Specific actions of cyanide on membrane potential and voltage-gated ion currents in rostral ventrolateral medulla neurons in rat brainstem slices

Wang, Gang; Zhou, Ping; Repucci, Michael A.; Golanov, Eugene V.; Reis, Donald J.

doi:10.1016/s0304-3940(01)02032-8

Cited by 21 publications

(15 citation statements)

References 18 publications

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“…Two potential downstream effectors of phosphorylated ERK1/2 in neuronal cells are voltage-dependent potassium channels and the transcription factor CREB [27,28]. Modulation of these potassium channels in the RVLM is involved in hypoxiainduced excitation of RVLM neurons [29], leading to acute hypertension. The lack of effects of U0126 on the angiotensin II-induced acute pressor response observed in this and a previous [15] study suggested that phosphorylated ERK1/2 in the ventrolateral medulla is not engaged in the short-term cardiovascular actions of the octapeptide.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of AT1 receptor gene on activation of protein kinase Cβ/nicotinamide adenine dinucleotide diphosphate oxidase/ERK1/2/c-fos signaling cascade mediates long-term pressor effect of angiotensin II in rostral ventrolateral medulla

Chan

Ling-lin

Tseng

et al. 2007

Journal of Hypertension

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Section: Discussionmentioning

confidence: 99%

Upregulation of AT1 receptor gene on activation of protein kinase Cβ/nicotinamide adenine dinucleotide diphosphate oxidase/ERK1/2/c-fos signaling cascade mediates long-term pressor effect of angiotensin II in rostral ventrolateral medulla

Chan

Ling-lin

Tseng

et al. 2007

Journal of Hypertension

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“…16,138 Neurons within the RVLM and spinal cord are known to be sensitive to hypoxia and can produce sympathoexcitation. 139,140 In humans, arterial compression at the ventrolateral medulla elevates muscle SNA 141 and causes hypertension, which can be reversed by surgical decompression. 142 Intriguingly, narrower lumens and thicker vessel walls are observed in the vertebral and basilar arteries of the pre-hypertensive SHR compared with normotensive rats.…”

Section: Drug-resistant Hypertension-how To Treat?mentioning

confidence: 99%

The sympathetic nervous system and blood pressure in humans: implications for hypertension

2011

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A neurogenic component to primary hypertension (hypertension) is now well established. Along with raised vasomotor tone and increased cardiac output, the chronic activation of the sympathetic nervous system in hypertension has a diverse range of pathophysiological consequences independent of any increase in blood pressure. This review provides a perspective on the actions and interactions of angiotensin II, inflammation and vascular dysfunction/brain hypoperfusion in the pathogenesis and progression of neurogenic hypertension. The optimisation of current treatment strategies and the exciting recent developments in the therapeutic targeting of the sympathetic nervous system to control hypertension (for example, catheter-based renal denervation and carotid baroreceptor stimulation) will be outlined. Keywords: sympathetic nerve activity; neurogenic hypertension; immune-to-brain signalling The sympathetic renaissancePrimary (or essential) hypertension (termed hypertension from here on) accounts for the vast majority of hypertensive cases (B95%).1 Although the aetiology of this condition is incompletely understood, it appears that along with genetic factors, several environmental and behavioural 'hypertensiogenic' factors have been identified, such as obesity, insulin resistance, high-salt intake, low physical activity levels and stress.1 Given the elevated risk of stroke, renal failure, myocardial infarction and coronary heart disease in those afflicted with high blood pressure, the elucidation of the key pathogenic features and optimisation of effective therapeutic strategies are critical.The most common form of hypertension is neurogenic hypertension, defined as high blood pressure with sympathetic overdrive, loss of parasympathetically mediated cardiac variability and excessive angiotensin II (Ang II) activity.2 The importance of the sympathetic nervous system in the short-term regulation of blood pressure via the modulation of peripheral vascular tone and cardiac output is well established, while the role of the sympathetic nerve activity (SNA) in long-term blood pressure control is more controversial. [3][4][5] Although the concept of a potential neurogenic component to hypertension is not new, 4 it has perhaps received less attention than the renin-angiotensin system (RAS), which has been a prominent therapeutic and research target in hypertension over the past few decades. Nevertheless, the activation of the sympathetic nervous system and the RAS in hypertension appears inextricably, and reciprocally, linked. Evidence from studies in both patients and animal models of hypertension strongly implicate the chronic sympathetic neural activation in the aetiology and progression of hypertension (Figure 1). 2,[6][7][8][9] The use of regional surgical sympathectomy to treat hypertension over 50 years ago before the availability of antihypertensive medications that lower sympathetic activity provides an early indication of the clinical appreciation for a significant neurogenic component to hypertension.10 Recent clini...

