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Chronic persistent non-productive cough is troublesome, whereas productive cough is physiologic and acts to remove abnormal secretions and foreign bodies from the lower respiratory tract. Atopic cough is a new clinical entity for bronchodilator-resistant non-productive cough associated with generalized atopy. Pathological characteristics of atopic cough included trachea bronchitis without Broncho Alveolar Lavage (BAL) eosinophilia, and the physiological characteristics included hypersensitivity of the cough reflex without bronchial hyper reactivity. Patients with atopic cough have eosinophilia of the nebulized hypertonic saline-induced sputum but normal spirometry findings and no variability of Peak Expiratory Flow (PEF). These features of atopic cough are distinct from those of cough variant asthma, since these patients have mild bronchial hyper reactivity and eosinophilic inflammation of the central and peripheral airways and their cough is responsive to bronchodilator treatment. Moreover cough-variant asthma is a precursor of typical asthma, while atopic cough is not, because nearly 30% of patients with cough-variant asthma eventually develop typical asthma but patients with atopic cough do not. Although nearly 60% of patients with atopic cough can be successfully treated with histamine H1-receptor antagonists, but other still require additional corticosteroid therapy because bronchoscopic study indicate that bronchial eosinophilic inflammation is more severe in the H1-receptor antagonist-resistant group. Further investigations are required for the clinical entity of eosinophilic bronchitis without asthma, since it seems to resemble to atopic cough and there seems to be considerable overlap of these two clinical entities.

The influence of muscarinic receptor stimulation and blockade on the central regulation of micturition was evaluated in conscious female rats. Saline was infused into the bladder to induce repeated bladder contractions and voiding. Increasing doses of a muscarinic agonist, oxotremorine-M (OXO-M; 0.01 to 1 microg/rat) or antagonist, atropine (0.1 to 30 microg/rat) were administered. Intrathecal OXO-M (0.1 microg) increased bladder capacity (BC; 85 +/- 17%), but did not change maximal voiding pressure (MVP), pressure threshold (PT), postvoiding intravesical pressure, or voiding efficiency (VE). Intracerebroventricular OXO-M (0.1 microg) increased BC (97 +/- 6%), MVP (45 +/- 19%), PT (158 +/- 49%), and reduced VE (-17 +/- 5%). A larger dose of OXO-M (1 microg, either i.c.v. or i.t.) produced greater changes. These effects were not reproduced by i.v. injections of OXO-M. The effects of OXO-M were blocked by pretreatment with atropine in a dose (1 microg i.c.v. or i.t.), which alone had no effect on voiding parameters. A larger dose of atropine (10 microg) reduced MP (-31 +/- 7% i.c.v. and -34 +/- 6% i.t.) and VE (-21 +/- 3% i.c.v. and -25 +/- 5% i.t.) but increased BC (52 +/- 8% i.c.v.). These results indicate that activation of muscarinic receptors in the brain or spinal cord can suppress voluntary voiding, but also stimulates bladder activity during bladder filling. The muscarinic inhibitory mechanisms do not appear to be tonically active. The effects of atropine (i.c.v. and i.t.) indicate that muscarinic excitatory mechanisms are tonically active. These findings raise the possibility that voiding function is regulated by both inhibitory and excitatory cholinergic mechanisms in the central nervous system.