Nitric oxide synthase-immunoreactive neurons in human and porcine respiratory tract

Rada, O; Villaro, A. C.; Montuenga, Luis M.; Martı́nez, Alfredo; Springall, David R.; Polak, J.M.

doi:10.1016/0304-3940(93)90575-6

Cited by 32 publications

(12 citation statements)

References 26 publications

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“…Our demonstration of an age and airway generation-related transition in functional control over smooth muscle tone is supported for immunohistochemical studies suggesting NOSimmunoreactive (NOS-IR) nerves decrease with age in both pig and man (Diaz de Rada et al, 1993). Our ®ndings of a predominantly central airway distribution of nitrergic relaxation in the adult is consistent with studies suggesting that NOS-IR nerves are most dense in the central airways of guinea-pig, horse, rat, pig and human respiratory tracts, but absent in the bronchioli (Fischer et al, 1993;Kobzik et al, 1993;Diaz de Rada et al, 1993;Yu et al, 1994;Ward et al, 1995a). In the cat there is evidence for actions of multiple inhibitory neurotransmitters at dierent levels of the tracheobronchial tree, with nitrergic mechanisms prominent in the central airway with a non-nitrergic mechanism prominent in bronchi, which is consistent with our ®ndings (Takahashi et al, 1995;Kondo et al, 1995).…”

Section: Discussionsupporting

confidence: 67%

Transition of functional innervation in the developing porcine airway from nitrergic to catecholaminergic

Connellan

Mitchell

1998

British J Pharmacology

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1 We determined the distribution and chemical nature of the inhibitory neurotransmitter(s) to the airway smooth muscle (ASM) before and after birth. 2 Relaxation responses to electrical ®eld stimulation (EFS) were studied in isovolumic bronchial segments from foetal (approximately 100/115 days gestation) and adult (25 kg) pigs, and in isovolumic tracheal segments from the foetus, and tracheal smooth muscle strips from the adult pig. Preparations were conditioned in low doses of atropine (10 77 M) to reduce the eects of excitatory neurotransmission and then exposed to carbachol to produce submaximal muscle tone. Some studies were also carried out on bronchial segments from 4 week old pigs. 3 EFS (65 V, 2 ms, 5 ± 20 Hz for 5 s) produced a TTX-sensitive relaxation in epithelium-intact and epithelium-denuded preparations. In foetal bronchial and tracheal preparations, EFS-induced relaxation was strongly inhibited by N G -nitro-L-arginine (L-NOARG, 10 76 to 10 74 M; P50.01 ± 0.001). However, in the adult, only relaxations of the trachea were inhibited by L-NOARG; bronchi were resistant to L-NOARG and also to N-nitro-L-arginine methyl ester (L-NAME, 5 The onset of relaxation to EFS was more prompt and the rate of relaxation more rapid in foetal bronchi than in adult bronchi (P50.0005). Maximum relaxation and recovery times were the same. 6 Foetal and adult bronchi were relaxed by sodium nitroprusside (SNP) with similar sensitivity and maximum eect. The rate of relaxation to SNP was not dierent in the two ages. 7 In the absence of atropine and carbachol, excitatory cholinergic responses to EFS (65 V, 2 ms, 5 Hz for 20 s) were not altered by L-NOARG (10 74 M) or L-NAME (10 74 M) in the adult bronchus but were modestly increased by L-NOARG in the foetal bronchus (P50.01). 8 The tracheobronchial tree appears functionally innervated by nitrergic input to the smooth muscle before birth. However, at or after 4 weeks of age the inhibitory neural input to the bronchi is catecholaminergic, but it remains nitrergic in the trachea. There is also a weak nitrergic pre-or postsynaptic inhibition of the eects of cholinergic neurotransmission in the foetal bronchus but not in the adult.

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Section: Discussionsupporting

confidence: 67%

Transition of functional innervation in the developing porcine airway from nitrergic to catecholaminergic

Connellan

Mitchell

1998

British J Pharmacology

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“…De Rada et al [75] revealed the presence of NOS-immunoreactive neurons in the human and porcine respiratory tract and blood vessels. From studies on NOS-containing nerve fibers in the human airway muscle and blood vessels, Fischer and Hoffmann [76] suggested the functional differences of the neural relaxant responses were mediated by nitric oxide at different levels of the airway tree.…”

Section: Neurogenic Nitric Oxide In Pulmonary Hypertensionmentioning

confidence: 98%

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

Toda¹,

Ayajiki²,

Okamura³

2009

Journal of Hypertension

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Nitric oxide formed by neuronal nitric oxide synthase (nNOS) in the brain, autonomic inhibitory (nitrergic) nerves, and heart plays important roles in the control of blood pressure. Activation of nitrergic nerves innervating the systemic vasculature elicits vasodilatation, decreases peripheral resistance, and lowers blood pressure. Impairment of nitrergic nerve function, as well as endothelial dysfunction, results in systemic and pulmonary hypertension and decreased regional blood flow. Blockade of nNOS activity in the brain, particularly the medulla and hypothalamus, causes systemic hypertension. Under hypertensive states, such as those in spontaneously hypertensive and Dahl salt-sensitive rats, the expression of the nNOS gene in the brain is increased; this appears to counteract the activated sympathetic function in the vasomotor center. The present article summarizes information concerning the modulation of systemic and pulmonary hypertension through nNOS-derived nitric oxide produced in the brain and periphery.

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“…11,12 Airway neurons that are immunoreactive for NOS are less prominent in peripheral than in central human airways. 13,14 NO also seems essential for ciliary motility, 15 and its antimicrobial properties have been shown to be important in host defense against various pathogens. 16,17 However, excess NO formation as in septic shock causes inflammation, oxidative tissue damage, and favors plasma leakage into perivascular spaces and the airway lumen 18 through reactive intermediates such as peroxynitrite anion (ONOO − ) or peroxynitrous acid (OONOH), both rapidly formed by the interaction of NO and superoxide anion (O 2 − ).…”

Section: Introductionmentioning

confidence: 99%

Cystic fibrosis lung disease: The role of nitric oxide

Grasemann

Ratjen

1999

Pediatr. Pulmonol.

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Nitric oxide synthase-immunoreactive neurons in human and porcine respiratory tract

Cited by 32 publications

References 26 publications

Transition of functional innervation in the developing porcine airway from nitrergic to catecholaminergic

Transition of functional innervation in the developing porcine airway from nitrergic to catecholaminergic

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

Cystic fibrosis lung disease: The role of nitric oxide

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