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R R He

Publications and source records attributed to R R He.

At least 19 recordsLinked to original sources
PubMed2001

[NADPH-diaphorase activity and Fos expression in brainstem nuclei involved in cardiovascular regulation following intracarotid injection of capsaicin].

The present study was undertaken to define whether intracarotid injection of capsaicin induces Fos expression associated with the activation of NOS-containing neurons in brainstem nuclei by combining the immunocytochemical method for Fos with NADPH-d histochemical technique for NOS. The results obtained are as follows: (1) Intracarotid injection of capsaicin caused a significant increase of Fos-like immunoreactive neurons in area postrema (AP), nucleus tractus solitarius (NTS), paragigantocellularis lateralis (PGL) and locus coeruleus (LC), without influence upon the neurons of raphe nuclei (RN) and periaqueductal gray (PAG). (2) NO-containing neurons in PGL and NTS and the double-labeled neurons in PGL were also increased significantly following intracarotid injection of capsaicin. Small numbers of NO-containing neurons were found in LC, but there was no change in the number of NO-containing neurons in RN and PAG. No NADPH-d histochemical activity could be found in AP. (3) The above responses to capsaicin were significantly inhibited by pretreatment with either a capsaicin receptor antagonist ruthenium red or a NMDA receptor antagonist MK-801. The above results indicate that intracarotid injection of capsaicin may activate the neurons in brainstem nuclei involved in cardiovascular regulation, and that NO only plays an indirect role in the modulation of the responses of brainstem nuclei to capsaicin. These effects of capsaicin are mediated by capsaicin receptors with involvement of glutamate.

Animals↗
PubMed2001

Role of renal nerve in cardioprotection provided by renal ischemic preconditioning in anesthetized rabbits.

The effects of renal ischemic preconditioning (RIP) on ischemia-reperfused myocardium were examined in the urethane-anesthetized rabbit to determine whether RIP may provide cardioprotection and to observe the role of the renal nerve in such condition. The results obtained are as follows: (1) During 45 min myocardial ischemia and subsequent 180 min reperfusion, blood pressure, heart rate and myocardial oxygen consumption decreased progressively. Epicardial electrographic ST-segment was elevated significantly in the period of ischemia and returned to the baseline gradually in the course of reperfusion. The myocardial infarct size occupied 55.80 +/- 1.25% of the area at risk. (2) RIP significantly reduced the myocardial infarct size to 36.51 +/- 2.80% (P < 0.01), indicating the cardioprotective effect of such an intervention. (3) Renal nerve section (RNS) completely abolished the cardioprotection afforded by RIP, though RNS per se did not affect the myocardial infarct size produced by ischemia-reperfusion. (4) During 10 min renal ischemia, the averaged multi-unit discharge rate of the renal afferent was increased from 0.14 +/- 0.08 to 0.65 +/- 0.12 imp/s (P < 0.01). (5) Pretreatment with an adenosine receptor antagonist 8-phenyltheophylline (10 mg/kg) markedly attenuated the discharge rate of the renal afferent induced by transient renal ischemia, implying that adenosine released in ischemic kidney activated the renal afferent. It is suggested that activation of renal afferents by transient renal ischemia-reperfusion plays an important role in the cardioprotection afforded by RIP.

Animals↗
PubMed2001

[Action of agmatine on tension of isolated aortic artery and its receptor mechanism in rats].

The effect of agmatine (Agm) on vascular tension and the underlying receptor mechanism were investigated in the isolated aortic artery of rats. The results are as follows. (1) Agm (10(-7)-10(-2) mol/L) relaxed aortic rings in a concentration-dependent manner under the condition of precontraction induced by phenylephrine (PE) at a concentration of 10(-6) mol/L. (2) Either in the intact or the endothelium-denuded rings, pretreatment with NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L) did not affect the vascular relaxant action of Agm, implying that the concentration-dependent vasorelaxation caused by Agm is not endothelium-dependent and NO is not involved. (3) Agm also relaxed aortic rings in a concentration-dependent manner under the condition of precontraction induced by CaCl2 at a concentration of 3 mmol/L. (4) Idazoxan (10(-4) mol/L), an alpha 2-adrenergic receptor (alpha 2-AR) and imidazoline receptor (IR) antagonist, abolished the Agm-induced vasorelaxation completely under the condition of CaCl2-induced precontraction. (5) Yohimbine (10(-4) mol/L), a selective alpha 2-AR antagonist, could partially block the vascular relaxant action of Agm. It is suggested that the vascular relaxant effect of Agm on the rat aortic artery may be mediated by alpha 2-AR and IR.

