Variable α2-adrenoceptor-mediated inhibition of bronchoconstriction and peptide release upon activation of pulmonary afferents

Lou, Ya‐Ping; Franco‐Cereceda, Anders; Lundberg, Jan M.

doi:10.1016/0014-2999(92)90668-t

Cited by 25 publications

(9 citation statements)

References 31 publications

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“…This explains why all patients affected by the obstructive sleep apnea syndrome present with raised NA/Ad plasma ratio (neural sympathetic overactivity) [24,174,[183][184][185][186][187]. The above phenomena are consistent with others showing that A6(NA) and A5(NA) axons display a black vs. white antagonism at the upper pharynx and respiratory areas; excitation by the former triggers the opening of it, whereas the latter provokes the closure of this segment [128,[183][184][185][186][187].…”

Section: Type N Diseases (Seesupporting

confidence: 76%

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Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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Abstract:The assessment of circulating neurotransmitters: noradrenaline, adrenaline, dopamine, platelet serotonin, plasma serotonin and plasma tryptophan before and after many types of stressor agents and neuropharmacological drugs carried out over the last thirty years allowed us to accumulate information dealing with the central nervous system (CNS) versus the peripheral autonomic nervous system (ANS) interactions in healthy as well as diseased mammals. Furthermore, the accurate knowledge about the CNS circuitry disorders which underlie both the CNS and peripheral clinical syndromes, has allowed us to prescribe successful neuropharmacological therapeutical strategies for many types of illnesses. In addition, the demonstration that the clinical improvement was always paralleled by the normalization of the neurochemical, hormonal, immunological and clinical profiles affords strong support to our point of view. According to all the above, the authors postulate the existence of two types of diseases: type A and Type N, which are underlain by two opposite CNS + ANS disorders. Type A diseases should be associated with the "uncoping stress" syndrome and are underlain by hyperactivity of the adrenocortical glands plus the CNS disorder characterized by the predominance of the C1(adrenergic) + DR(serotonergic) axis over the A5(noradrenergic) + MR(serotonergic) binomial, whereas the type N diseases depends on the opposite profile: "endogenous depression" syndrome. Finally, we quoted exhaustive evidence showing that the well known fading of both the A6(noradrenergic) + C1(adrenergic) CNS nuclei activity occurring during aging is responsible for the ANS + CNS disorder which is similar to that underlying psychosis, Alzheimer, post-traumatic stress disorder and deficit-attention hyperactive disorder.

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Section: Type N Diseases (Seesupporting

confidence: 76%

“…This ACh + NA interaction allows the fast excitation of the neural sympathetic branch. In addition to the above, sympathetic nerves innervate and inhibit the adrenal glands secretion by acting at alpha-2 receptors located at this level [128,192]. Fig.…”

Section: Neural Sympathetic or Adrenal Sympa-thetic Vs Parasympathetmentioning

confidence: 99%

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Lechín¹,

Dijs²

2008

TONEURJ

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“…Also, electrically induced nonadrenergic noncholinergic iris sphincter contractions were modulated by ␣ 2 -adrenoceptor mediated inhibition of sensory neurotransmitter release (10). Moreover, capsaicin-induced bronchoconstriction was reduced by ␣ 2 -adrenoceptor agonists (33).…”

Section: Discussionmentioning

confidence: 98%

Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE₂-dependent activation of α₁- and α₂-adrenoceptors on renal sensory nerve fibers

Kopp

Cicha²,

Smith³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Kopp UC, Cicha MZ, Smith LA, Mulder J, Hö kfelt T. Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE 2-dependent activation of ␣1-and ␣2-adrenoceptors on renal sensory nerve fibers. Am J Physiol Regul Integr Comp Physiol 293: R1561-R1572, 2007. First published August 15, 2007; doi:10.1152/ajpregu.00485.2007.-Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA). To test whether the ERSNA-induced increases in ARNA involved norepinephrine activating ␣-adrenoceptors on the renal sensory nerves, we examined the effects of renal pelvic administration of the ␣ 1-and ␣2-adrenoceptor antagonists prazosin and rauwolscine on the ARNA responses to reflex increases in ERSNA (placing the rat's tail in 49°C water) and renal pelvic perfusion with norepinephrine in anesthetized rats. Hot tail increased ERSNA and ARNA, 6,930 Ϯ 900 and 4,870 Ϯ 670% ⅐ s (area under the curve ARNA vs. time). Renal pelvic perfusion with norepinephrine increased ARNA 1,870 Ϯ 210% ⅐ s. Immunohistochemical studies showed that the sympathetic and sensory nerves were closely related in the pelvic wall. Renal pelvic perfusion with prazosin blocked and rauwolscine enhanced the ARNA responses to reflex increases in ERSNA and norepinephrine. Studies in a denervated renal pelvic wall preparation showed that norepinephrine increased substance P release, from 8 Ϯ 1 to 16 Ϯ 1 pg/min, and PGE 2 release, from 77 Ϯ 11 to 161 Ϯ 23 pg/min, suggesting a role for PGE 2 in the norepinephrineinduced activation of renal sensory nerves. Prazosin and indomethacin reduced and rauwolscine enhanced the norepinephrine-induced increases in substance P and PGE 2. PGE2 enhanced the norepinephrine-induced activation of renal sensory nerves by stimulation of EP4 receptors. Interaction between ERSNA and ARNA is modulated by norepinephrine, which increases and decreases the activation of the renal sensory nerves by stimulating ␣ 1-and ␣2-adrenoceptors, respectively, on the renal pelvic sensory nerve fibers. Norepinephrine-induced activation of the sensory nerves is dependent on renal pelvic synthesis/release of PGE 2. substance P; EP4 receptor; pelvis; prazosin; rauwolscine THERE IS CONSIDERABLE EVIDENCE for increased sympathetic nerve activation to further stimulate sensory nerve fibers following tissue injury (15). Studies on efferent renal sympathetic nerve activity (ERSNA) and afferent renal nerve activity (ARNA) suggest that such an interaction is not restricted to conditions of tissue injury but is an important mechanism regulating ERSNA during physiological conditions (30). The kidney has a rich supply of sympathetic nerves, which innervate all parts of the vasculature and the nephron (2). In contrast, the majority of the sensory nerve fibers are localized to the renal pelvic wall (25,26,32). There is anatomical support for an interaction between ERSNA and ARNA, as shown by the close relationship between unmyelinated sympathetic nerve fibers and myelinated afferent nerve fibers in renal tissue...

