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541 results on '"Chen, Shao-Rui"'

101. Differential responses of regional sympathetic activity and blood flow to visceral afferent stimulation

Author

PAN, HUI-LIN, DEAL, DWIGHT D., XU, ZEMIN, and CHEN, SHAO-RUI

Subjects
Physiology -- Research, Blood flow -- Physiological aspects, Efferent pathways -- Research, Portal vein -- Research, Vascular resistance -- Physiological aspects, Biological sciences
Abstract

The sympathetic nervous system is essential for the cardiovascular responses to stimulation of visceral afferents. It remains unclear how the reflex-evoked sympathetic output is distributed to different vascular beds to initiate the hemodynamic changes. In the present study, we examined changes in regional sympathetic nerve activity and blood flows in anesthetized cats. Cardiovascular reflexes were induced by either electrical stimulation of the right splanchnic nerve or application of 10 [micro]g/ml of bradykinin to the gallbladder. Blood flows were measured using colored microspheres or the Transonic flow meter system. Sympathetic efferent activity was recorded from the left splanchnic, inferior cardiac, and tibial nerves. Stimulation of visceral afferents decreased significantly blood flows in the celiac (from 49 [+ or -] 4 to 25 [+ or -] 3 ml/min) and superior mesenteric (from 35 [+ or -] 4 to 23 [+ or -] 2 ml/min) arteries, and the vascular resistance in the splanchnic bed was profoundly increased. Consistently, stimulation of visceral afferents decreased tissue blood flows in the splanchnic organs. By contrast, activation of visceral afferents increased significantly blood flows in the coronary artery and portal vein but did not alter the vascular resistance of the femoral artery. Furthermore, stimulation of visceral afferents increased significantly sympathetic efferent activity in the splanchnic (182 [+ or -] 44%) but not in the inferior cardiac and tibial nerves. Therefore, this study provides substantial new evidence that stimulation of abdominal visceral afferents differentially induces sympathetic outflow to the splanchnic vascular bed. sympathetic efferent nerves; celiac ganglia; mesenteric blood flow; portal vein; splanchnic circulation; vascular resistance

Published
2001

102. Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning

Author

PAN, HUI-LIN, CHEN, SHAO-RUI, SCICLI, GLORIA M., and CARRETERO, OSCAR A.

Subjects
Bradykinin -- Physiological aspects, Ischemia -- Physiological aspects, ACE inhibitors -- Physiological aspects, Captopril -- Usage, Heart muscle -- Physiological aspects, Biological sciences
Abstract

Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning. Am J Physiol Heart Circ Physiol 279: H116-H121, 2000.--Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardium (14.4 [+ or -] 2.8 vs. 7.3 [+ or -] 1.7 ng/ml, P [is less than] 0.05) during 30 min of ischemia. In seven animals subjected to preconditioning, myocardial bradykinin release was potentiated significantly from 2.4 [+ or -] 0.6 ng/ml during the control period to 23.1 [+ or -] 2.5 ng/ml during 30 min of myocardial ischemia compared with the non-preconditioning group (from 2.7 [+ or -] 0.6 to 13.4 [+ or -] 1.9 ng/ml, P [is less than] 0.05, n = 6). Thus this study provides further evidence that transmural gradients of bradykinin are produced during ischemia. The results also suggest that ischemic preconditioning enhances bradykinin release in the myocardial interstitial fluid during subsequent ischemia, which is likely one of the mechanisms of cardioprotection of ischemic preconditioning. cardiac microdialysis; angiotensin-converting enzyme inhibitors; captopril; kinin receptors; myocardium

Published
2000

119. Resistance to Morphine Analgesic Tolerance in Rats Deleted of TRPV1-Expressing Sensory Neurons

Author

Chen, Shao-Rui, Prunean, Adrian, Pan, Hao-Min, Welker, Kelli L., and Pan, Hui-Lin

Subjects
Male, Pain Threshold, Morphine, Receptors, Opioid, mu, Down-Regulation, Nociceptors, Pain, TRPV Cation Channels, Drug Tolerance, Article, Rats, Receptors, G-Protein-Coupled, Analgesics, Opioid, Posterior Horn Cells, Rats, Sprague-Dawley, Nerve Degeneration, Animals, Neurons, Afferent, Diterpenes, Protein Kinase C
Abstract

