Biomedical subjects

Guo-Qing Zhu

Publications and source records attributed to Guo-Qing Zhu.

13 recordsLinked to original sources

PubMed2006

NAD(P)H oxidase in paraventricular nucleus contributes to the effect of angiotensin II on cardiac sympathetic afferent reflex.

We previously reported that reactive oxygen species (ROS) in paraventricular nucleus (PVN) modulated cardiac sympathetic afferent reflex (CSAR) and mediated the effect of angiotensin II (Ang II) in the PVN on the CSAR. In the present study, we investigated whether the NAD(P)H oxidase in the PVN was a key source of ROS which modulated the CSAR and contributed to the effect of Ang II on the CSAR. In anesthetized rats with sinoaortic denervation and vagotomy, renal sympathetic nerve activity (RSNA) and arterial pressure were recorded. The CSAR was evaluated by the RSNA response to epicardial application of bradykinin (BK). The NAD(P)H oxidase activity in the PVN was measured with lucigenin-enhanced chemiluminescent method. Microinjection of the NAD(P)H oxidase inhibitor, either apocynin (1.0 nmol) or phenylarsine oxide (PAO, 1.0 nmol), into the PVN significantly inhibited the CSAR. Microinjection of Ang II (0.3 nmol) into the PVN significantly augmented the CSAR. The effects of Ang II were not only abolished by pretreatment with either apocynin or PAO in the PVN but also partially inhibited by xanthine oxidase inhibitor allopurinol. Either epicardial application of BK or microinjection of Ang II into the PVN significantly increased NAD(P)H oxidase activity in the PVN. The effect of Ang II on NAD(P)H oxidase activity was abolished by pretreatment with AT(1) receptor antagonist losartan in the PVN. These findings suggested that NAD(P)H oxidase in the PVN was a major source of the ROS in modulating the CSAR, and the NAD(P)H oxidase contributes to the effect of Ang II on the CSAR.

Afferent Pathways↗

PubMed2005

Resetting blood pressure by a closed-loop implanted chip system in normotensive rats.

A closed-loop implanted chip system was designed to control blood pressure without using drugs. The chip system instantaneously reset blood pressure by stimulating the left aortic depressor nerve according to the feedback signals of arterial blood pressure. The relationship between pressure signals and frequency of stimulation was identified in vitro and in vivo, and the efficiency of the chip system was evaluated in normal anesthetized Wistar rats. To determine whether the depressor effect of the chip was primarily independent on the bradycardia induced by the resetting, the effects of methyl atropine (1.5 g/kg, iv.) and bilateral vagotomy on depressor effect induced by the chip system were determined, respectively. The results indicated that the chip system worked well. The frequency of stimulus linearly increased following the elevation of pressure from 70 to 160 mm Hg. The frequency of the stimulus reached its maximum (100 Hz) when pressure exceeded 160 mm Hg, and the stimulation stopped when MAP was below 70 mm Hg. There were significant decreases in mean arterial pressure (MAP, -20.0+/-4.4 mm Hg) and heart rate (HR, -43.0+/-10.5 bpm) during the resetting in rats. After resetting, both MAP and HR recovered in a minute without any significant rebound. Pretreatment with either methyl atropine or bilateral vagotomy abolished the bradycardia effect but produced no significant effect on hypotension. The results demonstrated that the chip system successfully reset blood pressure in rats, and that the hypotension induced by the chip system was primarily independent on the bradycardia effect.

Anesthesia↗

PubMed2005

Reactive oxygen species in paraventricular nucleus modulates cardiac sympathetic afferent reflex in rats.

