Control of systemic and pulmonary blood pressure by nitric oxide formed through neuronal nitric oxide synthase

Toda, Noboru; Ayajiki, Kazuhide; Okamura, Tomio

doi:10.1097/hjh.0b013e32832e8ddf

Cited by 49 publications

(31 citation statements)

References 111 publications

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“…The interplay between NO and different components of the RAS, including the AT 2 R has been previously reported [16,41,42]. We therefore also evaluated whether the responses to icv C21 can be affected by central inhibition of NO-synthase.…”

Section: Discussionmentioning

confidence: 91%

Hypotensive and sympathoinhibitory responses to selective central AT2 receptor stimulation in spontaneously hypertensive rats

et al. 2015

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The type 2 angiotensin (AT2) receptor has been suggested to counterbalance the type 1 angiotensin (AT1) receptor in the central regulation of blood pressure and sympathetic tone. We here investigated the blood pressure responses to stimulation of central AT2 receptors by the selective agonist Compound 21 in conscious SHR and normotensive WKY rats. We also assessed the impact on norepinephrine plasma levels, autonomic function, spontaneous baroreflex sensitivity, and the possible involvement of the nitric oxide-pathway and the AT1 receptor. Chronic intracerebroventricular Compound 21 infusion lowered blood pressure and norepinephrine plasma levels in both rat strains. The nighttime hypotensive effect was greater in SHR compared to WKY. Compound 21 improved spontaneous baroreflex sensitivity more in SHR than in WKY. These effects were abolished by co-administration of AT2 receptor antagonist PD123319 or nitric oxide-synthase inhibitor L-NAME. Central AT1 receptor blockade did not enhance the hypotensive response to Compound 21. Chronic selective stimulation of central AT2 receptors lowers blood pressure through sympatho-inhibition, and improves spontaneous baroreflex sensitivity more in SHR than in WKY. These responses appear to require a functioning central nitric oxide-pathway, but are not modified by central AT1 receptor blockade. Collectively, the data demonstrate specific beneficial effects of stimulation of central AT2 receptors in hypertension associated with increased sympathetic tone and suggest that central AT2 receptors may represent a potential new therapeutic target for the treatment of neurogenic hypertension.

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Section: Discussionmentioning

confidence: 91%

Hypotensive and sympathoinhibitory responses to selective central AT2 receptor stimulation in spontaneously hypertensive rats

et al. 2015

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“…Also in the CNS, nNOS-derived NO is implicated in the central regulation of blood pressure. Blockade of nNOS activity in the medulla and hypothalamus makes systemic hypertension [31].…”

Section: Physiological Functions Of Nnosmentioning

confidence: 99%

Neuronal Nitric Oxide Synthase

Arami¹,

Jameie²,

AkbarMoosavi³

2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Nitric oxide synthase (NOS), a flavo-hemoprotein, regulates nitric oxide (NO) synthesis that has dual biological activities: as an important signalling molecule in vasodilatation and neurotransmission at low concentrations and at higher concentrations as a defensive cytotoxin. In central and peripheral nervous system, neuronal NOS (nNOS) produces NO that has been implicated in modulating physiological functions such as synaptic plasticity, learning, memory and neurogenesis as well as some pathological conditions in which overproduction of NO may lead to the generation of highly reactive species, such as peroxynitrite and stable nitrosothiols, which may cause irreversible cell damage in excitotoxicity, ischaemia, Parkinson, Alzheimer's disease (AD) and depression. NOSderived NO also involves in regulation of blood pressure, smooth muscle relaxation and gut peristalsis via peripheral nitrergic nerves.

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“…Nitric oxide synthesized via nNOS in the brain also participates in systemic and local hemodynamics, mainly associated with modifying central sympathetic nerve activities [56].…”

Section: Involvement Of Neuronal Nitric Oxide Synthase-derived Nitricmentioning

confidence: 99%

Salt-induced hemodynamic regulation mediated by nitric oxide

Toda

Arakawa

2011

Journal of Hypertension

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Excess daily salt intake impairs vasodilatation and enhances vasoconstriction, resulting in reduction of regional blood flow and elevation of blood pressure in healthy individuals and hypertensive patients with either salt sensitivity or not tested for salt sensitivity or not evaluated for salt sensitivity. The mechanism may involve decreased production of nitric oxide via endothelial nitric oxide synthase (eNOS), impaired bioavailability of nitric oxide, and elevated plasma levels of asymmetric dimethylarginine (ADMA). Experimental animals, irrespective of salt sensitivity, although less extensive in those with salt-resistance, fed a high-salt diet have deteriorated endothelial functions; the mechanisms involved include an impairment of eNOS activation, a decrease in eNOS expression, and an increase in oxidative stress and ADMA. The imbalance of interactions between nitric oxide and angiotensin II is also involved in salt sensitivity. Deficiency of nitric oxide formed via neuronal NOS and inducible NOS may contribute to salt-induced hypertension. Reduced daily salt intake, therefore, would be the most rational prophylactic measure against the development of hypertension.

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Control of systemic and pulmonary blood pressure by nitric oxide formed through neuronal nitric oxide synthase

Cited by 49 publications

References 111 publications

Hypotensive and sympathoinhibitory responses to selective central AT2 receptor stimulation in spontaneously hypertensive rats

Hypotensive and sympathoinhibitory responses to selective central AT2 receptor stimulation in spontaneously hypertensive rats

Neuronal Nitric Oxide Synthase

Salt-induced hemodynamic regulation mediated by nitric oxide

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