Effects of L-arginine-derived nitric oxide synthesis on neuronal activity in nucleus tractus solitarius

Ma, Sheng-Xing; Abboud, François M.; Felder, Robert B.

doi:10.1152/ajpregu.1995.268.2.r487

Cited by 84 publications

(85 citation statements)

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“…53,54 NTS neuronal activity was reduced by systemic injection of L-NAME at constant blood pressure 55 while L-arginine and the NO donor, sodium nitroprusside (SNP) increased discharge rate. 56 The RVLM, the final site of sympathetic processing in the brainstem, also appears to contain neurons susceptible to an inhibitory influence by NO.…”

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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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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“…Conversely, Chowdhary and Townend (28) have reported that NO serves to inhibit central sympathetic outflow and studies by Di Paola et al (29) show that the neurotransmitter L-glutamate which promotes the release of NO from nitrergic neurones stimulates, rather than inhibits, baroreflex processing within the NTS. Furthermore, singleneuron recordings within the NTS have shown reduced activity after systemic administration of L-NAME (30) and increased neuronal discharge after NO donors such as L-arginine and SNP (31). NO-mediated inhibition of the cardiac baroreflex appears not to be mediated at the level of the heart itself, since the available literature suggests that NO potentiates, rather than depresses, the magnitude of induced bradycardia (32)(33)(34).…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide Reduces Vagal Baroreflex Sensitivity in the Late Gestation Fetus

Thakor

Giussani

2009

Pediatr Res

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Goals to understand the etiology of essential hypertension have proposed that this problem arises, in part, because of changes within brainstem circuits involved in arterial blood pressure (ABP) control. It has been suggested that nitric oxide (NO) exerts inhibitory influences on the integration of afferent discharge from the arterial baroreceptors. This study tested the hypothesis that the inhibitory influence of NO on the arterial baroreflex is present in fetal life. Fetal baroreflex sensitivity was calculated in fetal sheep, before and during the NO-clamp; a technique that permits NO synthase (NOS) blockade with L-NAME while maintaining basal cardiovascular function with sodium nitroprusside. Under halothane anesthesia, five fetal sheep at 0.8 gestation were instrumented with vascular catheters. Five days later, fetuses received a range of bolus doses of phenylephrine (5-75 g I.A.) in randomized order either during saline or treatment with the NO clamp. Basal fetal ABP and heart rate before (50 Ϯ 4 mm Hg, 170 Ϯ 3 bpm) or during (51 Ϯ 4 mm Hg, 173 Ϯ 3 bpm) the NO-clamp were similar. The gradient of the pulse interval-ABP relationship was nearly doubled during NOS blockade (14.2 Ϯ 2.5 versus 7.8 Ϯ 1.6 ms/mm Hg). The data provide in vivo evidence that NO attenuates the sensitivity of the cardiac baroreflex during fetal life. (Pediatr Res 65: 269-273, 2009) T he arterial baroreflex plays an important role in maintaining cardiovascular homeostasis by continuously eliciting autonomic adjustments to maintain arterial blood pressure (ABP) within a narrow physiologic range. Baroreceptors are located in the carotid sinus and aortic arch, where they sense beat-by-beat changes in ABP. This information is relayed via primary afferent neurons to the brainstem, where the signal is processed and integrated. Compensatory adjustments in heart rate (HR) and vascular resistance, for any perturbations in ABP, are subsequently mediated via changes in efferent vagal and sympathetic outflow (1,2).Studies in both the adult and fetus have shown that there is an age-dependent fall in arterial baroreflex sensitivity (3,4). Accumulating evidence implicates nitric oxide (NO) in baroreflex pathways and its involvement in altering baroreflex sensitivity with ageing. For instance, NO synthase (NOS) immunoreactivity has been demonstrated in several locations of the baroreflex pathway, including the carotid sinus (5), the nucleus tractus solitarius (6), and the cardiac vagal and preganglionic sympathetic neurons (7,8). Further, the fall in baroreflex sensitivity with advancing age in conscious lambs is dependent on NO (9). However, it remains completely unknown whether the inhibitory influence on baroreflex sensitivity by NO is already present in fetal life. The present study tested the hypothesis that endogenous NO depresses baroreflex sensitivity during fetal life. Our own pilot studies and investigations by Schroder et al. (10) have shown that in fetal life, unloading of the arterial baroreceptors, for instance using bolus doses ...

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“…NO is linked to glutamatergic neurotransmission in the central nervous system (24,25) and activation of glutamate receptors in the nucleus tractus solitarius (NTS) and paragigantocellular nucleus is necessary to maintain normal levels of blood pressure and ventilation and also for a normal ventilatory CO 2 response to occur (26). It has been demonstrated that NO enhances the excitability and spontaneous discharge rates of neurons in the NTS (27) and may act as a retrograde messenger in an L-glutamate-releasing positive feedback system, also in the NTS, involved in the increase of ventilation during hypoxia (24). NO has an excitatory effect on the discharge rates of neurons in the pontine respiratory group, whereas L-NNA produces a disruption of the pneumotaxic mechanism (28).…”

Section: Discussionmentioning

confidence: 99%

Participation of nitric oxide in the nucleus isthmi in CO2-drive to breathing in toads

Gargaglioni

Branco

1999

Braz J Med Biol Res

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The nucleus isthmi (NI) is a mesencephalic structure of the amphibian brain. It has been reported that NI plays an important role in integration of CO 2 chemoreceptor information and glutamate is probably involved in this function. However, very little is known about the mechanisms involved. Recently, it has been shown that nitric oxide synthase (NOS) is expressed in the brain of the frog. Thus the gas nitric oxide (NO) may be involved in different functions in the brain of amphibians and may act as a neurotransmitter or neuromodulator. We tested the hypothesis that NO plays a role in CO 2 -drive to breathing, specifically in the NI comparing pulmonary ventilation, breathing frequency and tidal volume, after microinjecting 100 nmol/0.5 µl of L-NAME (a nonselective NO synthase inhibitor) into the NI of toads (Bufo paracnemis) exposed to normocapnia and hypercapnia. Control animals received microinjections of vehicle of the same volume. Under normocapnia no significant changes were observed between control and L-NAME-treated toads. Hypercapnia caused a significant (P<0.01) increase in ventilation only after intracerebral microinjection of L-NAME. Exposure to hypercapnia caused a significant increase in breathing frequency both in control and L-NAME-treated toads (P<0.01 for the control group and P<0.001 for the L-NAME group). The tidal volume of the L-NAME group tended to be higher than in the control group under hypercapnia, but the increase was not statistically significant. The data indicate that NO in the NI has an inhibitory effect only when the respiratory drive is high (hypercapnia), probably acting on tidal volume. The observations reported in the present investigation, together with other studies on the presence of NOS in amphibians, indicate a considerable degree of phylogenetic conservation of the NO pathway amongst vertebrates.

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Effects of L-arginine-derived nitric oxide synthesis on neuronal activity in nucleus tractus solitarius

Cited by 84 publications

References 0 publications

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

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

Nitric Oxide Reduces Vagal Baroreflex Sensitivity in the Late Gestation Fetus

Participation of nitric oxide in the nucleus isthmi in CO2-drive to breathing in toads

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