Animals↗
PubMed2001

[Agmatine inhibits the afferent activity of carotid baroreceptor in rats].

The effect of agmatine (Agm) on the carotid baroreceptor activity was examined in 24 anesthetized rats with perfused isolated carotid sinus by recording sinus nerve afferent discharges. The results are as follows. (1) By perfusing with 1 mmol/L Agm, the functional curve for the intrasinus pressure (ISP)-integral of sinus nerve activity (ISNA) relation was shifted to the right and downward with decreases in peak slope (PS) and peak integral value of carotid sinus afferent discharge (PIV). By perfusing with high concentrations of Agm (5 and 10 mmol/L), the curves were shifted to the right and downward further with marked decreases of PS and PIV. These results showed that Agm exerted an inhibitory action on the baroreceptor activity in a dose-dependent manner. (2) The Agm-induced decrease in sinus nerve afferent activity was eliminated by pretreatment with IR and alpha 2-AR blocker idazoxan (0.1 mmol/L). (3) Selective alpha 2-AR blocker yohimbine (15 mumol/L) partly abolished the inhibitory effect of Agm on baroreceptor. (4) Preperfusing with Bay K 8644 (500 nmol/L), an agonist of calcium channels, also eliminated the effect of Agm on carotid baroreceptor activity. These results indicate that Agm exerts an inhibitory action on carotid baroreceptor and such an action may be attributed to the reduction in calcium influx in carotid baroreceptor, which is mediated by IR and alpha 2-AR.

Afferent Pathways↗
PubMed2001

Agmatine inhibits carotid sinus baroreflex in anesthetized rats.

AIM: To study the effect of agmatine (Agm) on carotid sinus baroreflex. METHODS: The functional parameters of baroreflex were measured by perfusing the carotid sinus in anesthetized rats. RESULTS: (1) Agm 1, 5, and 10 mmol/L shifted the functional curve of carotid sinus baroreflex to the right and upwards in a concentration-dependent manner with a reduction in peak slope and a reflex decrease in mean arterial pressure, indicating that Agm exerted an inhibitory effect on the carotid baroreflex. (2) The inhibitory effect of Agm (5 mmol/L) on baroreflex was eliminated by pretreatment with idazoxan (Ida, 0.1 mmol/L), an alpha2-adrenoceptor (alpha2-AR) and imidazoline receptor (IR) antagonist, and partially blocked by yohimbine (Yoh, 15 micromol/L), a selective alpha2-AR antagonist. (3) NG-nitro-L-arginine methyl ester (L-NAME, 500 micromol/L), an NOS inhibitor, did not affect the inhibitory effect of Agm. CONCLUSION: Agm inhibits carotid baroreflex via IR and alpha2-AR.

Adrenergic alpha-Antagonists↗
PubMed2001

17 beta-Estradiol inhibits carotid sinus baroreceptor activity in anesthetized male rats.

AIM: To study the effect of 17beta-estradiol (E2) on carotid baroreceptor activity (CBA). METHODS: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus. RESULTS: E2 3, 10, and 30 micromol/L shifted FCCB to the right and downward, with a marked decrease in peak slope (PS) and peak integral value of carotid sinus nerve discharge (PIV) in a concentration-dependent manner, indicating the inhibitory effect of E2 on CBA. Pretreatment with tamoxifen (TAM) 10 micromol/L, an inhibitor of estrogen receptor, did not block the effect of E2 on CBA. Preperfusion with L-NAME 100 micromol/L, an inhibitor of NO synthase, could completely abolish the effect of E2 on CBA. NO donor SIN-1 10 micromol/L could potentiate the inhibitory effect of E2. CONCLUSION: E2 inhibits CBA via endothelial NO release.

Anesthesia↗
PubMed2001

Effect of dipfluzine on L-type calcium current in guinea pig ventricular myocytes.

