Eclamptic Plasma Stimulates Norepinephrine Release in Cultured Sympathetic Nerve

Khatun, Selina; Kanayama, Naohiro; Sato, Eiji; Belayet, Hossain Md; Kobayashi, Takao; Terao, Toshihiko

doi:10.1161/01.hyp.31.6.1343

Cited by 15 publications

(14 citation statements)

References 30 publications

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“…13,14 Recently, we demonstrated that plasma from eclamptic and pre-eclamptic women stimulates the NE release in cultured sympathetic neuron and bupivacaine blunted the increase NE level that have been seen in stimulation with eclamptic and preeclamptic plasma. 15 Considering the recent reports and current results, we suggest that vasoconstriction induced by the sympathetic nerve may play a causative role in pre-eclampsia, and to relieve this condition, long-term epidural anaesthesia is very effective.…”

Section: Discussionmentioning

confidence: 71%

“…13,14 Recently we reported that eclamptic and pre-eclamptic plasma has an excitotoxic effect on the sympathetic nerve via axoplasmic membrane depolarisation, thus increasing noradrenaline secretion that is blocked by bupivacaine. 15 Lumbar epidural anaesthesia, which blocks the abdominal sympathetic nerve, improves hypertension and biochemical parameters during pre-eclamptic labour. [16][17][18] Thus, epidural anaesthesia has been recommended by many authors as the analgesic method of choice in preeclamptic labour.…”

Section: Introductionmentioning

confidence: 99%

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A new treatment of severe pre-eclampsia by long-term epidural anaesthesia

et al. 1999

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We hypothesised that long term epidural anaesthesia suppresses sympathetic overactivity in pre-eclampsia. Two equal groups of severe pre-eclamptic patients were treated either with long-term epidural anaesthesia (epidural group) or bed rest, diet control, and an antihypertensive drug (control group). After 7 days of epidural block, mean arterial blood pressures decreased, platelet count and serum total protein increased in all cases while proteinuria decreased in four cases. All patients treated with a long-term epidural therapy continued their pregnancies for more than 3 weeks after admission. The infants in the epidural group had 1-min Apgar scores above 8, a body weight of 2240 ± 310 g (mean ± s.d.) and

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

A new treatment of severe pre-eclampsia by long-term epidural anaesthesia

et al. 1999

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“…The postganglionic sympathetic nerve activity in skeletal muscle blood vessels is more than three times as high in preeclamptic as in normotensive pregnant women (104). Stimulation of sympathetic neurons with plasma from eclamptic and preeclamptic women significantly increases norepinephrine release, but whether this is mediated through ANG II has not been defined (63). ANG II-mediated experimental hypertension in the nonpregnant state is associated with a marked increase in vascular smooth muscle immunostaining for endothelin, and blockade of the endothelin receptor ET A corrects the vasoconstrictor hyperresponsiveness (96).…”

Section: Vasomotor Events and Vascular-endothelial Dysfunctionmentioning

confidence: 99%

Role of the renin-angiotensin system in the pathogenesis of preeclampsia

Shah

2005

American Journal of Physiology-Renal Physiology

129

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Shah, Dinesh M. Role of the renin-angiotensin system in the pathogenesis of preeclampsia. Am J Physiol Renal Physiol 288: F614 -F625, 2005; doi:10.1152/ ajprenal.00410.2003.-Preeclampsia is a hypertensive disorder unique to pregnancy with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression observed both in human preeclampsia and in a transgenic mouse model with a human preeclampsia-like syndrome supports the concept that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. A novel disease paradigm of the two-kidney one-clip (2K-1C) Goldblatt model is presented for preeclampsia, wherein the gravid uterus is the clipped "kidney" and the two maternal kidneys represent the unclipped kidney. Validation of the 2K-1C Goldblatt model analogy requires evidence of elevated angiotensin II in the peripheral circulation before vascular maladaptation in preeclampsia. Convincing evidence of the elevation of angiotensin II in preeclampsia does not exist despite the fact that much of vascular pathogenesis appears to be due to angiotensin type I (AT 1) receptor activation. Vascular maladaptation with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT 1 and bradykinin B2 receptor heterodimerization and the production of an autoantibody against AT1. Various organ systems with a predilection for involvement in preeclampsia are each a site of a tissue-based RAS. How angiotensin II-mediated mechanisms may explain the primary clinical-pathological features of preeclampsia is described. Future investigations are proposed to more precisely define the role of activation of the uteroplacental RAS in the mechanisms underlying preeclampsia.HYPERTENSIVE DISORDERS COMPLICATE approximately 5-7% of all pregnancies (35a). These disorders include 1) chronic hypertension of whatever origin, including essential hypertension and chronic renal disease; 2) gestational hypertension, a hypertensive disorder occurring in pregnancy without multisystem involvement; 3) preeclampsia syndrome superimposed on chronic hypertension; 4) preeclampsia syndrome occurring de novo and only in the first pregnancy; and 5) preeclampsia syndrome occurring in a subsequent pregnancy and/or recurring with an underlying susceptibility state.Preeclampsia is a unique syndrome of pregnancy characterized by hypertension, proteinuria, and, frequently, edema. Several pathophysiological mechanisms have been implicated in the development of preeclampsia. These include endothelial dysfunction (36), an inflammatory p...

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“…Stimulation of sympathetic neurons with plasma from eclamptic and preeclamptic women significantly increases norepinephrine release, but whether this is mediated through Ang II has not been defined [62]. Whether systemic levels of endothelin are increased in preeclampsia is controversial [63][64][65], but endothelin may mediate the vascular response locally in preeclampsia without change in the circulating levels [64].…”

Section: Hypertension and Vascular-endothelial Dysfunctionmentioning

confidence: 99%

The role of RAS in the pathogenesis of preeclampsia

Shah

2006

Current Science Inc

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Preeclampsia is a hypertensive disorder that is unique to pregnancy, with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression in human preeclampsia and in transgenic mouse models with a human preeclampsia-like syndrome shows that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. Vascular maladaptation in preeclampsia with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms through angiotensin receptor type I (AT1) activation. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1 and bradykinin B2 receptor heterodimerization and the production of autoantibody against AT1. Various organ systems with predilection for involvement in preeclampsia are sites of tissue-based RAS. Angiotensin II-mediated mechanisms may explain the primary clinicopathologic features of preeclampsia. In this review, these various aspects are critically examined and an integrated concept on the role of RAS in preeclampsia is presented.

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Eclamptic Plasma Stimulates Norepinephrine Release in Cultured Sympathetic Nerve

Cited by 15 publications

References 30 publications

A new treatment of severe pre-eclampsia by long-term epidural anaesthesia

A new treatment of severe pre-eclampsia by long-term epidural anaesthesia

Role of the renin-angiotensin system in the pathogenesis of preeclampsia

The role of RAS in the pathogenesis of preeclampsia

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