induced by Cro were dose-dependent. (2) By pretreatment with glibenclamide (10 micromol/L), a K(ATP) channel blocker, the above effects of Cro on the carotid baroreflex were abolished. (3) The Cro-induced change in the baroreflex was enhanced by preperfusing with adenosine (125 micromol/L). On the basis of the above results, it is concluded that Cro facilitates the carotid baroreflex, an effect attributable to the enhanced stretch of baroreceptors by dilation of sinus wall as a result of K(ATP) channel activation.

Animals↗
PubMed1999

Effect of moxonidine on carotid sinus baroreflex in anesthetized rats.

AIM: To study the effect of moxonidine (Mox) on carotid sinus baroreflex. METHODS: By perfusing the carotid sinus in anesthetized rats, the functional parameters of baroreflex were measured. The femoral artery was perfused with constant flow and the change of perfusing pressure was recorded to determine the effect of Mox on vascular tone. RESULTS: Mox 32 and 100 mumol.L-1 shifted the functional curve of carotid sinus baroreflex to the right and upward, with the reduction in peak slope and in reflex decrease of mean arterial pressure, suggesting that Mox produced an inhibitory effect on baroreflex. The effect of Mox 100 mumol.L-1 on baroreflex was completely blocked by efaroxan 100 mumol.L-1. Mox increased vascular resistance. CONCLUSION: Mox inhibits carotid baroreflex via its constrictive action on sinus wall.

Adrenergic alpha-Antagonists↗
PubMed1999

Effects of agmatine on afterdepolarizations induced by isoproterenol in guinea pig papillary muscles.

AIM: To study the effects of agmatine (Agm) on early afterdepolarizations (EAD) and delayed afterdepolarizations (DAD) induced by isoproterenol (Iso) in guinea pig papillary muscles. METHODS: EAD and DAD were recorded using intracellular glass microelectrode technique. RESULTS: (1) EAD and DAD induced by Iso 20 nmol.L-1 were markedly inhibited by pretreatment with Agm 1.0-2.0 mmol.L-1 in a concentration-dependent manner. (2) NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol.L-1), a NOS inhibitor, did not affect the inhibitory effects of Agm (1.0 mmol.L-1) on EAD and DAD induced by Iso. (3) The inhibitory effects of Agm (1.0 mmol.L-1) on EAD and DAD induced by Iso (20 nmol.L-1) were eliminated by pretreatment with idazoxan (Ida, 0.1 mmol.L-1), an alpha-2 adrenergic receptor (alpha 2-AR) and imidazoline receptor (IR) antagonist. CONCLUSION: The inhibitory effects of Agm on EAD and DAD induced by Iso in papillary muscles is related to the reduction in calcium influx and mediated by alpha 2-AR and/or IR.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1999

Electrophysiologic effects of agmatine on pacemaker cells in sinoatrial node of rabbits.

AIM: To study the electrophysiologic effects of agmatine (Agm) on pacemaker cells in sinoatrial (SA) node. METHODS: Parameters of action potential (AP) in SA node were recorded using intracellular microelectrode technique. RESULTS: Agm not only slowed down the amplitude of action potential (APA), maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), and rate of pacemaker firing (RPF), but also prolonged 90% duration of action potential (APD90) in a concentration-dependent manner. The effects of Agm (10 mmol.L-1) could be blocked completely by pretreatment with idazoxan (0.15 mmol.L-1), an alpha 2-adrenergic receptor (alpha 2-AR) and imidazoline receptor (IR) antagonist. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 1 mmol.L-1), an NOS inhibitor, did not affect the electrophysiologic effects of Agm on pacemaker cells in SA node. Elevation of Ca2+ concentration (5 mmol.L-1) in perfusate antagonized the effects of Agm (10 mmol.L-1). Lemakalim (Lem, 30 mumol.L-1), an opener of ATP-sensitive potassium channels, partially inhibited the prolonging effect of Agm on repolarization. CONCLUSION: The electrophysiologic effects of Agm on pacemaker cells in SA node were likely attributed to the reduction in calcium influx and potassium efflux and mediated by alpha 2-AR and IR.

Action Potentials↗
PubMed1999

Biphasic activation of renal afferent by intrarenal artery injection of bradykinin in anesthetized rabbits.

