Evaluation of aerosols of prostaglandins E1 and E2 as bronchodilators

Kawakami, Yoshikazu; Uchiyama, Kiyoshi; Irie, Tadashi; Murao, Makoto

doi:10.1007/bf00562439

Cited by 60 publications

(33 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In aspirin-sensitive patients the peak bronchodilation occurred immedi ately at the end of PGE2 inhalation. In con trast, in the remaining asthmatic patients the bronchodilating effect was most pronounced 30-60 min later, this observation being in accordance with other authors [8]. This dif ferent response was also reflected by signifi cant differences in mean PEF changes be tween the two groups studied at 5 and 10 min after inhalation.…”

Section: Discussionsupporting

confidence: 79%

Bronchial Reactivity to Prostaglandins F2α, E2, and Histamine in Different Types of Asthma

Szczeklik¹,

Nizankowska²,

Niżankowski³

1977

Respiration

View full text Add to dashboard Cite

Bronchial reactivity to prostaglandins F_2α (PGF_2α), E₂ (PGE2) and histamine has been studied in 27 patients with aspirin-sensitive asthma and in 28 asthmatics without this sensitivity. Of the latter group, 13 patients had atopic, 9 infectious, and 6 mixed type of asthma. Atopic patients were characterized by vivid reactivity to low doses of both PGF_2α and histamine. In patients with infectious asthma significantly higher doses of both PGF_2α and histamine were necessary to induce bronchoconstriction as compared to atopies. Aspirin-sensitive patients responded quickly with bronchial spasm to similar doses of histamine as atopies, but tolerated significantly higher doses of PGF_2α. There was no difference in reactivity to PGF_2α between patients with aspirin sensitivity and those with infectious asthma. 5 and 10 min after administration of 60 μg PGE₂ significantly better improvement in ventilation occurred in aspirin-sensitive patients than in those of either atopic or infectious groups. The results obtained point to differences in bronchial reactivity to prostaglandins and histamine depending on type of asthma and severity of its symptoms.

show abstract

Section: Discussionsupporting

confidence: 79%

Bronchial Reactivity to Prostaglandins F2α, E2, and Histamine in Different Types of Asthma

Szczeklik¹,

Nizankowska²,

Niżankowski³

1977

Respiration

View full text Add to dashboard Cite

show abstract

“…Receptors present on the vagal nerve termini situated in and under the airway epithelium can be activated by a wide variety of stimuli. These include mechanical stimuli such as punctate touch and lung inflation (Canning 2004), inflammatory mediators released during disease such as PGE 2 and bradykinin (Kawakami et al 1973;Choudry et al 1989;Maher et al 2009;Grace et al 2012), environmental irritants such as cigarette smoke and pollutants (Lee et al 2007;Belvisi et al 2011), changes in osmolarity of the airways (Lowry et al 1988;Koskela et al 2005) and changes in pH or temperature (McGarvey et al 1998;Wong et al 1999). Activation of these receptors causes a localized membrane depolarization, and if this reaches a certain threshold, then, an action potential is generated following activation of voltage-gated sodium channels (VGSCs) and carried up by the vagus nerve to the brainstem.…”

Section: Cough and Airway Sensory Nervesmentioning

confidence: 99%

Targeting TRP channels for chronic cough: from bench to bedside

Bonvini

Birrell

Smith

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

Cough is currently the most common reason for patients to visit a primary care physician in the UK, yet it remains an unmet medical need. Current therapies have limited efficacy or have potentially dangerous side effects. Under normal circumstances, cough is a protective reflex to clear the lungs of harmful particles; however, in disease, cough can become excessive, dramatically impacting patients' lives. In many cases, this condition is linked to inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD), but can also be refractory to treatment and idiopathic in nature. Therefore, there is an urgent need to develop therapies, and targeting the sensory afferent arm of the reflex which initiates the cough reflex may uncover novel therapeutic targets. The cough reflex is initiated following activation of ion channels present on vagal sensory afferents. These ion channels include the transient receptor potential (TRP) family of cation-selective ion channels which act as cellular sensors and respond to changes in the external environment. Many direct activators of TRP channels, including arachidonic acid derivatives, a lowered airway pH, changes in temperature, and altered airway osmolarity are present in the diseased airway where responses to challenge agents which activate airway sensory nerve activity are known to be enhanced. Furthermore, the expression of some TRP channels is increased in airway disease. Together, this makes them promising targets for the treatment of chronic cough. This review will cover the current understanding of the role of the TRP family of ion channels in the activation of airway sensory nerves and cough, focusing on four members, transient receptor potential vanilloid (TRPV) 1, transient receptor potential ankyrin (TRPA) 1, TRPV4, and transient receptor potential melastatin (TRPM) 8 as these represent the channels where most information has been gathered with relevance to the airways. We will describe recent data and highlight the possible therapeutic utility of specific TRP channel antagonists as antitussives in the clinic.

show abstract

“…Inhaled prostaglandin E 2 (PGE 2 ) has been shown to be a bronchodilator in subjects with asthma (Melillo et al, 1994) or COPD (Kawakami et al, 1973). However, PGE 2 itself has the potential to cause the adverse effects of cough and retrosternal burning when inhaled by humans, particularly in subjects with asthma (Choudry et al, 1989).…”

Section: G E-prostanoid Receptor 4 Agonistsmentioning

confidence: 99%