Our previous studies showed that angiotensin II (Ang II) in the paraventricular nucleus (PVN) potentiated the cardiac sympathetic afferent reflex (CSAR) in rats. This study investigated whether the reactive oxygen species (ROS) in the PVN modulated the CSAR and contributed to the effect of Ang II on the CSAR in rats. Under alpha-chloralose and urethane anesthesia, renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate were recorded in sinoaortic-denervated and cervical-vagotomized rats. The CSAR was evaluated by the RSNA response to epicardial application of bradykinin (0.04 and 0.4 microCompared with microinjection of saline into the PVN, superoxide anion scavenger, either tempol (20 nmol) or tiron (10 nmol), significantly decreased the CSAR (P < 0.05). Conversely, superoxide dismutase (SOD) inhibitor diethyldithio-carbamic acid (DETC, 10 nmol) potentiated the CSAR (P < 0.05). Microinjection of Ang II (0.3 nmol) into the PVN resulted in an enhanced CSAR (P < 0.05). The effect of Ang II on the CSAR was completely inhibited by pretreatment with either tempol or tiron (P < 0.05) but was not affected by DETC. On the other hand, either tempol or tiron decreased the RSNA (P < 0.05), but DETC increased the RSNA (P < 0.05). Ang II increased the RSNA (P < 0.05) and MAP (P < 0.05). The effect of Ang II on the RSNA and MAP was abolished by pretreatment with either tempol or tiron but was not affected by DETC. These results indicated that the ROS in the PVN modulated the CSAR and contributed to the effect of Ang II in the PVN on the CSAR.

Action Potentials↗

PubMed2005

AT1 receptor in paraventricular nucleus mediates the enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure.

Our previous studies have shown that the cardiac sympathetic afferent reflex (CSAR) was enhanced in the chronic heart failure in dogs and rats. Exogenous angiotensin II (Ang II) in the paraventricular nucleus (PVN) potentiated this reflex which was mediated by AT1 receptor. The aim of the present study was to determine if the abnormal endogenous Ang II and AT1 receptor in the PVN were responsible for the enhanced CSAR in rats with coronary ligation-induced chronic heart failure (CHF). Under urethane and alpha-chloralose anesthesia, mean arterial pressure, heart rate and renal sympathetic nerve activity (RSNA) were recorded in sino-aortic denervated and cervical vagotomized CHF and sham-operated rats. The effects of bilateral microinjection of AT1 receptor antagonist losartan and angiotensin converting enzyme inhibitor captopril on the CSAR evoked by epicardial application of bradykinin (BK, 0.04 and 0.4 microg) were determined respectively. Both AT1 receptor mRNA and AT1 receptor protein in the PVN were measured. Bilateral microinjection of either captopril (10 nmol) or losartan (50 nmol) into the PVN inhibited the enhanced CSAR evoked by BK in rats with CHF, but had no significant effects in sham-operated rats. AT1 receptor protein in the PVN significantly increased in CHF rats compared with sham-operated rats. These results indicated that either decrease of Ang II or blockage of AT1 receptor in the PVN normalized the enhanced CSAR evoked by epicardial application of BK in rats with CHF, and that increased expression of AT1 receptor in the PVN contributed to the enhanced CSAR in the CHF state.

Animals↗

PubMed2005

Interaction of central Ang II and NO on the cardiac sympathetic afferent reflex in dogs.

The aim of this study was to test the hypothesis that the central angiotensin II (Ang II) and nitric oxide (NO) systems interact to modulate the cardiac sympathetic afferent reflex (CSAR). All dogs were anesthetized with alpha-chloralose (100 mg/kg, iv). They were sino-aortic baroreceptor denervated and vagotomized throughout the experiment renal sympathetic nerve activity responses to cardiac sympathetic afferent stimulation and the central gain of the CSAR were measured. Three protocols were performed: (1) intracerebroventricular injection (icv, 3 microg/h or 6 microg/h) of Ang II with and without N(omega)-nitro-L-arginine methyl ester (L-NAME) (icv, 1 mg/kg), (2) L-NAME (icv) with and without Ang II (icv, 6 microg/h), and (3) administration of the specific neural NO synthase (nNOS) inhibitor, S-Methyl-L-thiocitrulline (MeTC) (icv, 0.1 or 1 mM, 0.5 ml in 5 min) with and without pretreatment with the angiotensin type 1 receptor antagonist, losartan (icv, 0.125 mg/kg). The primary findings were (1) Ang II alone did not significantly affect the central sensitivity of the CSAR. However, Ang II with L-NAME enhanced this reflex, (2) even though L-NAME alone augmented the CSAR, this excitatory effect was further potentiated in the presence of Ang II and (3) MeTC significantly enhanced the central sensitivity of the CSAR. However, this enhancement did not occur after pretreatment with losartan. These data suggest that Ang II interacts with NO in the brain to modulate the CSAR and that inhibition of NO is required for facilitation of the CSAR by Ang II.

