PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 3966270

Sympathetic nerve activity: a link to stroke?

S M Mueller·W L Black
View original source ↗Export metadata ↓

Abstract

Spontaneously hypertensive rats (SHR) have been shown to have an increased capacity for superior cervical sympathetic nerve activity which may protect against stroke (Mueller et al: Stroke 13: 115, 1982). Sympathetic nerve activity has never been examined in the stroke-prone substrain of SHR (SP). In this study we measured superior cervical sympathetic nerve activity during rest and during a maximal sympathetic response in SHR, SP, and their normotensive controls, Wistar-Kyoto (WKY). The resting superior cervical sympathetic nerve activity of SP was significantly less than SHR (p less than 0.02) but not different from WKY. During central ischemia, used to induce maximal sympathetic response, the increase in SP sympathetic nerve activity was significantly less than SHR (p less than 0.001) but was not different from WKY. This diminished capacity for elevated superior cervical sympathetic nerve activity in stroke-prone SHR may relate to their increased predisposition to stroke because sympathetic hyperactivity cannot protect cerebral vessels during acute hypertension.

Explore related subjects

Adrenergic FibersAnimalsCerebrovascular DisordersDisease SusceptibilityHypertensionMaleRatsRats, Inbred SHRRats, Inbred WKYJournal ArticleResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S M Mueller, W L Black. Sympathetic nerve activity: a link to stroke?. https://doi.org/10.1161/01.str.16.1.73

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Exercise training-induced remodeling of paraventricular nucleus (nor)adrenergic innervation in normotensive and hypertensive rats.

Activation of oxytocin (OT)ergic projections from the hypothalamic paraventricular nucleus (PVN) to the nucleus tractus solitarii contributes to cardiovascular adjustments during exercise training (EXT). Moreover, a deficit in this central OTergic pathway is associated with altered cardiovascular function in hypertension. Since PVN catecholaminergic inputs, known to be activated during EXT, modulate PVN cardiovascular-related functions, we aimed here to determine whether remodeling of PVN (nor)adrenergic innervation occurs during EXT and whether this phenomenon is affected by hypertension. Confocal immunofluorescence microscopy and tract tracing were used to quantify changes in (nor)adrenergic innervation density in PVN subnuclei and in identified dorsal vagal complex (DVC) projecting neurons (PVN-DVC) in EXT normotensive [Wistar-Kyoto rat (WKY)] and hypertensive [spontaneously hypertensive rat (SHR)] rats. In WKY, EXT increased the density of PVN dopamine beta-hydroxylase immunoreactivity (DBHir) (160%). Furthermore, the number and density of DBHir boutons overlapping PVN-DVC OTergic neurons were also increased during EXT (130%), effects that were blunted in SHR. Conversely, while DBHir in the medial parvocellular subnucleus (an area enriched in corticotropin-releasing hormone neurons) was not changed by EXT in WKY, a diminished DBHir was observed in trained SHR. Overall, these data support the concept that the PVN (nor)adrenergic innervation undergoes plastic remodeling during EXT, an effect that is differentially affected during hypertension. The functional implications of PVN (nor)adrenergic remodeling in relation to the central peptidergic control of cardiovascular function during EXT are discussed.

Adrenergic Fibers↗
PubMed2007

Central command regulation of circulatory function mediated by descending pontine cholinergic inputs to sympathoexcitatory rostral ventrolateral medulla neurons.

Central command is a feedforward neural mechanism that evokes parallel modifications of motor and cardiovascular function during arousal and exercise. The neural circuitry involved has not been elucidated. We have identified a cholinergic neural circuit that, when activated, mimics effects on tonic and reflex control of circulation similar to those evoked at the onset of and during exercise. Central muscarinic cholinergic receptor (mAChR) activation increased splanchnic sympathetic nerve activity (SNA) as well as the range and gain of the sympathetic baroreflex via activation of mAChR in the rostral ventrolateral medulla (RVLM) in anesthetized artificially ventilated Sprague-Dawley rats. RVLM mAChR activation also attenuated and inhibited the peripheral chemoreflex and somatosympathetic reflex, respectively. Cholinergic terminals made close appositions with a subpopulation of sympathoexcitatory RVLM neurons containing either preproenkephalin mRNA or tyrosine hydroxylase immunoreactivity. M2 and M3 receptor mRNA was present postsynaptically in only non-tyrosine hydroxylase neurons. Cholinergic inputs to the RVLM arise only from the pedunculopontine tegmental nucleus. Chemical activation of this region produced increases in muscle activity, SNA, and blood pressure and enhanced the SNA baroreflex; the latter effect was attenuated by mAChR blockade. These findings indicate a novel role for cholinergic input from the pedunculopontine tegmental nucleus to the RVLM in central cardiovascular command. This pathway is likely to be important during exercise where a centrally evoked facilitation of baroreflex control of the circulation is required to maintain blood flow to active muscle.

Adrenergic Fibers↗