The effect of intrarenal artery injection of bradykinin (BK, 5.0 micrograms/kg) on multi- and single-unit recordings of afferent renal nerve activity (ARNA) was examined in anesthetized 48 rabbits. The results obtained are as follows. (1) There were two phases of increase in ARNA following intrarenal BK. The early phase occurred immediately while the delayed phase made its appearance about 7 min later. The degree of increase in ARNA of the delayed phase induced by intrarenal BK was more prominent than that in the early phase. BP was actually unaltered following intrarenal BK. (2) By pretreatment with indomethacin (Indo, 5.0 mg/kg), the delayed phase of increase in ARNA induced by intrarenal BK was attenuated, while the early phase was not affected. (3) Pretreatment with L-NAME (30 mg/kg) led the delayed phase to be blocked completely while the early phase was partially decreased. From the above-mentioned observations, it is concluded that intrarenal BK induces a significant increase in ARNA in two phases. The early phase may be due to the direct action of BK and partially due to the NO action, while the delayed phase may be attributed to the action of released prostaglandin and NO as a result of intrarenal BK.

Afferent Pathways↗
PubMed1999

Effect of intracarotid administration of adenosine on the activity of area postrema neurons in barodenervated rats.

To observe the effect of intracarotid administration of adenosine on the electrical activity of area postrema (AP) neurons, 76 spontaneous active units were recorded from 45 sino-aortic denervated Sprague-Dawley rats using extracellular recording technique. The results obtained are as follows. (1) Following intracarotid administration of adenosine (Ado, 25 micrograms/kg), the discharge rate of 29 out of 42 units decreased markedly from 6.26 +/- 0.75 to 4.74 +/- 0.76 spikes/s (P < 0.01), whereas that of 6 units increased from 4.13 +/- 0.77 to 4.72 +/- 0.83 spikes/s (P < 0.05), and the other 7 showed no response. Blood pressure (BP) and heart rate (HR) were unaltered throughout the experiment. (2) 8-phenyltheophylline (8-PT, 15 micrograms/kg), a nonselective adenosine receptor antagonist, completely blocked the inhibitory effect of Ado in 10 units. (3) Selective A1 adenosine receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 50 micrograms/kg), blocked the effect of Ado in 12 units to a remarkable extent. (4) Glibenclamide (500 micrograms/kg), a blocker of ATP-sensitive potassium channel, abolished the effect of Ado in 12 units. The above results indicate that Ado can inhibit spontaneous electrical activity of AP neurons, which is mediated by adenosine A1-receptor with the involvement of ATP-sensitive potassium channels.

Adenosine↗
PubMed1999

[Effects of intracarotid injection of capsaicin on electrical activity of rostral ventrolateral medullary neurons in rats].

The effects of intracarotid injection of capsaicin on spontaneous electrical activity of nucleus paragigantocellularis lateralis (PGL) neurons in rostral ventrolateral medulla (RVLM) were examined in 35 anesthetized rats with sino-aortic denervation by using extracellular recording technique. The results obtained were as follows: (1) In response to intracarotid injection of capsaicin (10 mumol, 0.1 ml), MAP was increased from 10.74 +/- 0.13 to 12.56 +/- 0.21 kPa (P < 0.001), and HR from 374 +/- 4 to 395 +/- 5 bpm (P < 0.001). All of 30 PGL neurons recorded responded to intracarotid injection of capsaicin with an increase in spontaneous discharge rate from 12.6 +/- 0.7 to 20.9 +/- 1.1 spikes/s (P < 0.001); (2) In 10 units, the excitatory response of PGL neurons to intracarotid injection of capsaicin was significantly inhibited by pretreatment with the vanilloid receptor (capsaicin receptor) antagonist ruthenium red (200 mmol, 0.1 ml). These results suggest that capsaicin may stimulate the vanilloid receptor of neurons in RVLM, thereby resulting in activation of PGL neurons.

Animals↗
PubMed1999

Intracarotid injection of endothelin-1 facilitates the activity of rostral ventrolateral medullary neurons via area postrema in rats.

To observe the effect of intracarotid administration of endothelin (ET-1) on electrical activity of neurons within rostral ventrolateral medulla (RVLM) region, 87 spontaneous active units were extracellularly recorded in 35 Sprague-Dawley rats with sino-aortic denervation. The results obtained are as follows. (1) Intracarotid administration of ET-1 (0.3 nmol/kg) increased the discharge firing rate from 17.8 +/- 1.5 to 20.9 +/- 1.4 spikes/s (P < 0.01) in 30 out of 36 RVLM neurons, while blood pressure and heart rate had no significant change. (2) BQ-123 (0.67 nmol/kg), a selective ETA blocker, completely blocked the facilitatory effects of ET-1 in 11 out of 14 units. (3) In 10 out of 11 units, glibenclamide (3.3 nmol/kg), a blocker of ATP-sensitive potassium channel, had no effect on the action of ET-1. (4) After ablation of area postrema (AP), the facilitatory action of intracarotid administration of ET-1 on 19 units of RVLM was abolished, while in 7 units of sham ablation animals the response of neurons to ET-1 remained unchanged. Taken together, intracarotid-administered ET-1 may act on the ETA receptors in neurons of AP, thereby resulting in the facilitating effect on RVLM neurons through the efferent projection of AP.