Afferent Pathways↗

PubMed2005

Tempol reduces reperfusion-induced arrhythmias in anaesthetized rats.

The generation of reactive oxygen species (ROS) contributes to reperfusion-induced arrhythmias. In the present study, the antiarrhythmic effects of tempol and tiron, two membrane-permeable radical scavengers, on reperfusion-induced arrhythmias in rats in vivo were investigated. The anaesthetized rats were subjected to 5 min of left descending coronary artery (LAD) occlusion followed by 30 min of reperfusion. All rats pretreated with saline developed ventricular tachycardia (VT) and ventricular fibrillation (VF) at the onset of reperfusion, and most of the rats died from irreversible VF at the end of reperfusion. However, pretreatment with tempol (30 or 100 mg kg(-1)) 5 min before reperfusion reduced mortality, arrhythmia score and the incidence and duration of VT and VF. In the rats pretreated with high dose of tempol (100 mg kg(-1)), no VF happened and all rats were alive at the end of the experiment. The arrhythmia score was also significantly decreased compared with that of rats pretreated with saline (0.80 +/- 0.4 versus 5.6 +/- 0.4, P < 0.01). Tiron also provided nearly complete protection against reperfusion-induced arrhythmias when given 2 min before reperfusion. On the other hand, intravenous administration of tempol induced decreases in mean arterial pressure (MAP), heart rate (HR) and pressure rate index (PRI), a relative indicator of myocardial oxygen consumption. In order to determine whether the antiarrhythmic effects of tempol were secondary to the reduction of myocardial oxygen consumption, continuous electrical stimulation of the aortic depressor nerve (3 V, 10 ms and 10 Hz) was carried out in a group of rats to induce decreases in MAP, HR and PRI similar to those in the high dose of Tempol group. However, these rats did not show significant changes in the severity of reperfusion-induced arrhythmias. We conclude that both tempol and tiron significantly reduce reperfusion-induced arrhythmias in rats, and this protective action is independent of hemodynamic effects.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

PubMed2005

[Study on eco-climatic applicability of Angelica sinensis].

OBJECTIVE: In the interest of establish planting base of Angelica sinensis on a large scale, enhance economic benefit, and improve decision-making reasons, the eco-climatic applicability of A. sinensis was studied. METHOD: Using integral regression, eco-climatic applicability and the effect of meteorological conditions for the yield of A. sinensis' were analysed by field experimental data. RESULT: Selected > or =0 degrees C accumulated temperature and annual precipitation as leading index, altitude as assistant index, yield and rate of finished products as reference index, the integrated eco-climatic division index and the planting division applicability of A. sinensis was confirmed. CONCLUSION: Accordancing to theory of climate similitude and leading index summarisation, combining with assistant index and reference index, the integrated division index of eco-climate was confirmed. The planting division of co-climate applicability was divided into 5 grades as best suitable, suitable hypo-suitable, just suitable and no suitable regions. At the same time,the way to enhanced utilizing efficiency of eco-climate resources was brought forward.

Angelica sinensis↗

PubMed2004

Baroreceptor reflex in heart failure.

Congestive heart failure is a syndrome that is usually initiated by a reduction in pump function of the heart, i.e. a decrease in cardiac output. Initially, a reduction in cardiac output leads to unloading of baroreceptor reflex that, in turn, increases heart rate through vago-sympathetic mechanisms and total peripheral resistance via an increase in sympathetic outflow to vascular beds. In this review we are thinking on how baroreceptor reflex plays a role in the abnormal control of the circulation in heart failure. This review and our recent studies suggest that: (1) baroreceptor reflex is blunted in heart failure; (2) central angiotensin II and reactive oxygen species play an important role in blunted baroreceptor reflex; (3) cardiac sympathetic afferent stimulation and chemoreceptor reflex inhibit baroreceptor reflex; and (4) exercise training normalizes abnormal reflexes in the heart failure state.

Angiotensin II↗

PubMed2004

Reduced nitric oxide in the rostral ventrolateral medulla enhances cardiac sympathetic afferent reflex in rats with chronic heart failure.

