General Pharmacology: The Vascular System
ReviewNANC neural control of airway smooth muscle tone☆
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Cited by (13)
Sex, Cells, and Asthma
2021, Mayo Clinic ProceedingsCitation Excerpt :The roles of sympathetic and particularly parasympathetic innervation in regulation of airway tone and reactivity are well recognized, as are roles in defensive reflexes of the upper airway, such as coughing and sneezing.152 Human airways are innervated by nonadrenergic, noncholinergic (NANC) pathways involving excitatory bronchoconstriction through tachykinins, substance P, and neurokinin A and bronchodilation, whereas inhibitory NANC pathways involve vasoactive intestinal peptide and NO.153-159 Thus, imbalances between excitatory and inhibitory NANC pathways can contribute to AHR.153,160 No specific information is available regarding how sex steroids influence NANC pathways and their potential contribution to sex differences in asthma.
COPD Therapy: Beyond Conventional Pharmacology
2020, Archivos de BronconeumologiaSex Differences in Pulmonary Anatomy and Physiology: Implications for Health and Disease
2016, Sex Differences In PhysiologySex steroid signaling: Implications for lung diseases
2015, Pharmacology and TherapeuticsCitation Excerpt :Human airway has non-adrenergic, non-cholinergic (NANC) innervation which mediates (excitatory) bronchoconstriction via tachykinins, substance P and neurokinin A. The inhibitory component of NANC mediates bronchodilation via vasoactive intestinal peptide and NO (Lammers et al., 1992; Belvisi et al., 1995; Ward et al., 1995; Linden, 1996; Mackay et al., 1998; van der Velden & Hulsmann, 1999; Joos et al., 2000). Neuronal NOS in NANC nerve fibers generates NO from arginine which then induces ASM relaxation.
Pharmacological characterization of the interaction between the dual phosphodiesterase (PDE) 3/4 inhibitor RPL554 and glycopyrronium on human isolated bronchi and small airways
2015, Pulmonary Pharmacology and TherapeuticsCitation Excerpt :As expected, the loss of Emax to acetylcholine in the presence of the competitive antagonist glycopyronnium, resembles the response observed for indirectly acting substances that release endogenous intermediaries, the concentrations of which are the limiting factor and therefore cannot compete with antagonist-occupied receptors [21]. In addition, this peculiar profile might be caused by the intrinsic characteristic of bronchial contraction induced by transmural stimulation of postganglionic nerve fibers that is characterized by the release of both acetylcholine, through activation of parasympathetic nerves, and tachykinins such as substance P (SP), neurokinin A (NKA) and calcitonin gene-related peptide (CGRP), through activation of excitatory non-adrenergic non-cholinergic (NANC) mechanisms, although the latter system is of greater significance in animals than in human airways [41–46]. The alternative pA2 analysis suggests that glycopyrronium was a very potent compound in reducing the bronchial contraction induced by EFS, although the pA2 calculated during our study was slightly different compared with the pIC50 = 10.4 detected in a previous study on the pharmacological characterization of the potency of glycopyrronium in human isolated bronchi [47].
The relationship between dose-dependent antitussive and bronchodilatory effects of Opilia celtidifolia polysaccharide and nitric oxide in guinea pigs
2010, International Journal of Biological MacromoleculesCitation Excerpt :In addition to the classical cholinergic bronchoconstrictor and adrenergic bronchodilator neural mechanisms, there is a variety of species which are neither adrenergic nor cholinergic, the non-adrenergic, non-cholinergic (NANC) mechanisms. NANC neural mechanisms play an important role in the maintenance and regulation of bronchomotor tone, either via the direct effects of the transmitters released or by neuromodulation of autonomic control mechanisms [22]. Excitatory NANC (e-NANC) bronchoconstrictor responses are mediated by the release of sensory neuropeptides from e-NANC nerves, which release tachykinins such as substance P (SP), neurokinin A (NKA) and the peptide calcitonin gene-related peptide (CGRP).
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This work was supported by Hermann Krefting's Foundation, the Swedish Heart-Lung Fund, the Swedish Society of Medicine, the Swedish Medical Research Council (B94-19F-10715-01) and Tore Nilsson's Foundation.