• The Korean Journal of Physiology and Pharmacology
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• v.17 no.4
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• pp.367-373
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• 2013

Contribution of the vestibular end organ to regulation of arterial pressure was quantitatively compared with the role of baroreceptors in terms of baroreflex sensitivity and c-Fos protein expression in the rostral ventrolateral medulla (RVLM). Baroreflex sensitivity and c-Fos protein expression in the RVLM were measured in conscious rats that had undergone bilateral labyrinthectomy (BL) and/or baroreceptor unloading. BL attenuated baroreflex sensitivity during intravenous infusion of sodium nitroprusside (SNP), but did not significantly affect the sensitivity following infusion of phenylephrine (PE). Baroreflex sensitivity became positive following sinoaortic denervation (SAD) during infusion of PE and attenuated sensitivity during infusion of SNP. Baroreflex sensitivity also became positive following double ablation (BL+SAD) during infusion of PE, and attenuated sensitivity during infusion of SNP. c-Fos protein expression increased significantly in the RVLM in the sham group after SNP administration. However, the BL, SAD, and SAD+BL groups showed significant decreases in c-Fos protein expression compared with that in the sham group. The SAD group showed more reduced c-Fos protein expression than that in the BL group, and the SAD+BL group showed less expression than that in the SAD group. These results suggest that the vestibular system cooperates with baroreceptors to maintain arterial pressure during hypotension but that baroreceptors regulate arterial pressure during both hypotension and hypertension. Additionally, afferent signals for maintaining blood pressure from the vestibular end organs and the baroreceptors may be integrated in the RVLM.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.181-194
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• 1990

Antidromically activated spinoreticular tract (SRT) cell units in the lumbosacral enlargement of ${\alpha}-chloralose$ anesthetized cats were classified as medial and lateral SRT units according to the location of their axonal termination. Identified SRT units were tested fer antidromic conduction velocity, laterality of their axonal projection, the location in spinal gray, peripheral receptive field, the response pattern to graded mechanichal stimulation and the responsiveness to $A{\delta}$ and C volley of the peripheral nerve. 1) The 59% of 34 medial SRT units were recorded in ipsilateral side to the antidromic stimulation site, but 60% of the 47 lateral SRT units projected to contralateral side. 2) Most of the medial SRT cells and rostral ventrolateral medulla (RVLM)-projecting lateral SRT cells were recorded in lamina VII & VIII. The LRN (lateral reticular nucleus)-projecting SRT cells, however, distributed through all the laminae except superficial ones (I & II). 3) The identified SRT units were classified as low theshold (LT), deep, high threshold (HT), wide dynamic range (WDR) cells, based on the response patterns to graded mechanical stimuli. The proportion of SRT units which receive noxious input was 37.5%, 25% and 75% in the medial, LRN-projecting and RVLM SRT group, respectively. 4) There was no significant difference in the mean conduction velocities between the 3 groups. But the deep cells had significantly higher velocity than that of the HT cells. The above results show that the peripheral inputs to the SRT units are different in the 3 groups: medial, LRN & RVLM SRT group. Especially in case of the SRT cells projecting to RVLM which is a probable candidate fur the integration center of various pressor reflexes such as somatosympathetic reflex, the noxious informations occupy higher proportion of input to them than in other groups. Therefore the noxious information transmitted through the lateral SRT destined for RVLM is expected to play a role in somatosymapthetic reflex.

• Journal of Biomedical Engineering Research
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• v.17 no.1
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• pp.71-80
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• 1996

A number of experimental evidences suggest that the rnun ventrolateral medulla(RVLM) is the final common pathway in the regulation of arterial blood pressure. A Voup of neurons in the RVLM, called the cardiovascular neurons (UN), show spontaneous activity temporally synchronized with the periodic cardiac cycle. These neurons affect the sympathetic nerve discharge(SND), thus are believed to be responsible for blood pressure control. The present experiment identified 98 UVNs in 42 cats based on the temporal relationships between each neuron's activity with both the cardiac cycle and SWD. In 20 UWL changes of spontaneous firing rate(FR) during the somatosympathetic reflex(SSR) were studied Five different firing patterns were observed during the pressor and depressor responses of SSR, implying that they form an interconnected neuronal circuit interacting with one another to generate efferent signals for blood pressure regulation. In the following companion paper, the firing patterns of CVN are analyzed to develop a minimal neuronal circuit model explaining the present experimental outcome.

