Sympathetic nerves protect against blood-brain barrier disruption in the spontaneously hypertensive rat.

Mueller, Shirley M.; Ertel, Phillip J.; Felten, David L.; Overhage, J. Marc

doi:10.1161/01.str.13.1.83

Cited by 27 publications

(14 citation statements)

References 17 publications

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“…In addition, attenuation of medial hypertrophy in spontaneously hypertensive and stroke-prone spontaneously hypertensive rats increased the susceptibility of the BBB to disruption during acute hypertension. 13,14 Therefore, it appears that hypertension-induced cerebral artery hypertrophy can stiffen the vascular wall, making cerebral arteries more resistant to forced dilatation during acute hypertension, thereby protecting the BBB. 5,6 Cerebral arteries can also undergo eutrophic remodeling in response to chronic hypertension, defined as a decrease in external and internal diameter such that cross-sectional area does not change.…”

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Pregnancy Prevents Hypertensive Remodeling of Cerebral Arteries

2006

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Abstract-We investigated how hypertension during pregnancy affected passive structural (wall:lumen, wall stress) and active (myogenic activity) responses of the cerebral circulation. Female nonpregnant (NP; nϭ8) Sprague Dawley rats were compared with late-pregnant (LP; day 19 to 20, nϭ6) rats. Some animals were treated with the NO synthase inhibitor nitro-L-arginine in their drinking water to raise blood pressure. LP rats (nϭ6) were treated for the last 7 days of pregnancy (last trimester) to mimic preeclampsia and compared with NP rats treated for the same duration (nϭ8). Active and passive responses were determined on isolated and pressurized third-order posterior cerebral arteries. Nitro-L-arginine treatment significantly raised blood pressure in both groups of animals that was associated with increased wall thickness and wall:lumen ratio in the NP hypertensive animals versus controls (PϽ0.05). In contrast, this response to pressure was absent in LP animals, which had similar wall measurements. In addition, arteries from NP hypertensive animals had increased myogenic tone and pressure of forced dilatation compared with NP control animals (PϽ0.01). Again, this response was lacking in the LP hypertensive animals that had similar tone and pressure of forced dilatation as normotensive controls. The increased tone and wall thickness decreased wall stress in the NP hypertensive animals, a response that did not occur in LP hypertensive animals. Because medial hypertrophy is considered a protective response to elevated blood pressure, these results suggest that hypertension in pregnancy may predispose the cerebral circulation to autoregulatory breakthrough and blood-brain-barrier disruption when blood pressure is elevated, as during eclampsia. Key Words: hypertension, pregnancy Ⅲ cerebral arteries Ⅲ pregnancy Ⅲ eclampsia Ⅲ hypertrophy T he neurological complications of eclampsia are thought to be similar to hypertensive encephalopathy in which an acute, excessive elevation in pressure causes forced dilatation of cerebral artery myogenic tone, autoregulatory breakthrough, and edema formation. 1-3 Our previous work demonstrated that normal pregnancy may predispose the brain to eclampsia by lowering the pressure at which forced dilatation of cerebral arteries occurs. 4 Whereas this effect may not be consequential if mean arterial pressure remains within the normal autoregulatory pressure range, it may cause bloodbrain barrier (BBB) disruption and edema formation if pressure is elevated, as during hypertension in pregnancy and preeclampsia/eclampsia.It is now established that chronic hypertension is associated with medial hypertrophy of both large and small cerebral arteries that increases the wall:lumen ratio. [5][6][7][8][9] This response of the cerebrovascular smooth muscle to chronically elevated blood pressure is considered to be an important protective function. 6 Several studies have shown that spontaneously hypertensive rats 10,11 and stroke-prone spontaneously hypertensive rats 12 were less susceptible to BBB di...

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Pregnancy Prevents Hypertensive Remodeling of Cerebral Arteries

2006

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“…10 It has been suggested that this long term effect is due to a "trophic" influence on smooth muscle proliferation in the vessel wall.…”

Section: Discussionmentioning

confidence: 99%

“…An elevated sympathetic nerve activity to the cerebral vessels in SHR may be protective against stroke both acutely 8 -9 and chronically. 10 -" One can conjecture that alterations in superior cervical sympathetic nerve activity, possibly genetic in origin, may contribute to stroke in selected hypertensive individuals.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic nerve activity: a link to stroke?