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“…Furthermore, 4-aminopyridine is known to enhance stimulation-evoked transmitter release from a variety of neurones (Rudy 1988) although its effect on peptide release from pulmonary afferents is not known. The CGRP release from sensory nerves can be inhibited by a2-adrenoceptor stimulation (Lou et al 1992b) and a,-adrenoceptor regulation of transmitter release has been suggested to involve Ca2+ activated K + channels (Stjarne 1989). Recently, Stretton et al (1992) suggested that high conductance Ca2+activated K+-channel activation may often be the mechanism underlying the prejunctional modulation of sensory nerve function in airways.…”

mentioning

confidence: 99%

Different Effects of the K⁺ Channel Blockers 4‐Aminopyridine and Charybdotoxin on Sensory Nerves in Guinea‐pig Lung

Lou

Lundberg

1993

Pharmacology & Toxicology

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In the isolated guinea-pig bronchus, the potassium channel blocking agent 4-aminopyridine (10(-4) M) caused a contraction which was abolished by capsaicin tachyphylaxis, suggesting involvement of sensory neuropeptides. Charybdotoxin (10(-8), 5 x 10(-8) M), which is a potent blocker of the high-conductance Ca(2+)-activated K+ channel in smooth muscle, caused slowly developing and long lasting bronchoconstriction, which was resistant to capsaicin tachyphylaxis. Neither 4-aminopyridine (10(-3), 10(-4) M) nor charybdotoxin (10(-8), 5 x 10(-8) M) had any significant effect on the bronchoconstriction induced by electrical field stimulation. Furthermore, charybdotoxin had no significant influence on the inhibitory effect of the alpha 2-adrenoceptor agonist SKF 35886 (5 x 10(-7) M) on the bronchoconstriction induced by electrical field stimulation. In the isolated perfused guinea-pig lung, 4-aminopyridine (3 x 10(-5) -10(-3) M) caused bronchoconstriction and enhanced both basal and (at 3 x 10(-5) M) vagal nerve stimulation-evoked calcitonin gene-related peptide outflow from pulmonary sensory nerves. In conclusion, 4-aminopyridine stimulated capsaicin-sensitive sensory neurons and enhanced the sensory activation induced by vagal nerve stimulation in guinea-pig lung. Charybdotoxin, on the other hand, caused bronchial contraction independently of capsaicin-sensitive nerves.

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Variable α2-adrenoceptor-mediated inhibition of bronchoconstriction and peptide release upon activation of pulmonary afferents

Cited by 25 publications

References 31 publications

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE₂-dependent activation of α₁- and α₂-adrenoceptors on renal sensory nerve fibers

Different Effects of the K⁺ Channel Blockers 4‐Aminopyridine and Charybdotoxin on Sensory Nerves in Guinea‐pig Lung

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Variable α2-adrenoceptor-mediated inhibition of bronchoconstriction and peptide release upon activation of pulmonary afferents

Cited by 25 publications

References 31 publications

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2-dependent activation of α1- and α2-adrenoceptors on renal sensory nerve fibers

Different Effects of the K+ Channel Blockers 4‐Aminopyridine and Charybdotoxin on Sensory Nerves in Guinea‐pig Lung

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Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE₂-dependent activation of α₁- and α₂-adrenoceptors on renal sensory nerve fibers

Different Effects of the K⁺ Channel Blockers 4‐Aminopyridine and Charybdotoxin on Sensory Nerves in Guinea‐pig Lung