Mechanisms of vasomotor rhinitis

Abstract

Nonallergic non-infectious perennial rhinitis (NANIPER) is a heterogeneous disorder comprising several pathophysiological entities. The etiology of some of these disorders (e.g. drug-induced rhinitis, nonallergic rhinitis with eosinophilia syndrome [NARES], occupational rhinitis, hormonal rhinitis, emotion-induced rhinitis, physical/chemical irritant-induced rhinitis) is well established. In contrast, the aetiology of idiopathic forms of rhinitis (also known as vasomotor rhinitis) is largely unknown. Mechanistic studies have suggested that non-IgE-mediated inflammatory and/or neurogenic processes may be involved. There is evidence that localized inflammation is the underlying cause of symptoms in drug-induced rhinitis and NARES, since eosinophilia is an important pathophysiological component in these conditions. In contrast, neurogenic reflex mechanisms initiated by environmental factors appear to be involved in idiopathic rhinitis. It has been suggested that there may be an imbalance of the sympathetic and parasympathetic nervous systems, with parasympathetic hyper-activity and sympathetic hypo-activity resulting in nasal congestion and rhinorrhoea. Indirect evidence suggests that C-fibres may also play an important role in the pathophysiology of idiopathic rhinitis.

Effects of adrenergic and cholinergic antagonists on diameter of nasolacrimal drainage system

“…This control of the nasal vessels plays a crucial role in regulating the patency of the nasal passages through erectile tissues [5,6,17]. The erectile tissues, the so-called "cavernous tissues" of the nasal mucosa, are involved in the congestion of the nasal passage [8].…”

“…Under normal circumstances, the nasal blood vessels are kept in a state of partial constriction by "continuous sympathetic vascular tone" [5,6,14]. That is, under normal conditions, both the resistance and capacitance of the vessels of the nasal mucosa are under the tonic control of the sympathetic system via the cervical sympathetic trunk [17].…”

“…This vasoconstrictive action of adrenergic agents on the human nasal mucosa maintains the patency of the nasal passage [6] and is almost exclusively mediated through α-1 receptors, and the α-2 receptors are of only a minor importance [14]. Kawarai and associates [14] reported that prazosin, a selective α-1 adrenergic antagonist, blocked the evoked nasal vasoconstrictor response.…”

“…In contrast, stimulation of the parasympathetic nervous system leads to vasodilation and a swelling of the mucosa [17], and this mechanism plays an essential role in the "protective" nasal cleaning reflex [6]. This vasodilation is not blocked by atropine, and thus appears to be due to a non-cholinergic mechanism [4].…”

Inmunohistochemical Evaluation of Estrogen Receptors Alpha and Beta in Normal Inferior Turbinate Mucosa

“…Chronic nasal non-allergic inflammation can be called non-allergic rhinitis. The incidence of nonallergic rhinitis ranges from 17 to 52% in the literature, and 58 to 74% of such cases occur in women (Settipane & Lieberman, 2001;Bachert, 2004;Garay, 2004).…”