Differentiated hemodynamic changes controlled by splanchnic nerve

Sato, Mônica Akemi; Morrison, Shaun F.; Lopes, Oswaldo Ubrı́aco; Colombari, Eduardo

doi:10.1016/j.autneu.2006.01.017

Cited by 7 publications

(5 citation statements)

References 18 publications

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“…Overactivity of renal sympathetic nerve is considered a major cause of the pathophysiology of hypertension [26, 27]. The splanchnic nerve is thought to influence the regulation of a number of basic functions, such as arterial blood pressure, heart rate, vascular tone [28]. Nerve discharge for three age groups of F344 rats were compared (young (3.3 months), mature (12.6 months), and senescent (24 months)).…”

Section: Discussion Of Specific Organs and Organ Systemsmentioning

confidence: 99%

Thresholds for thermal damage to normal tissues: An update

Yarmolenko

Moon

Landon

et al. 2011

International Journal of Hyperthermia

565

474

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The purpose of this review is to summarise a literature survey on thermal thresholds for tissue damage. This review covers published literature for the consecutive years from 2002–2009. The first review on this subject was published in 2003. It included an extensive discussion of how to use thermal dosimetric principles to normalise all time-temperature data histories to a common format. This review utilises those same principles to address sensitivity of a variety of tissues, but with particular emphasis on brain and testis. The review includes new data on tissues that were not included in the original review. Several important observations have come from this review. First, a large proportion of the papers examined for this review were discarded because time–temperature history at the site of thermal damage assessment was not recorded. It is strongly recommended that future research on this subject include such data. Second, very little data is available examining chronic consequences of thermal exposure. On a related point, the time of assessment of damage after exposure is critically important for assessing whether damage is transient or permanent. Additionally, virtually no data are available for repeated thermal exposures which may occur in certain recreational or occupational activities. For purposes of regulatory guidelines, both acute and lasting effects of thermal damage should be considered.

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Section: Discussion Of Specific Organs and Organ Systemsmentioning

confidence: 99%

Thresholds for thermal damage to normal tissues: An update

Yarmolenko

Moon

Landon

et al. 2011

International Journal of Hyperthermia

565

474

View full text Add to dashboard Cite

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“…Electrical stimulation of the splanchnic nerve causes mesenteric vasoconstriction and simultaneous hindquarter vasodilatation. Hindquarter vasodilation was abolished after intravenous administration of L-NAME, suggesting that nitric oxide mediates this response [47]. Nitric oxide containing factors are also thought to mediate the hindlimb vasodilation evoked by electrical stimulation of the superior laryngeal nerve in rats [48].…”

Section: Discussionmentioning

confidence: 99%

Swimming Exercise Changes Hemodynamic Responses Evoked by Blockade of Excitatory Amino Receptors in the Rostral Ventrolateral Medulla in Spontaneously Hypertensive Rats

Ogihara

Schoorlemmer

Lazari

et al. 2014

BioMed Research International

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Exercise training reduces sympathetic activity in hypertensive humans and rats. We hypothesized that the swimming exercise would change the neurotransmission in the rostral ventrolateral medulla (RVLM), a key region involved in sympathetic outflow, and hemodynamic control in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Bilateral injections of kynurenic acid (KYN) were carried out in the RVLM in sedentary- (S-) or exercised- (E-) SHR and WKY rats submitted to swimming for 6 weeks. Rats were α-chloralose anesthetized and artificially ventilated, with Doppler flow probes around the lower abdominal aorta and superior mesenteric artery. Injections into the RVLM were made before and after i.v. L-NAME (nitric oxide synthase, NOS, inhibitor). Injections of KYN into the RVLM elicited a major vasodilation in the hindlimb more than in the mesenteric artery in E-SHR compared to S-SHR, but similar decrease in arterial pressure was observed in both groups. Injections of KYN into the RVLM after i.v. L-NAME attenuated the hindlimb vasodilation evoked by KYN and increased the mesenteric vasodilation in E-SHR. Swimming exercise can enhance the hindlimb vasodilation mediated by peripheral NO release, reducing the activation of neurons with EAA receptors in the RVLM in SHR.

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“…In contrast, rat models of salt-sensitive neurogenic hypertension did not benefit from renal denervation - in these models, the splanchnic sympathetic nerves were a better therapeutic target ( Osborn and Kuroki, 2012 ). However, stimulation of the postganglionic splanchnic nerves has been shown to produce both mesenteric vasoconstriction and hindquarter vasodilation ( Sato et al, 2006 ). Before selective denervation and manipulation of sympathetic nerves can become a mainstream therapeutic strategy, it will be critical to elucidate these nuanced mechanisms of differential sympathetic nerve control.…”

Section: Discussionmentioning

confidence: 99%

Revisiting differential control of sympathetic outflow by the rostral ventrolateral medulla

2023

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The rostral ventrolateral medulla (RVLM) is an important brain region involved in both resting and reflex regulation of the sympathetic nervous system. Anatomical evidence suggests that as a bilateral structure, each RVLM innervates sympathetic preganglionic neurons on both sides of the spinal cord. However, the functional importance of ipsilateral versus contralateral projections from the RVLM is lacking. Similarly, during hypotension, the RVLM is believed to rely primarily on withdrawal of tonic gamma aminobutyric acid (GABA) inhibition to increase sympathetic outflow but whether GABA withdrawal mediates increased activity of functionally different sympathetic nerves is unknown. We sought to test the hypothesis that activation of the ipsilateral versus contralateral RVLM produces differential increases in splanchnic versus adrenal sympathetic nerve activities, as representative examples of functionally different sympathetic nerves. We also tested whether GABA withdrawal is responsible for hypotension-induced increases in splanchnic and adrenal sympathetic nerve activity. To test our hypothesis, we measured splanchnic and adrenal sympathetic nerve activity simultaneously in Inactin-anesthetized, male Sprague-Dawley rats during ipsilateral or contralateral glutamatergic activation of the RVLM. We also produced hypotension (sodium nitroprusside, i.v.) before and after bilateral blockade of GABAA receptors in the RVLM (bicuculline, 5 mM 90 nL). Glutamate (100 mM, 30 nL) injected into the ipsilateral or contralateral RVLM produced equivalent increases in splanchnic sympathetic nerve activity, but increased adrenal sympathetic nerve activity by more than double with ipsilateral injections versus contralateral injections (p < 0.05; n = 6). In response to hypotension, increases in adrenal sympathetic nerve activity were similar after bicuculline (p > 0.05), but splanchnic sympathetic nerve activity responses were eliminated (p < 0.05; n = 5). These results provide the first functional evidence that the RVLM has predominantly ipsilateral innervation of adrenal nerves. In addition, baroreflex-mediated increases in splanchnic but not adrenal sympathetic nerve activity are mediated by GABAA receptors in the RVLM. Our studies provide a deeper understanding of neural control of sympathetic regulation and insight towards novel treatments for cardiovascular disease involving sympathetic nervous system dysregulation.

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Differentiated hemodynamic changes controlled by splanchnic nerve

Cited by 7 publications

References 18 publications

Thresholds for thermal damage to normal tissues: An update

Thresholds for thermal damage to normal tissues: An update

Swimming Exercise Changes Hemodynamic Responses Evoked by Blockade of Excitatory Amino Receptors in the Rostral Ventrolateral Medulla in Spontaneously Hypertensive Rats

Revisiting differential control of sympathetic outflow by the rostral ventrolateral medulla

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