Deletion of transient receptor potential vanilloid type 1 (TRPV1)-expressing afferent neurons reduces presynaptic mu opioid receptors but paradoxically potentiates the analgesic efficacy of mu opioid agonists. In this study, we determined if removal of TRPV1-expressing afferent neurons by resiniferatoxin (RTX), an ultrapotent capsaicin analog, influences the development of opioid analgesic tolerance. Morphine tolerance was induced by daily intrathecal injections of 10 microg of morphine for 14 consecutive days or by daily i.p. injections of 10 mg/kg of morphine for 10 days. In vehicle-treated rats, the effect of intrathecal or systemic morphine on the mechanical withdrawal threshold was gradually diminished within 7 days. However, the analgesic effect of intrathecal and systemic morphine was sustained in RTX-treated rats at the time the morphine effect was lost in the vehicle group. Furthermore, the mu opioid receptor-G protein coupling in the spinal cord was significantly decreased ( approximately 22%) in vehicle-treated morphine tolerant rats, but was not significantly altered in RTX-treated rats receiving the same treatment with morphine. Additionally, there was a large reduction in protein kinase Cgamma-immunoreactive afferent terminals in the spinal dorsal horn of RTX-treated rats. These findings suggest that loss of TRPV1-expressing sensory neurons attenuates the development of morphine analgesic tolerance possibly by reducing mu opioid receptor desensitization through protein kinase Cgamma in the spinal cord. These data also suggest that the function of presynaptic mu opioid receptors on TRPV1-expressing sensory neurons is particularly sensitive to down-regulation by mu opioid agonists during opioid tolerance development.

Published
2007

128. Signalling pathway of nitric oxide in synaptic GABA release in the rat paraventricular nucleus

Author

Li, De-Pei, Chen, Shao-Rui, Finnegan, Thomas F, and Pan, Hui-Lin

Subjects
Male, Patch-Clamp Techniques, Penicillamine, Excitatory Postsynaptic Potentials, Receptors, Cytoplasmic and Nuclear, Neural Inhibition, Nitric Oxide, Research Papers, Membrane Potentials, Rats, Rats, Sprague-Dawley, Soluble Guanylyl Cyclase, nervous system, Guanylate Cyclase, Synapses, Cyclic GMP-Dependent Protein Kinases, Animals, Calcium, Female, Nitric Oxide Donors, Calcium Channels, Cyclic GMP, gamma-Aminobutyric Acid, Paraventricular Hypothalamic Nucleus, Signal Transduction
Abstract

In the paraventricular nucleus (PVN) of the hypothalamus, nitric oxide (NO) inhibits sympathetic outflow through increased GABA release. However, the signal transduction pathways involved in its action remain unclear. In the present study, we determined the role of cGMP, soluble guanylyl cyclase, and protein kinase G in the potentiating effect of NO on synaptic GABA release to spinally projecting PVN neurones. The PVN neurones were retrogradely labelled by a fluorescent tracer injected into the thoracic spinal cord of rats. Whole-cell voltage-clamp recordings were performed on labelled PVN neurones in the hypothalamic slice. Bath application of the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), reproducibly increased the frequency of miniature GABAergic inhibitory postsynaptic currents (mIPSCs) without changing the amplitude and the decay time constant. Neither replacement of Ca2+ with Co2+ nor application of Cd2+ to block the Ca2+ channel altered the effect of SNAP on mIPSCs. Also, the effect of SNAP on mIPSCs was not significantly affected by thapsigargin, a Ca2+-ATPase inhibitor that depletes intracellular Ca2+ stores. Application of a membrane-permeant cGMP analogue, pCPT-cGMP, mimicked the effect of SNAP on mIPSCs in the presence of a phosphodiesterase inhibitor, IBMX. Furthermore, both the soluble guanylyl cyclase inhibitor, ODQ, and the specific protein kinase G inhibitor, Rp pCPT cGMP, abolished the effect of SNAP on mIPSCs. Thus, these data provide substantial new information that NO potentiates GABAergic synaptic inputs to spinally projecting PVN neurones through a cGMP-protein kinase G pathway.

Published
2003

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