AIM: To study the effect of dipfluzine (Dip) on L-type calcium current in guinea pig ventricular myocytes. METHODS: Single myocytes were dissociated by enzymatic dissociation method. The current was recorded with the whole-cell configuration of the patch-clamp technique. RESULTS: Dip (0.3 - 30 micromol/L) reduced the voltage-dependently activated peak value of I(Ca-L) in a concentration-dependent manner. The characteristics of I-V relationship were not greatly altered by Dip, and the maximal activation voltage of I(Ca-L) in the presence of Dip was not different from that of control. Steady-state activation of I(Ca-L) was not affected markedly, and the half activation potential V(0.5)) and the slope factor (kappa) in the presence of Dip 3 micromol/L were not markedly different from those of the control. V(0.5) value was (-12.8 +/- 1.7) mV in the control and (-13.2 +/- 2.4) mV in the presence of Dip 3 micromol/L. The kappa value was (7.1 +/- 0.4) mV in the control and (7.5 +/- 0.5) mV in the presence of Dip 3 micromol/L (n = 7 cells from 3 hearts, P > 0.05). Dip 3 micromol/L markedly shifted the steady-state inactivation curve of I(Ca-L) to the left, and accelerated the voltage-dependent steady-state inactivation of calcium current. V(0.5) value was (-19.7 +/- 2.4) mV in the control and (-31 +/- 6) mV in the presence of Dip 3 micromol/L. The kappa value was (3.6 +/- 0.3) mV in the control and (1.8 +/- 0.2) mV in the presence of Dip 3 micromol/L (n = 4 cells from 2 hearts, P < 0.05). Dip 3 micromol/L markedly delayed half-recovery time of Ca2+ channel from inactivation from (40 +/- 11) to (288 +/- 63) ms (n = 4, P < 0.01). CONCLUSION: Dip mainly acts on the inactivated state of L-type calcium channel, accelerates the inactivation of calcium channel, and slows the recovery of calcium channel from inactivated state in guinea pig ventricular myocytes, through which the I(Ca-L) is inhibited.

Animals↗
PubMed2001

Hemodynamic effects of agmatine in Dahl salt-sensitive hypertensive and Dahl salt-resistant rats.

The hemodynamic effects of agmatine were investigated in anaesthetized Dahl salt-sensitive (DS) hypertensive and Dahl salt-resistant (DR) rats. The results are as follows. (1) Agmatine (1, 10, 20 mg/kg i.v.) decreased heart rate (HR), mean arterial pressure (MAP), left ventricular blood pressure (LVP), the first derivative of LVP (LV dp/dt), cardiac index (CI) and total peripheral resistance index (TPRI) in a dose-dependent manner in both DS and DR rats, and the decreases in MAP, LVP, +/- LV dp/dtmax and TPRI at the same dose of agmatine in DR rats were less than those in DS hypertensive rats. Specifically, agmatine at high dose (20 mg/kg) induced a delayed increment of hemodynamic parameters in DS hypertensive rats, but not in DR rats. (2) Idazoxan (2.5 mg/kg), an antagonist for I2 over I1-imidazoline receptors and alpha 2-adrenoceptor receptors (alpha 2-AR), only partially blocked the effects of agmatine (10 mg/kg). (3) Yohimbine (4 mg/kg), a selective alpha 2-AR antagonist, also partially attenuated the effects of agmatine. (4) Efaroxan (2.5 mg/kg), a selective antagonist for I1 over I2-imidazoline receptors and alpha 2-AR, could completely block the effects of agmatine. Taken together, the results indicate that agmatine can dose-dependently decrease HR, MAP, LVP, +/- LV dp/dtmax, CI and TPRI in DS hypertensive and DR normotensive rats. The hemodynamic effects of agmatine are mediated mainly by I1-IR with the participation of I2-IR and alpha 2-AR.

Agmatine↗
PubMed2001

Renal ischemia enhances electrical activity and Fos protein expression of the rostral ventrolateral medullary neurons in rats.

