Mechanism of the Reversal Effect of Acupuncture on the Fall of Blood Pressure Induced by Angiotensin-(1-7)in the Caudal Ventrolateral Medulla of Rats

Objective：To investigate the mechanism of the reversal effect of acupuncture on the fall of blood pressure induced by angiotensin （1-7）[Ang-（1 7）] in the caudal ventrolateral medulla （CVLM） of rats. Methods： Ang-（1-7） and its selective receptor antagonist （DAla7）, Ang（1-7） and Ang（779） were microinjected into the CVLM respectively to induce the change of blood pressure, during which, the concentrations of amino acid neurotransmitters were detected by means of microdialysis and high performance liquid chromatography （HPLC）combined with fluorescent detector, on the other hand, the effects of electro-acupuncture （EA） on the level of blood pressure and the concentrations of amino acid neurotransmitters were also observed. Results： Unilateral microinjection of Ang（1 7） into the CVLM could decrease the blood pressure （BP）, which was accompanied by an increase in the release of Glu and a decrease in the release of Tau in the same site; Whereas microinjection of Ang-779 into the CVLM could elevate BP, which was accompanied by a decrease in the release of Glu and an increase in the release of Tau; EA at acupoint Zusanli （ST 36） for 20 min could inhibit the fall of blood pressure induced by microinjection of Ang-（1-7） into the CVLM and the elevation of blood pressure induced by microinjection of Ang-779 into the CVLM, and in the meantime, it could inhibit the changes of the release of Glu and Tau induced by microinjection of Ang-（1-7） and Ang-779 into the CVLM. Conclusion： The reversal effect of EA on the fall or elevation of blood pressure induced by microinjection of Ang-（1-7） or Ang-779 into the CVLM might be related to the changes of Glu and Tau release.

ANGIOTENSIN Ⅱ IMMUNOREACTIVITIES IN CARDIOVASCULAR BRAIN AREAS OF DEVELOPING SPONTANEOUSLY HYPERTENSIVE AND NORMOTENSIVE WISTAR KYOTO RATS:AGE-AND SEX-RELATED DIFFERENCES

Angiotensin Ⅱ immunoreactivity (ir-Ang Ⅱ) was measured in brain areas,known to be involved in the control of circulation, in spontaneously hypertensive rats(SHR) and normotensive, Wistar Kyoto rats as controls (WKY) of 1-]2 weeks old and of both sexes. The systolic pressure (SP), in rats of 4-12 weeks old,increased with age and was signifficantly higher in SHR than WKY. In SHR, the increase was also significantly greater in male than female. The ir-Ang Ⅱ increased with age in all cardiovascular brain areas up to 12 weeks old in SHR, but only up to 4 weeks old in WKY. There was also sex difference in SHR. The changes in ir-Ang Ⅱ, particularly in the ventrolateral medulla (VLM), correlated well with changes in SP. The findings suggest thal interaction between brain Ang Ⅱ and cardiovascular brain areas, particularly the VLM and hypothalamus, may be crucial in the development of hypertension. The results also indicale sexual dimorphism in brain Ang Ⅱ in addition to blood pressure reaction in the developing SHR.

Angiotensin Ⅱ-derived reactive oxygen species underpinning the processing of the cardiovascular reflexes in the medulla oblongata

The brainstem is a major site in the central nervous system involved in the processing of the cardiovascular reflexes such as the baroreflex and the peripheral chemoreflex. The nucleus tractus solitarius and the rostral ventrolateral medulla are 2 important brainstem nuclei, and they play pivotal roles in autonomic cardiovascular regulation. Angiotensin II is one of the neurotransmitters involved in the processing of the known that one of the mechanisms by which angiotensin II exerts cardiovascular reflexes within the brainstem. It is well- its effect is via the activation of pathways that generate reactive oxygen species （ROS）. In the central nervous system, ROS are reported to be involved in several pathological dis- eases such as hypertension, heart failure and sleep apnea. However, little is known about the role of ROS in the processing of the cardiovascular reflexes within the brainstem. The present review mainly discussed some recent findings documenting a role for ROS in the processing of the baroreflex and the peripheral chemoreflex in the brainstem.