Animals↗
PubMed1999

[Bradykinin inhibits carotid sinus baroreflex in anesthetized rats].

The effects of bradykinin (BK) on the carotid baroreflex were examined in 36 anesthetized rats with isolated carotid sinus perfusion. The results obtained are as follows. (1) By perfusing the isolated carotid sinus with BK (1.0 mumol/L), the functional curve of baroreflex was shifted to the right and upward, its peak slope (PS) decreasing from 0.44 +/- 0.14 to 0.31 +/- 0.01 kPa (P < 0.01) and the reflex decrease in mean arterial pressure (RD) was lowered from 6.85 +/- 0.18 to 4.46 +/- 0.16 kPa (P < 0.05), while the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly enhanced from 7.76 +/- 0.20 to 10.04 +/- 0.09 kPa (P < 0.001), 12.72 +/- 0.29 to 13.74 +/- 0.31 kPa (P < 0.05) and 23.28 +/- 0.24 to 25.31 +/- 0.20 kPa (P < 0.01), respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP induced by BK were dose-dependent. (2) By pretreatment with indomethacin (10 mumol/L), an inhibitor of prostaglandin synthesis, the above-mentioned effects of BK on carotid baroreflex were not affected. (3) Preperfusion with an inhibitor of NO synthase L-NAME (100 mumol/L) could completely eliminate the effects of BK. (4) Pretreatment with angiotensin-converting enzyme inhibitor captopril (20 mumol/L) could potentiate the effects of BK. Taken together, it is indicated that BK may cause vascular endothelium to release NO, thereby inhibiting the carotid baroreflex.

Animals↗
PubMed1999

[Electrophysiological effects of agmatine on guinea pig papillary muscles in vitro].

The cardiac electrophysiological effects of agmatine (AGM) were examined in guinea pig papillary muscle using intracellular microelectrode technique. The results obtained are as follows. (1) Duration of action potential (APD) in normal papillary muscles were decreased by AGM in a concentration-dependent manner. (2) In partially depolarized papillary muscles, amplitute of action potential, overshoot, maximal velocity of phase 0 depolarization and APD were depressed by AGM. (3) Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L) did not affect the above effects of AGM (1 mmol/L) on papillary muscles. (4) The effects of AGM (1 mmol/L) could be blocked completely by pretreatment with idazoxan (0.1 mmol/L), an alpha 2-adrenoceptor (alpha 2-AR) and imidazoline receptor (IR) antagonist. All these results indicate that the effects of AGM on papillary muscles are likely due to a decrease of intracellular calcium mediated by alpha 2-AR and IR.

Action Potentials↗
PubMed1999

[Expression of c-fos in the medulla oblongata after carotid baroreceptor activation by elevated intrasinus pressure and adenosine].

Expression of c-fos protein in the medulla oblongata after baroreceptor activation by elevated intrasinus pressure (ISP) and perfusion of adenosine (Ado) was examined in 14 vascularly isolated carotid sinus perfusion rats. The results showed that Fos-like immunoreactive (FLI) neurons were distributed throughout nucleus tractus solitarius, area postrema, rostral ventrolateral medulla and nucleus raphe pallidus, and the number of FLI was increased with the elevation of ISP. Furthermore, perfusing the carotid sinus with Ado at a given ISP markedly increased the FLI in the above regions. From the results obtained, it is concluded that the c-fos expression in baroreflex pathway in medulla oblongata may be enhanced by elevated ISP and intrasinus perfusion of Ado, and Ado is capable of facilitating the baroreflex.

Adenosine↗
PubMed1999

[Hemodynamic effects of agmatine and its cellular mechanism in anesthetized rats].

The hemodynamic effects of intravenous injection of agmatine and their cellular mechanism were investigated in anesthetized rats. The results obtained are as follows. (1) Following intravenous injection of agmatine (10 mg/kg), HR, MAP, LVP, +/- LV dp/dtmax, CI and TPRI were significantly decreased. (2) Pretreatment with N-nitro-L-arginine (15 mg/kg) or methylene blue (50 mg/kg), did not affect the hypotensive effect of agmatine. (3) The hemodynamic effects induced by agmatine could be inhibited by prior intravenous injection of idazoxan (2 mg/kg), an alpha 2-adrenoceptor (alpha 2-AR) and imidazoline receptor antagonist. The results indicate that the hypotensive effect induced by i.v. agmatine may be attributed to the decrease in cardiac output resulting from depression of myocardial contractility, as well as to the reduction in total peripheral resistance resulting from vasodilatation. These effects of agmatine may be mediated by imidazoline receptor and/or alpha 2-AR.

Adrenergic alpha-Antagonists↗