The effects of renal ischemia on spontaneous electrical activity and Fos protein expression of nucleus paragigantocellularis lateralis (PGL) in rostral ventrolateral medulla (RVLM) were observed in 67 anesthetized Sprague-Dawley rats with sinoaortic denervation by using extracellular recording and immunohistochemical techniques. The results obtained are as follows. (1) Renal ischemia increased the discharge rate from 11.40 +/- 1.08 to 21.1 +/- 1.74 spikes/s (P < 0.001) in 28 out of 30 PGL neurons, while blood pressure and heart rate had no significant change (P > 0.05). (2) Administration of 8-phenyltheophylline (8-PT), an adenosine receptor antagonist, did not affect the discharge rate of PGL neurons, but could partially inhibit the effects of renal ischemia in 17 units (P < 0.05). (3) Renal ischemia resulted in a remarkable increase in the number of Fos-like protein immunoreactive PGL neurons in the RVLM (P < 0.01). (4) Fos protein expression induced by renal ischemia was significantly inhibited by pretreatment with 8-PT (P < 0.05). Taken together, it is concluded that renal ischemia induces an increase in spontaneous electrical activity and Fos protein expression in PGL neurons of RVLM, and that adenosine released within ischemic kidney may be involved in such effects.

Animals↗
PubMed2001

Differential responses of regional vascular beds to local injection of agmatine in rats.

In 66 anaesthetized rats, the effects of local injection of agmatine on femoral, renal, and mesenteric vascular beds were investigated respectively by constant flow perfusion method. The results are as follows. (1) Agmatine (0.1, 0.5, 1 mg/kg) increased the perfusion pressure (PP) of femoral vascular bed in a dose dependent manner. The effect of agmatine (1 mg/kg) was completely blocked by pretreatment with idazoxan (0.5 mg/kg), an antagonist for imidazoline receptors (IR) and alpha(2)-adrenergic receptors (alpha(2)-AR), and yohimbine (1 mg/kg), a selective alpha(2)-AR antagonist. (2) Agmatine also increased the PP of renal vascular bed in a dose-dependent manner, and agmatine at high dose (1 mg/kg) caused a biphasic increase of PP in renal vascular bed. Idazoxan blocked these effects completely, while yohimbine led the agmatine induced effect to a decrease in the PP of renal vascular bed. (3) Agmatine decreased the PP of mesenteric vascular bed in a dose-dependent manner, an effect which was completely blocked by idazoxan, but unaffected by yohimbine. From the results obtained, it is concluded that agmatine differentially affects the vascular tone in the femoral, renal, and mesenteric vascular beds.

Agmatine↗
PubMed2000

Electrophysiological effects of agmatine on human atrial fibers.

The objective of the present study was to study the electrophysiological effects of agmatine on human atrial fibers obtained at cardiac surgery using standard microelectrode techniques. Agmatine (1 to approximately 10 mM) decreased the action potential amplitude (APA), maximum upstroke velocity of phase 0 depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), rate of pacemaker firing (RPF), and action potential duration at 50 and 90% of repolarization (APD(50-90)) in a concentration-dependent manner. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 0.5 mM), a NOS inhibitor, did not affect the electrophysiological effects of agmatine (5 mM) on human atrial fibers. The effects of agmatine (5 mM) could be blocked completely by pretreatment with idazoxan (0.1 mM), an alpha-2 adrenergic receptor (alpha2-AR) and imidazoline receptor (IR) antagonist. All these results indicate that the effects of agmatine on human atrial fibers are likely due to a decrease of intracellular calcium mediated by IR and/or alpha2-AR.

Action Potentials↗
PubMed2000

Effect of anoxic preconditioning on ATP-sensitive potassium channels in guinea-pig ventricular myocytes.