• The Korean Journal of Physiology and Pharmacology
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• v.6 no.3
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• pp.149-154
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• 2002

The blood pressure (BP) is regulated by the nervous system and humoral factors, such as renin- angiotensin system, vasopressin and others. In the present study, we examined the central effects of glutamate and GABA on the cardiovascular regulation by injection of these substances into the lateral ventricle and also investigated the relationship between these central effects and the action of angiotensin II (Ang). Male Sprague Dawley rats, $350{\sim}400$ g, were anesthetized with urethane and instrumented with an arterial catheter for direct measurement of BP and heart rate (HR), and an guide cannula in the lateral ventricle for drug injection. A glass microelectode was inserted into the rostral ventrolateral medulla (RVLM) for recording single unit spikes. Barosensitive neurons were identified by changes of single unit spikes in RVLM following intravenous injection of nitroprusside and phenylephrine. The effects of GABA and glutamate injected into the lateral ventricle were studied in single neuronal activity of the RVLM in addition to changes in BP and heart rate, and compared the results before and after treatment with intravenous losartan, nonpeptide Ang II-type 1 receptor antagonist (1 mg/100 g BW). Intracerebroventricular administration of GABA decreased systolic blood pressure (SBP) and HR, but increased the firing rates in the RVLM. However, intracerebroventricular glutamate injection produced effects opposite to GABA. After pretreatment of intravenous losartan, the central effects of GABA on BP and firing rate in the RVLM were significantly attenuated and that of glutamate showed a tendency of attenuation. These results suggested that central GABA and glutamate regulated BP and firing rates in RVLM were inversely related to BP change. The central effects of GABA or glutamate on the autonomic nervous function were modulated by humoral factor, Ang II, by maintaining BP.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.133-141
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• 1994

The discharge patterns and peripheral nerve inputs to cardiovascular neurons were investigated in rostral ventrolateral medulla (RVLM) and raphe nucleus of cats. The data from the two were compared to determine their roles in cardiovascular regulation and the endogenous analgesic system. Animals were anesthetized with ${\alpha}-chloralose$ and single cell activities were recorded by carbon-filament microelectrode and their relationships with cardiovascular activity were analyzed. In RVLM area, a total of thirty-three cells were identified as cardiovascular neurons. During one cardiac cycle, the mean discharge rate of the neurons was $1.96{\pm}0.29$ and the peak activity was observed 45 ms after the systolic peak of arterial blood pressure. Thirteen cells could be activated antidromically by stimulation of the the $T_2$ intermediolateral nucleus. Forty-three raphe neurons were identified as cardiovascular neurons whose mean discharge rate during one cardiac cycle was $1.02{\pm}0.12$. None of these cells could be activated antidromically. Study of the interval time histogram of RVLM neurons revealed that the time to the first peak was $128{\pm}20.0\;ms$, being shorter than the period of a cardiac cycle. The same parameter found from the raphe neurons was $481{\pm}67.2\;ms$, which was much longer than the cardiac cycle length. Of seventeen RVLM neurons examined ten received only the peripheral $A{\delta}-afferent$ inputs, whereas six RVLM neurons received both $A{\delta}-$ and C-inputs; the remaining one cell received an inhibitory peripheral C-input. In contrast, nine of eleven raphe neurons were found to receive $A{\delta}-inputs$ only. We conclude that the main output of cardiovascular regulatory influences are mediated through the RVLM neurons. The cardiovascular neurons in the raphe nucleus appear to serve as interneurons transferring cardiovascular afferent information to the raphespinal neurons mediating the endogenous analgesic mechanisms.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.6
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• pp.675-686
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• 2017

Orthostatic hypotension (OH) is associated with symptoms including headache, dizziness, and syncope. The incidence of OH increases with age. Attenuation of the vestibulosympathetic reflex (VSR) is also associated with an increased incidence of OH. In order to understand the pathophysiology of OH, we investigated the physiological characteristics of the VSR in the disorder. We applied sodium nitroprusside (SNP) to conscious rats with sinoaortic denervation in order to induce hypotension. Expression of pERK in the intermediolateral cell column (IMC) of the T4~7 thoracic spinal regions, blood epinephrine levels, and blood pressure were evaluated following the administration of glutamate and/or SNP. SNP-induced hypotension led to increased pERK expression in the medial vestibular nucleus (MVN), rostral ventrolateral medullary nucleus (RVLM) and the IMC, as well as increased blood epinephrine levels. We co-administered either a glutamate receptor agonist or a glutamate receptor antagonist to the MVN or the RVLM. The administration of the glutamate receptor agonists, AMPA or NMDA, to the MVN or RVLM led to elevated blood pressure, increased pERK expression in the IMC, and increased blood epinephrine levels. Administration of the glutamate receptor antagonists, CNQX or MK801, to the MVN or RVLM attenuated the increased pERK expression and blood epinephrine levels caused by SNP-induced hypotension. These results suggest that two components of the pathway which maintains blood pressure are involved in the VSR induced by SNP. These are the neurogenic control of blood pressure via the RVLM and the humoral control of blood pressure via epinephrine release from the adrenal medulla.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.2
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• pp.121-125
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• 2013

