Role of nitric oxide in regulation of baroreceptor reflex

Jimbo, Masahito; Suzuki, Hiromichi; Ichikawa, Masashi; Kumagai, Kazuhiro; Nishizawa, Masahiko; Saruta, Takao

doi:10.1016/0165-1838(94)90011-6

Cited by 64 publications

(35 citation statements)

References 22 publications

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“…It has been shown in animals that nitric oxide has central nervous effects and decreases sympathetic outflow. 43 A similar central nervous effect of nitric oxide in humans may be suggested by its bradycardic effect in patients with interruption of low-pressure baroreceptor transmission (cardiac transplant) 44 and in patients with baroreflex failure and integrity of the efferent vagal innervation of the heart (selective baroreflex failure). 31 We did not observe a bradycardia with nitroprusside after interruption of the efferent arc of the baroreflex with N N -cholinergic blockade.…”

Section: Discussionmentioning

confidence: 99%

Uncoupling of the Baroreflex by N _N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

et al. 1998

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Abstract-Systemic administration of adrenergic agonists and nitric oxide donors is used extensively to determine cardiovascular receptor sensitivity. Conclusions regarding receptor sensitivity in the presence of the baroreflex may be misleading. In 8 normal volunteers, we determined the heart rate and blood pressure changes after incremental bolus doses of isoproterenol, phenylephrine, and sodium nitroprusside before and during neuronal nicotinic

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Section: Discussionmentioning

confidence: 99%

Uncoupling of the Baroreflex by N _N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

et al. 1998

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“…Conversely, in baroreceptor intact rabbits, stimulation of NO synthesis with intravenous L-arginine caused a decrease in cervical sympathetic nerve activity and RSNA despite a fall in blood pressure. 47 The use of modulators of the NO pathway which lack specificity for a particular isoform of NOS and the systemic route of their administration does not allow us to determine where NO acts to inhibit sympathetic nerve activity. Nor does it determine which of the two constitutively expressed isoforms (eNOS or nNOS) is involved.…”

Section: Nitrergic Modulation Of Sympathetic Nervous Activitymentioning

confidence: 99%

“…45,49,61 However, a number of studies have failed to show any influence of NO on the reflex control of sympathetic activity. 47,62 This inconsistency is only partially explained by species differences or the effect of anaesthetics.…”

Section: Journal Of Human Hypertensionmentioning

confidence: 99%

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Chowdhary

Townend

2001

J Hum Hypertens

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The importance of endothelial nitric oxide (NO) generation in sustaining a tonic systemic vasodilatation is well established. Inhibiting NO production produces hypertension in animals and in humans and not surprisingly there has been considerable interest in establishing whether deficiencies of endothelial NO pathway activity are implicated in the aetiology of essential hypertension. The results of these investigations have been inconsistent with some suggestion that observed deficiencies of both basal and stimulated endothelial NO generation in hypertensive subjects may be an effect rather than the cause of raised arterial pressure. It is increasingly recognised that neuronal production of NO also influences cardiovascular homeostasis through its action as a neuromodulator within the autonomic nervous system. Overall NO has been shown to have sym-

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“…Some studies reported that baroreflex control of HR and/or sympathetic nerve activity were not changed in response to NO. 9,24,25 Other studies reported that baroreceptor reflex gain was increased by NO in the bradycardic component in the conscious state, although these studies were performed to examine the role of NO on baroreflex function by systemic administration of NOS inhibitors. 26,27 It has also been shown that there is a disorder of the L-arginine-NO pathway in stroke-prone spontaneously hypertensive rats (SHRSP).…”

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confidence: 99%

Overexpression of eNOS in RVLM Improves Impaired Baroreflex Control of Heart Rate in SHRSP

et al. 2003

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Abstract-We previously demonstrated that the overexpression of endothelial nitric oxide synthase (eNOS) in the rostral ventrolateral medulla (RVLM) decreases blood pressure, heart rate (HR), and sympathetic nerve activity and that these effects are enhanced in stroke-prone spontaneously hypertensive rats (SHRSP). The aim of this study was to determine if an increase in NO production in the RVLM caused by the overexpression of eNOS improves the impaired baroreflex control of HR in SHRSP. We transfected adenovirus vectors encoding eNOS (AdeNOS) into the RVLM of SHRSP or Wistar-Kyoto rats (WKY). Mean arterial pressure and HR were measured by a radio-telemetry system in the conscious state. Reflex changes in HR were elicited by intravenous infusion of either phenylephrine, sodium nitroprusside, or hydralazine at day 7 after the gene transfer. The maximum gain of the baroreflex control of HR was significantly decreased in SHRSP compared with WKY. Overexpression of eNOS in the RVLM of SHRSP improved the impaired maximum gain of the baroreflex control of HR. After treatment with atropine, the maximum gain was still significantly greater in SHRSP in the AdeNOS-transfected group than in the nontransfected group, although it was decreased in both groups. In contrast, after treatment with metoprolol, the maximum gain did not differ between the two groups. These results indicate that an increase in NO production in the RVLM improves the impaired baroreflex control of HR in SHRSP and that these effects may have resulted from a cardiac sympathoinhibitory effect of NO in the RVLM of SHRSP. Key Words: genes Ⅲ nitric oxide Ⅲ sympathetic nervous system Ⅲ brain Ⅲ baroreflex I t is well established that the central nervous system plays an important role in controlling arterial baroreflex function. 1,2 The major baroreceptor reflex pathway exits in the brain stem, such as the nucleus tractus solitarii (NTS), the caudal ventrolateral medulla (CVLM), and the rostral ventrolateral medulla (RVLM). 1,2 In particular, the RVLM contains sympathetic premotor neurons responsible for maintaining sympathetic outflow. 3 It is also well known that the baroreceptor reflex control of heart rate is impaired in various animal models of hypertension 4 -9 and in patients with hypertension. 10 Reduced arterial baroreceptor sensitivity has been shown to be responsible for this impaired baroreflex function. 4 -8 However, recent studies have suggested that central nervous mechanisms may also be involved in the impaired baroreceptor reflex function in hypertension. 9,11 There is considerable evidence that neuronal nitric oxide synthase (nNOS) exists within the brain stem, including the RVLM and NTS, 12 and plays an important role in regulating sympathetic nerve activity. [13][14][15][16] At resting conditions, microinjection studies into the RVLM with NO donors or NOS inhibitors have produced conflicting results, including both pressor or depressor responses, and explanation of these results remains to be elucidated. 16 -22 It is possible that anesthesia...

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Role of nitric oxide in regulation of baroreceptor reflex

Cited by 64 publications

References 22 publications

Uncoupling of the Baroreflex by N _N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

Uncoupling of the Baroreflex by N _N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Overexpression of eNOS in RVLM Improves Impaired Baroreflex Control of Heart Rate in SHRSP

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Role of nitric oxide in regulation of baroreceptor reflex

Cited by 64 publications

References 22 publications

Uncoupling of the Baroreflex by N N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

Uncoupling of the Baroreflex by N N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Overexpression of eNOS in RVLM Improves Impaired Baroreflex Control of Heart Rate in SHRSP

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Uncoupling of the Baroreflex by N _N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation

Uncoupling of the Baroreflex by N _N -Cholinergic Blockade in Dissecting the Components of Cardiovascular Regulation