Ischemic or hypoxic preconditioning in experimental animals and humans is described. The mechanism of preconditioning may involve several endogenous substances released from ischemic or hypoxic tissues (such as adenosine, noradrenaline and bradykinin) that stimulate protein kinase C (PKC), which then phosphorylates ATP-sensitive potassium channels (K(ATP) channels). However, the effect of hypoxic preconditioning on K(ATP) channels in guinea-pig ventricular myocytes is unclear. The uncoupler carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone (FCCP) has been shown to activate K(ATP) channels in isolated cardiac cells. In the present study we tested whether anoxic preconditioning (APC) could affect the opening of K(ATP) channels activated by metabolic inhibition (MI) induced by FCCP in cell-attached and inside-out patches from guinea-pig ventricular myocytes. We measured the channel activity as NP(o)i and calculated it using the formula Po=I/(Ni), where Po is open-state probability, I is the mean patch current carried by all K(ATP) channels activated in a particular patch for a certain period of time, N is the number of functioning channels in the patch, and i is the unitary current of the K(ATP) channels. In cell-attached membrane patches, after about 5 min of initiating MI, K(ATP) channels were activated at a holding potential of +40 mV (NP(o)i=3.70+/-0.9 pA); APC pretreatment (3 min of anoxia followed by 7 min of reoxygenation) before MI (APC+MI group) shortened the time to activate K(ATP) channels by MI (2.3+/-0.5 min) and increased the activity of K(ATP)currents (NP(o)i=8.4+/-0.5 pA). This effect of APC was eliminated by administration of a PKC blocker, chelerythrine (5 microM), for 5 min before the APC pretreatment. In the inside-out patches, the IC50 of intracellular ATP against the K(ATP) channels in the APC+MI group was significantly increased to 642 microM compared to that in the MI group (IC50 of intracellular ATP =252 microM). Chelerythrine inhibited the effect of APC on the sensitivity of K(ATP) channels to the intracellular ATP concentration (IC50 of [ATP]i=301 microM). Our results demonstrate that APC can increase and accelerate the opening of K(ATP) channels induced by MI, and decrease the sensitivity of K(ATP) channels to [ATP]i, which is mediated by promoting the activation of PKC induced by APC.

Adenosine Triphosphate↗
PubMed2000

Inhibition by agmatine on spontaneous activity of rabbit atrioventricular node cells.

AIM: To study the effects of agmatine on spontaneous activity of atrioventricular (AV) node and its action mechanisms. METHODS: Action potentials in AV node cells were recorded using intracellular microelectrode technique. RESULTS: Agmatine not only reduced the amplitude of action potential (APA), maximal rate of depolarization (Vmax), velocity of diastolic (phase 4) depolarization (VDD), and rate of spontaneous firing (RSF), but also prolonged 90% duration of action potential (APD90) in a concentration-dependent manner. The effects of agmatine (10 mmol/L) could be blocked completely by pretreatment with idazoxan (0.1 mmol/L), an imidazoline receptor (IR) and alpha 2-adrenergic receptor (alpha 2-AR) antagonist. Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L), a nitric oxide (NO) synthase inhibitor, did not affect the effects of agmatine on AV node cells. Elevation of Ca2+ concentration (5 mmol/L) in perfusate antagonized the effects of agmatine (10 mmol/L). Lemakalim (30 mumol/L), an ATP-sensitive potassium channel opener, inhibited the prolonging effects of agmatine on repolarization. CONCLUSION: The inhibitory effects of agmatine on spontaneous activity of AV node cells in rabbits were likely mediated by IR and/or alpha 2-AR, and were related to the reduction in calcium influx and potassium efflux.

Action Potentials↗
PubMed2000

Changes in heart rate, blood pressure and renal sympathetic nerve activity induced by microinjection of capsaicin into area postrema in rats.

The effects of capsaicin microinjection into area postrema (AP) on mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in 36 anesthetized Sprague-Dawley rats. The results obtained are as follows. (1) Following microinjection of capsaicin (10 micromol/L, 50 nl) into the AP, MAP, HR and RSNA were significantly increased from 12.34+/-0.53 kPa, 328.52+/-7.54 bpm and 100+/-0% to 15.17+/-0.25 kPa (P<0.001), 354.81+/-8.54 bpm (P<0.001) and 156.95+/-7.57% (P<0.001), respectively. (2) Ruthenium red (RR, 100 mmol/L, 0.2 ml, iv), a capsaicin receptor antagonist, significantly inhibited these effects of capsaicin. (3) Pretreatment with a NMDA receptor antagonist MK-801 (500 microgram/kg, 0.2 ml, iv) also reduced these effects of capsaicin. The above results indicate that microinjection of capsaicin into AP induces excitatory effects on MAP, HR and RSNA, which are mediated by capsaicin receptors with glutamate involvement.

Animals↗
PubMed2000

[17beta -estradiol inhibits carotid sinus baroreflex in male rats].