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“…The methods used to retrogradely label RVLM neurons are identical to previous descriptions from our laboratory (59,60). P20 rats were anesthetized with isoflurane (2% in oxygen), rhodamine-microbeads were microinjected bilaterally into the spinal cord at T 2-T4, and 2-3 days later, the P20 rats were killed.…”

Section: Animalsmentioning

confidence: 99%

“…P20 rats were anesthetized with isoflurane (2% in oxygen), rhodamine-microbeads were microinjected bilaterally into the spinal cord at T 2-T4, and 2-3 days later, the P20 rats were killed. The brain stems were removed, immersed in an ice-cold, oxygenized sucrose, artificial cerebrospinal fluid [ACSF (58,60)] and sectioned coronally into 300 -400 m slices using a Vibratome. These slices were incubated at 35°C in: 1) a lactic acid (l)-ACSF (59, 60) with 0.02% pronase for 1 h, and 2) an oxygenated l-ASCF (22) with 0.02% thermolysin for 1 h. To dissociate RVLM neurons, the region was first identified under an E600 fluorescence microscope by the presence of dye-labeled neurons, was then punched out, and the tissue stirred in 1-ASCF.…”

Section: Animalsmentioning

confidence: 99%

“…Whole cell patch-clamp recording of RVLM neurons was performed with an Axoclamp-2A amplifier with pClamp Window 8.0 (Molecular Devices, Sunnyvale, CA) as previously described (57,58,60). To determine whether ANG II affected cell currents, patched neurons were exposed to either vehicle (0.01% BSA in l-ASCF) or other drugs and then ANG II in vehicle (continuously for at least 10 min) or other drug-containing buffers by using a custom-designed double-barrel perfusion system.…”

Section: Animalsmentioning

confidence: 99%

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Sex differences in angiotensin signaling in bulbospinal neurons in the rat rostral ventrolateral medulla

Wang

Milner²,

Speth³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Wang G, Milner TA, Speth RC, Gore AC, Wu D, Iadecola C, Pierce JP. Sex differences in angiotensin signaling in bulbospinal neurons in the rat rostral ventrolateral medulla. Am J Physiol Regul Integr Comp Physiol 295: R1149 -R1157, 2008. First published August 6, 2008 doi:10.1152/ajpregu.90485.2008.-Sex differences may play a significant role in determining the risk of hypertension. Bulbospinal neurons in the rostral ventrolateral medulla (RVLM) are involved in the tonic regulation of arterial pressure and participate in the central mechanisms of hypertension. Angiotensin II (ANG II) acting on angiotensin type 1 (AT 1) receptors in RVLM neurons is implicated in the development of hypertension by activating NADPH oxidase and producing reactive oxygen species (ROS). Therefore, we analyzed RVLM bulbospinal neurons to determine whether there are sex differences in: 1) immunolabeling for AT 1 receptors and the key NADPH oxidase subunit p47 using dual-label immunoelectron microscopy, and 2) the effects of ANG II on ROS production and Ca 2ϩ currents using, respectively, hydroethidine fluoromicrography and patch-clamping. In tyrosine hydroxylase-positive RVLM neurons, female rats displayed significantly more AT 1 receptor immunoreactivity and less p47 immunoreactivity than male rats (P Ͻ 0.05). Although ANG II (100 nM) induced comparable ROS production in dissociated RVLM bulbospinal neurons of female and male rats (P Ͼ 0.05), an effect mediated by AT 1 receptors and NADPH oxidase, it triggered significantly larger dihydropyridine-sensitive longlasting (L-type) Ca 2ϩ currents in female RVLM neurons (P Ͻ 0.05). These observations suggest that an increase in AT 1 receptors in female RVLM neurons is counterbalanced by a reduction in p47 levels, such that ANG II-induced ROS production does not differ between females and males. Since the Ca 2ϩ current activator Bay K 8644 induced larger Ca 2ϩ currents in females than in male RVLM neurons, increased ANG IIinduced L-type Ca 2ϩ currents in females may result from sex differences in calcium channel densities or dynamics. C1 neurons; reactive oxygen species; NADPH oxidase; calcium channel; estrogen THERE IS INCREASING EVIDENCE that sex differences contribute to the risk of cardiovascular disease, including hypertension (14, 44). Under the age of 45 yr, fewer women than men die from cardiovascular disease (1), a pattern which is reversed after menopause (52). Similar sex-associated differences exist in animal hypertension models: females develop hypertension later, and less severely, than males (11,35,62). Studies in humans and animal models indicate that central nervous system pathways play a critical role in the development and maintenance of hypertension (27). Specifically, increases in sympathetic nerve activity and changes in arterial baroreflex function are strongly implicated in the pathogenesis of the disorder. The rostral ventrolateral medulla (RVLM) contains tonically active presympathetic bulbospinal neurons, most of which express tyrosine hydroxylase (TH) [the C1 cell...

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Specific actions of cyanide on membrane potential and voltage-gated ion currents in rostral ventrolateral medulla neurons in rat brainstem slices

Cited by 21 publications

References 18 publications

Upregulation of AT1 receptor gene on activation of protein kinase Cβ/nicotinamide adenine dinucleotide diphosphate oxidase/ERK1/2/c-fos signaling cascade mediates long-term pressor effect of angiotensin II in rostral ventrolateral medulla

Upregulation of AT1 receptor gene on activation of protein kinase Cβ/nicotinamide adenine dinucleotide diphosphate oxidase/ERK1/2/c-fos signaling cascade mediates long-term pressor effect of angiotensin II in rostral ventrolateral medulla

The sympathetic nervous system and blood pressure in humans: implications for hypertension

Sex differences in angiotensin signaling in bulbospinal neurons in the rat rostral ventrolateral medulla

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