The purpose of this study was to determine the effect of nitric oxide (NO) in the rostral ventrolateral medulla (RVLM) on the central integration of the cardiac sympathetic afferent reflex (CSAR) in normal rats and in rats with coronary ligation-induced chronic heart failure (CHF). Under alpha-chloralose and urethane anesthesia, mean arterial pressure, heart rate and renal sympathetic nerve activity (RSNA) were recorded at baseline and during elicitation of the CSAR evoked by electrical stimulation of the cardiac afferent sympathetic nerves in sino-aortic denervated and cervical vagotomized rats. A cannula was inserted into the left RVLM for microinjection of NO synthase inhibitor, S-methyl-L-thiocitruline (MeTC) or NO donor, S-nitroso-N-acetyl-penicillamine (SNAP). The CSAR was tested by electrical stimulation (5, 10, 20 and 30 Hz at 10 V for 1 ms) of the afferent cardiac sympathetic nerves. It was observed that (1) the responses of RSNA to stimulation were enhanced in rats with CHF; (2) MeTC (80 nmol) potentiated the responses of RSNA to stimulation in sham rats but not in rats with CHF; (3) SNAP (50 nmol) depressed the enhanced RSNA response to stimulation in CHF rats but had no effect in sham rats; and (4) MeTC increased the baseline RSNA and MAP only in sham rats, but SNAP inhibited the baseline RSNA and MAP in both sham and CHF rats. These results indicate that reductance of NO in the RVLM is involved in the augmentation of CSAR in CHF rats.

Afferent Pathways↗

PubMed2004

AT1 receptor mRNA antisense normalizes enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure.

Previous studies showed that the cardiac sympathetic afferent reflex (CSAR) is enhanced in dogs and rats with chronic heart failure (CHF) and that central ANG II type 1 receptors (AT(1)R) are involved in this augmented reflex. The aim of this study was to determine whether intracerebroventricular administration and microinjection of antisense oligodeoxynucleotides targeted to AT(1)R mRNA would attenuate the enhanced CSAR and decrease resting renal sympathetic nerve activity (RSNA) in rats with coronary ligation-induced CHF. The CSAR was elicited by application of bradykinin to the epicardial surface of the left ventricle. Reflex responses to epicardial administration of bradykinin were enhanced in rats with CHF. The response to bradykinin was determined every 50 min after intracerebroventricular administration (lateral ventricle) or microinjection (into paraventricular nucleus) of antisense or scrambled oligonucleotides to AT(1)R mRNA. AT(1)R mRNA and protein levels in the paraventricular nucleus were significantly reduced 5 h after administration of antisense. Antisense significantly decreased resting RSNA and normalized the enhanced CSAR responses to bradykinin in rats with CHF. Scrambled oligonucleotides did not alter resting RSNA or the enhanced responses to bradykinin in rats with CHF. No significant effects were found in sham-operated rats after administration of either antisense or scrambled oligonucleotides. These results strongly suggest that central AT(1)R mRNA antisense reduces expression of AT(1)R protein and normalizes the augmentation of this excitatory sympathetic reflex and that genetic manipulation of protein expression can be used to normalize the sympathetic enhancement in CHF.

Animals↗

PubMed2004

ANG II in the paraventricular nucleus potentiates the cardiac sympathetic afferent reflex in rats with heart failure.

Chronic heart failure (CHF) is characterized by sympathoexcitation, and the cardiac sympathetic afferent reflex (CSAR) is a sympathoexcitatory reflex. Our previous studies have shown that the CSAR was enhanced in CHF. In addition, central angiotensin II (ANG II) is an important modulator of this reflex. This study was performed to determine whether the CSAR evoked by stimulation of cardiac sympathetic afferent nerves (CSAN) in rats with coronary ligation-induced CHF is enhanced by ANG II in the paraventricular nucleus (PVN). Under alpha-chloralose and urethane anesthesia, renal sympathetic nerve activity (RSNA) was recorded. The RSNA responses to electrical stimulation (5, 10, 20, and 30 Hz) of the CSAN were evaluated. Bilateral microinjection of the AT1-receptor antagonist losartan (50 nmol) into the PVN had no significant effects in the sham group, but it abolished the enhanced RSNA response to stimulation in the CHF group. Unilateral microinjection of three doses of ANG II (0.03, 0.3, and 3 nmol) into the PVN resulted in dose-related increases in the RSNA responses to stimulation. Although ANG II also potentiated the RSNA response to electrical stimulation in sham rats, the RSNA responses to stimulation after ANG II into the PVN in rats with CHF were much greater than in sham rats. The effects of ANG II were prevented by pretreatment with losartan into the PVN in CHF rats. These results suggest that the central gain of the CSAR is enhanced in rats with coronary ligation-induced CHF and that ANG II in the PVN augments the CSAR evoked by CSAN, which is mediated by the central angiotensin AT1 receptors in rats with CHF.

