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KMID : 0358619930270020185
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Korean Journal of Physiology
1993 Volume.27 No. 2 p.185 ~ p.197
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To study the underlying mechanism through which the endothelium-dependent relaxation is inhibited by blocking the pump, the effects of pump blockade on the release of EDRF and its relaxing activity were examined, using organ bath study, bioassay technique, and cGMP measurement. Endothelium-dependent relaxation was attenuated by blocking the pump in the vascular ring with intact endothelium. In bioassay experiment EDRF release was decreased with the blockade of the pump in the EDRF donor strip. Endothelium-dependent increase of cGMP level was suppressed by inhibiting the pump in the test strips. The magnitude of relaxation of test strip which was induced by the perfusate that had passed through the EDRF donor strip was decreased with the blockade of the pump in the test strip. Therefore, it could be suggested that the attenuation of endothelium-dependent relaxation caused by inhibiting pump activity is due to both the decreased release of EDRF from endothelial cells and the decreased sensitivity of the smooth muscle cells to EDRF.
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Goo Yong-Sook
Kim Sang-Jeong
Kim Jun
Sung Ho-Kyung
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Abstract
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The rostral ventrolateral medulla (RVLM) includes vasopressor neurons, which transmit activation signals to the intermediolateral nucleus (IML) of the spinal cord, where the preganglionic sympathetic nucleus is located, to raise arterial blood pressure (BP). However, controversy exists as to the possible depressor area in the RVLM and the pathway involved. The present study persued evidence far the location of depressor neurons and the pathway by simultaneously observing changes in BP and the firing rate (FR) of cardiovascular neurons (CVNs) in the RVLM during the somatosympathetic reflex (SSR) elicited by peripheral nerve stimulation, since CVNs are known to contribute to the generation of the sympathetic nerve discharge. In 42 cats, anaesthetized with , single unit recording was performed, using carbon filament electrodes inserted into the RVLM, enabling estimation of the post R wave unit histogram (PR-UNlT) and the spike triggered average of sympathetic nerve discharge (STA-SND), allowing identification of CVNs. Antidromic stimulation of spinal segment was followed to determine whether the identified CVN projects axonal endings to the spinal cord (reticulospinal neuron). The sciatic nerve was electrically stimulated at (1 mA, 0.1 ms), 1 Hz and C-intensity (10 mA, 0.5 ms), 20 Hz to elicit the depressor, and pressor responses of the SSR, respectively. Simultaneous measurement of CVN firing rate was made. Experimental results are summarized as follows. 1) 20 out of 98 CVNs had axonal projections to the spinal cord and 17 out of 98 CVNs showed FR changes during SSR. 2) Response patterns of FR and BP during SSR were classified into 8 types. 3) These 8 different response patterns could be further classified into those from pressor and depressor neurons. These results demonstrate that some CVNs were identifiable as reticulospinal neurons responding to anti-dromic stimulation and that CVNs operating as depressor neurons as well as pressor neurons exist in the RVLM, both of which are involved with SSR mediation. Therefore, evidence was found that an independent depressor pathway might be involved in the mediation of SSR.
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KEYWORD
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Rostral ventrolateral medulla (RVLM), Cardiovascular neuron (CVN), Somatosympathetic reflex (SSR), Pressor neuron, and Depressor neuron
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