延髓头端腹外侧区在电针预处理减轻心肌缺血再灌注损伤中的作用

ObjectiveTo observe the effects of pretreatment with electroacupuncture (EA) on neuron activity in the rostral ventrolateral medulla (RVLM) of rats with myocardial ischemia-reperfusion injury (MIRI) and explore the central regulatory mechanism of EA in attenuating MIRI.MethodsOf 72 SD rats, 12 were randomly allocated into the group of EA pretreatment + RVLM nucleus damage (EA + RVLM lesion group). The other 60 rats were randomized (20 rats each) into a sham-operation group, a model group, and an EA pretreatment group (EA group). Except for the rats in the sham-operation group, the models of MIRI were prepared by ligating the left anterior descending coronary artery in the model, EA, and EA + RVLM lesion groups. The rats of the EA group were intervened with EA at “Shénmén (神门HT7)” and “Tōnglĭ (通里HT5)”, 1 mA in current intensity and 2 Hz in frequency, for 20 min each time per day. Before modeling, the intervention was given for seven consecutive days. In the EA + RVLM lesion group, 3 weeks after microinjection with the neuronal apoptotic virus at bilateral RVLM, the same EA intervention as the EA group was provided. Afterward, the MIRI models were prepared. In the model group, no EA intervention was given. Using Powerlab electrophysiolograph, ST segment displacement value and arrhythmia score were recorded and analyzed before modeling, 30 min after ligation, and 120 min after reperfusion in each group. The concentration of cardiac troponin (cTnl) was detected with an ELISA assay kit. Using immunofluorescence staining, the expression level of c-fos protein of RVLM was detected in the sham-operation, model, and EA groups separately. Plexon multichannel acquisition processor was adopted to record the neuronal firing and field potential of RVLM in the sham-operation, model, and EA groups.ResultsST segment displacement value, arrhythmia score, and cTnl concentration 30 min after ligation and 120 min after reperfusion were all elevated in the model group compared to the sham-operation group (all P < 0.01). ST segment displacement value, arrhythmia score, and cTnl concentration were lower in the EA group compared to the model and EA + RVLM lesion groups (P < 0.01). Compared with the sham-operation group, the expression level of c-fos and the total firing frequency in RVLM were significantly higher in the model group (P < 0.01). However, the expression level of c-fos and the total firing frequency in RVLM were lower in the EA group compared with the model group (P < 0.01).ConclusionElectroacupuncture pretreatment may induce changes in c-fos protein expression and neuronal activity in RVLM to mitigate myocardial lesions. RVLM plays an important role in electroacupuncture pretreatment for alleviating MIRI.

Circuit-Specific Control of Blood Pressure by PNMT‑Expressing Nucleus Tractus Solitarii Neurons

The nucleus tractus solitarii(NTS)is one of the morphologically and functionally defined centers that engage in the autonomic regulation of cardiovascular activity.Phenotypically-characterized NTS neurons have been implicated in the differential regulation of blood pressure(BP).Here,we investigated whether phenylethanolamine N-methyltransferase(PNMT)-expressing NTS(NTS^(PNMT))neurons contribute to the control of BP.We demonstrate that photostimulation of NTS^(PNMT)neurons has variable effects on BP.A depressor response was produced during optogenetic stimulation of NTS^(PNMT)neurons projecting to the paraventricular nucleus of the hypothalamus,lateral parabrachial nucleus,and caudal ventrolateral medulla.Conversely,photostimulation of NTS^(PNMT)neurons projecting to the rostral ventrolateral medulla produced a robust pressor response and bradycardia.In addition,genetic ablation of both NTS^(PNMT)neurons and those projecting to the rostral ventrolateral medulla impaired the arterial baroreflex.Overall,we revealed the neuronal phenotype-and circuit-specific mechanisms underlying the contribution of NTS^(PNMT)neurons to the regulation of BP.