Mechanism of decongestant activity of α2-adrenoceptor agonists

Drugs That May Cause or Exacerbate Heart Failure

“…When these agents are topically applied, case reports have suggested that excessive use or prolonged exposure beyond package labeling can lead to systemic exposure resulting in stroke, hypertension, and bradycardia. [306][307][308][309] Inhaled and oral OTC asthma products may contain potent nonselective sympathomimetic amines such as racepinephrine and ephedrine, and they have been associated with chest pain, hypertension, tachycardia, and hemoptysis. [310][311][312][313] Many of the newer aluminum-and magnesium-containing antacids have minimal to no sodium; however, other products for cough/cold and gastrointestinal ailments may contain sodium.…”

Pharmacological Characterization of a Novel α2C-Adrenoceptor AgonistN-[3,4-dihydro-4-(1H-imidazol-4-ylmethyl)-2H-1, 4-benzoxazin-6-yl]-N-ethyl-N′-methylurea (Compound A)

“…Indeed, nasal decongestion is triggered by an active constriction of the venous sinusoids (Kristiansen et al, 1993), and a decrease in nasal cavity pressure after ␣-adrenoceptor agonist administration reflects shrinkage of nasal capacitance vessels (Berridge and Roach, 1986). Several other studies in different species (Lacroix, 1989;Corboz et al, 2003Corboz et al, , 2007Corboz et al, , 2008Wang and Lung, 2003), including human (Johannssen et al, 1997;Corboz et al, 2005), indicated a predominance of the ␣ 2 -adrenenoceptor mechanism in the regulation of capacitance vessels. In addition, ␣ 2 -adrenoceptor proteins are expressed in human nasal mucosa (Corboz et al, 2005) and levels of ␣ 2 -adrenoceptor protein are higher than ␣ 1 -adrenoceptor protein in nasal mucosa of nonallergic and allergic patients (van Megen et al, 1991).…”

“…An ␣ 2 -adrenoceptor agonist, by preferentially constricting venous capacitance blood vessels over arterial resistance blood vessels in nasal mucosa (Corboz et al, 2005(Corboz et al, , 2008, should thus avoid the hypertensive liability of ␣ 1 -adrenoceptor agonists. It is known that ␣ 2 -adrenoceptor agonists produce decongestion in humans, and in the 1960s, the ␣ 2 -adrenoceptor agonist clonidine was initially developed for the treatment of nasal congestion (Stahle, 2000), as was Tinazoline (Nagarajan et al, 1981), and more recently, an ␣ 2 -adrenoceptor agonist demonstrated significant relief of nasal congestion in human subjects with allergic rhinitis (Berkowitz et al, 2005).…”

Oxymetazoline adds to the effectiveness of fluticasone furoate in the treatment of perennial allergic rhinitis

“…The initial development, however, is believed to be linked to the loss of a-receptors. 13 Patients with a long history of the problem develop inflammation within the mucosa and epithelial changes. 14 The potential for topical decongestants to cause rhinitis medicamentosa is listed as a side effect in the Physicians' Desk Reference and prompts limiting their usage to twice per day for 3 to 5 days.…”