By perfusing isolated carotid sinus, the effect of 17beta-estradiol (E(2)) on carotid sinus baroreflex was observed in anesthetized male rats. The results obtained are as follows. (1) By perfusing with E(2) (10 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a peak slope (PS) decrease from 0.49+/-0.03 to 0.25+/-0.01 (P<0.01) and a reflex decrease in mean arterial pressure (reflex decrease, RD) from 7.37+/-0.42 kPa to 3.49+/-0.20 kPa (P<0.001), while the threshold pressure (TP) and saturation pressure (SP) were significantly increased from 9.52+/-0.68 kPa to 13.3+/-0.11 kPa (P<0.001) and 24.53+/-0.48 kPa to 27.52+/-0.20 kPa (P<0.01) respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS, TP and SP were dose-dependent. (2) Pretreatment with different doses of tamoxifen (1, 5, 10, 30 micromol/L), an inhibitor of estrogen receptor, did not block the effect of E(2) on carotid baroreflex. (3) Preperfusion with an inhibitor of NO synthase L-NAME (100 micromol/L) could completely abolish the effect of E(2) on carotid baroreflex. It is concluded that the inhibitory effect of E(2)on carotid sinus baroreflex may be mediated by NO release from endothelial cells, but not by a genomic mechanism.

Animals↗
PubMed2000

[Role of calcium in the mechanism underlying the inhibitory effect of streptomycin on carotid sinus baroreflex in rats].

The effect of streptomycin (SM) on carotid baroreflex was examined in 23 anesthetized rats with isolated carotid sinus perfusion. The results obtained are as follows. (1) In response to perfusion with SM (200 micromol/L), the functional curve of carotid baroreflex was shifted to the right and upward with a decrease of peak slope (PS) and a reflex decrease in mean arterial pressure (RD)(P<0.01), indicating an inhibitory effect of SM on carotid sinus baroreflex. (2) By perfusing the isolated carotid sinus with high Ca(2+) solution (4 mmol/L), the inhibitory effect of SM on carotid baroreflex was partially eliminated. The functional curve of SM was shifted to the left and downward with PS increasing from 0.27+/-0.04 kPa to 0.37+/-0.02 kPa (P<0.01) and RD was enhanced from 4.32+/-0.14 kPa to 6.18+/-0.17 kPa (P<0.01). On the other hand, the threshold pressure (TP) and saturation pressure (SP) were significantly decreased from 10.29+/-0.29 kPa to 9.98+/-0.33 kPa (P<0.05) and from 27.26+/-0.42 kPa to 25.22+/-0.38 kPa (P<0.05), respectively. (3) By pretreatment with Bay K 8644 (500 nmol/L), an agonist of calcium channels, the effect of SM on carotid baroreflex was completely abolished. (4) Exposure of the carotid sinus to SM following pretreatment with charybdotoxin (ChTX,100 nmol/L), a blocker of the Ca(2+)-activated K(+) channel (KCa), still inhibited the baroreflex. These results suggest that the inhibitory action of SM on carotid baroreflex may be mediated by suppressing Ca(2+) influx.

Animals↗
PubMed2000

[Modulatory effects of 17beta-estradiol on the electrical activity of subfornical organ neurons].

The effects of 17beta-estradiol (E(2) ) on electrical activity of neurons in subfornical organ (SFO) slices were examined using extracelluar recording technique. The results are as follows. (1) In 15 SFO units, a low dose of E(2) (0.1 nmol/L) applied into superfusate induced an increase in discharge rate from 3.21+/-0.37 to 6.79+/-0.71 Hz (P<0.001), whereas a high dose of E(2) (100 nmol/L ) caused a decrease in discharge rate from 3.44+/-0.40 to 1.44+/-0.36 Hz (P<0.01); (2) glutamate NMDA receptor antagonist MK-801 (50 pmol/L) blocked the excitatory effects induced by low dose of 17beta-estradiol in 7 units; (3) L-arginine (L-arg, 1 mmol/L), a physiological precursor of NO, abolished the excitatory effects induced by low dose of 17beta-estradiol in 7 units; (4) application of N-omega-nitro-L-arginine methyl ester (L-NAME, 10 mmol/L), an inhibitor of NOS, blocked the inhibitory effects induced by high dose of 17beta-estradiol in 6 units. The above results suggest that the estrogen exerts dual action on SFO neuron. E(2) at low dosage increases the discharge rate of SFO neuron, an effect which may be related to the activation of NMDA receptors, whereas E(2) at high dosage decreases the discharge rate, an effect which may be attributed to the activation of NOS with resultant production of NO.

Animals↗