Mueller¹,

Black²

1985

Stroke

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73ac output in unanesthetized rats. J Appl Physiol 30: [879][880][881][882][883][884] 1971 9. Pannier JL, Leusen I: Circulation to the brain of the rat during acute and prolonged respiratory changes in the acid-base balance. SUMMARY 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 < 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 < 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. Stroke Vol 16, No 1, 1985 HYPERTENSION is among the important risk factors for stroke. However, it is seldom clear why one hypertensive individual has a stroke and another does not. Study of animal models analogous to human essential hypertension, the spontaneously hypertensive rat, (SHR), and the substrain of the SHR that is susceptible to stroke as well as hypertension, stroke-prone SHR (SP), could contribute to our understanding in this regard.Some authors 1 -2 have demonstrated elevated sympathetic nerve activity in the lumbar and renal nerves of the spontaneously hypertensive rat which they believed contributed to the development and maintenance of hypertension. Ikeda, et al,3 carried this concept further and postulated that if elevated superior cervical sympathetic nerve activity was present in the stroke-prone strain of SHR, decreased cerebral blood flow might result leading to cerebral ischemia and an From the

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“…We used the same experimental protocol that we used in our previous study. 1 Profound cerebral vasodilation was induced with acute hypertension (norepinephrine) and seizures (bicuculline). We hypothesized that if a reduction in SHR intraparenchymal cerebral vessel wall thickness was present after chronic denervation, it would lead to a significantly enhanced wall tension (tension = pressure X radius/wall thickness) 2 as blood pressure and vessel radius were increased.…”

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“…1 A possible "trophic" influence of sympathetic nerves on cerebral vessels of adult SHR with established hypertension has not been examined. Thus, the purpose of this study was to determine the effect of chronic sympathetic denervation on cerebral vessels of SHR when superior cervical ganglionectomy was performed in adulthood rather than adolescence.…”

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The chronic influence of sympathetic nerves on cerebral vessels is age-related.

Mueller¹,

Ertel²,

Felten³

et al. 1983

Stroke

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SUMMARY The purpose of this study was to determine the effect of chronic sympathetic denervation on cerebral vessels of the spontaneously hypertensive rat when superior cervical ganglionectomy was performed in adulthood. In a previous study, we have demonstrated increased protein transfer across the cerebral vessels of the chronically denervated hemisphere when superior cervical ganglionectomy was performed in adolescent spontaneously hypertensive rats. After four weeks of sympathetic denervation, the adult rats in this study did not demonstrate increased protein transfer in the denervated compared to the innervated cerebral hemisphere. Thus, the "trophic" effect of sympathetic nerves on cerebral vessels appears to be age-related.Stroke, Vol 14, No 2, 1983 WE HAVE PREVIOUSLY demonstrated a "trophic" influence of sympathetic nerves on the cerebral vasculature of spontaneously hypertensive rats (SHR) during the development of hypertension. 1 A possible "trophic" influence of sympathetic nerves on cerebral vessels of adult SHR with established hypertension has not been examined. Thus, the purpose of this study was to determine the effect of chronic sympathetic denervation on cerebral vessels of SHR when superior cervical ganglionectomy was performed in adulthood rather than adolescence. We used the same experimental protocol that we used in our previous study.1 Profound cerebral vasodilation was induced with acute hypertension (norepinephrine) and seizures (bicuculline). We hypothesized that if a reduction in SHR intraparenchymal cerebral vessel wall thickness was present after chronic denervation, it would lead to a significantly enhanced wall tension (tension = pressure X radius/wall thickness) 2 as blood pressure and vessel radius were increased. Enhanced blood-brain barrier (BBB) permeability, proportional to vessel wall tension, 3 would be expected to occur. We determined protein permeability in the cerebral hemispheres and temporalis muscle of SHR four weeks after unilateral superior cervical ganglionectomy performed in nine to 19 week old young adult animals. The tissue with normal chronic innervation served as a control for the contralateral denervated tissue. Successful sympathetic denervation was demonstrated by using a histofluorescence technique. radioiodinated albumin was used to determine quantitative protein transfer in 11 of these rats. Successful sympathetic denervation was demonstrated in another three rats by a histofluorescence technique. 4Denervation Unilateral cervical ganglionectomies were performed alternately on the right and left side so that half of the animals had a right superior cervical ganglionectomy and the other half had a left superior cervical ganglionectomy. The ganglionectomy produced ptosis and enophthalmous on the side ipsilateral to the ganglionectomy in all rats indicating a functionally successful sympathetic denervation.In order to objectively demonstrate the presence or absence of vascular sympathetic innervation, we used the sucrose-phosphate-glyoxylic acid (SPG) his...

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Sympathetic nerves protect against blood-brain barrier disruption in the spontaneously hypertensive rat.

Cited by 27 publications

References 17 publications

Pregnancy Prevents Hypertensive Remodeling of Cerebral Arteries

Pregnancy Prevents Hypertensive Remodeling of Cerebral Arteries

Sympathetic nerve activity: a link to stroke?

The chronic influence of sympathetic nerves on cerebral vessels is age-related.

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