Angiotensin II↗

PubMed2002

Central AT1 receptors are involved in the enhanced cardiac sympathetic afferent reflex in rats with chronic heart failure.

The purpose of this study was to determine if the cardiac sympathetic afferent reflex (CSAR) was augmented in rats with coronary ligation-induced chronic heart failure (CHF), and if central angiotensin II (ANG II) was involved in this enhancement. Under alpha-chloralose and urethane anesthesia, mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded in sino-aortic denervated and cervical vagotomized rats. An intracerebroventricular cannula was implanted. The CSAR was examined by epicardial application of bradykinin (BK, 0.04 and 0.4 microg in 2.0 microl) or capsaicin (0.04 and 0.4 microg in 2.0 microl) to the anterior and posterior wall of the left ventricle. The CSAR evoked by BK or capsaicin was augmented in rats with CHF. In sham rats, there was no significant difference of the CSAR induced by BK or capsaicin between anterior and posterior epicardial application. However, in rats with CHF, the CSAR induced by BK (0.04 microg) to anterior epicardial application was blunted compared with posterior application. Intracerebroventricular injection of losartan (500 nmol) normalized the enhanced CSAR in rats with CHF, but had no significant effects on the CSAR in sham rats. However, intravenous application of the same dose of losartan only decreased the baseline MAP, but did not alter baseline RSNA or the CSAR in sham or CHF rats. Pre-treatment with epicardial application of lidocaine to the anterior wall abolished the CSAR evoked by application of BK or capsaicin but had no effects on the CSAR evoked by epicardial application of BK or capsaicin to the posterior wall. These results suggest that the CSAR induced by epicardial application of BK and capsaicin is enhanced in the rats with CHF, and the enhanced CSAR is mediated by central AT(1) receptors.

Anesthetics, Local↗

PubMed2002

Microinjection of ANG II into paraventricular nucleus enhances cardiac sympathetic afferent reflex in rats.

The aims of present study were to determine whether angiotensin II (ANG II) in the paraventricular nucleus (PVN) is involved in the central integration of the cardiac sympathetic afferent reflex and whether this effect is mediated by the ANG type 1 (AT(1)) receptor. While the animals were under alpha-chloralose and urethane anesthesia, mean arterial pressure, heart rate, and renal sympathetic nerve activity (RSNA) were recorded in sinoaortic-denervated and cervical-vagotomized rats. A cannula was inserted into the left PVN for microinjection of ANG II. The cardiac sympathetic afferent reflex was tested by electrical stimulation (5, 10, 20, and 30 Hz in 10 V and 1 ms) of the afferent cardiac sympathetic nerves or epicardial application of bradykinin (BK) (0.04 and 0.4 microg in 2 microl). Microinjection of ANG II (0.03, 0.3, and 3 nmol) into the PVN resulted in dose-related increases in the RSNA responses to electrical stimulation. The percent change of RSNA response to 20- and 30-Hz stimulation increased significantly at the highest dose of ANG II (3 nmol). The effects of ANG II were prevented by pretreatment with losartan (50 nmol) into the PVN. Microinjection of ANG II (0.3 nmol) into the PVN significantly enhanced the RSNA responses to epicardial application of BK, which was abolished by pretreatment with losartan (50 nmol) into the PVN. These results suggest that exogenous ANG II in the PVN augments the cardiac sympathetic afferent reflex evoked by both electrical stimulation of cardiac sympathetic afferent nerves and epicardial application of BK. These central effects of ANG II are mediated by AT(1) receptors.

Afferent Pathways↗