The purpose of this study is to investigate the antinociceptive effects of ginsenosides on toothache. c-Fos immunoreactive (IR) neurons were examined after noxious intrapulpal stimulation (NS) by intrapulpal injection of 2 M KCl into upper and lower incisor pulps exposed by bone cutter in Sprague Dawley rats. The number of Fos-IR neurons was increased in the trigeminal subnucleus caudalis (Vc) and the transitional region between Vc and subnucleus interpolaris (Vi) by NS to tooth. The intradental NS raised arterial blood pressure (BP) and heart rate (HR). The number of Fos-IR neurons was also enhanced in thalamic ventral posteromedial nucleus (VPMN) and centrolateral nucleus (CLN) by NS to tooth. The intradental NS increased the number of Fos-IR neurons in the nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM), hypothalamic supraoptic nucleus (SON) and paraventricular nucleus (PVN), central cardiovascular regulation centers. Ginsenosides reduced the number of c-Fos-IR increased by NS to tooth in the trigeminal Vc and thalamic VPMN and CLN. Naloxone, an opioid antagonist, did not block the effect of ginsenoside on the number of Fos-IR neurons enhanced by NS to tooth in the trigeminal Vc and thalamic VPMN and CLN. Ginsenosides ameliorated arterial BP and HR raised by NS to tooth and reduced the number of Fos-IR neurons increased by NS to tooth in the NTS, RVLM, hypothalamic SON, and PVN. These results suggest that ginsenosides have an antinociceptive effect on toothache through non-opioid system and attenuates BP and HR increased by NS to tooth.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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• pp.89-94
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• 2004

The arterial pressure is regulated by the nervous and humoral mechanisms. The neuronal regulation is mostly carried out by the autonomic nervous system through the rostral ventrolateral medulla (RVLM), a key area for the cardiovascular regulation, and the humoral regulation is mediated by a number of substances, including the angiotensin (Ang) II and vasopressin. Recent studies suggest that central interleukin-1 (IL-1) activates the sympathetic nervous system and produces hypertension. The present study was undertaken to elucidate whether IL-1 and Ang II interact in the regulation of cardiovascular responses to the stress of hemorrhage. Thus, Sprague-Dawley rats were anesthetized and both femoral arteries were cannulated for direct measurement of arterial pressure and heart rate (HR) and for inducing hemorrhage. A guide cannula was placed into the lateral ventricle for injection of IL-1 $(0.1,\;1,\;10,\;20\;ng/2\;{\mu}l)$ or Ang II $(600\;ng/10\;{\mu}l)$. A glass microelectrode was inserted into the RVLM to record the single unit spike potential. Barosensitive neurons were identified by an increased number of single unit spikes in RVLM following intravenous injection of nitroprusside. I.c.v. $IL-1\;{\beta}$ increased mean arterial pressure (MAP) in a dose-dependent fashion, but HR in a dose-independent pattern. The baroreceptor reflex sensitivity was not affected by i.c.v. $IL-1\;{\beta}$. Both i.c.v. $IL-1\;{\alpha}\;and\;{\beta}$ produced similar increase in MAP and HR. When hemorrhage was induced after i.c.v. injection of $IL-1\;{\beta}$, the magnitude of MAP fall was not different from the control. The $IL-1\;{\beta}$ group showed a smaller decrease in HR and a lower spike potential count in RVLM than the control. MAP fall in response to hemorrhage after i.c.v. injection of Ang II was not different from the control. When both IL-1 and Ang II were simultaneously injected i.c.v., however, MAP fall was significantly smaller than the control, and HR was increased rather than decreased. These data suggest that IL-1, a defense immune mediator, manifests a hypertensive action in the central nervous system and attenuates the hypotensive response to hemorrhage by interaction with Ang II.