Other pharmacologic agents that may affect bronchial hyperreactivity.

C T Furukawa

doi:10.1016/0091-6749(84)90308-7

Home/Archive/PubMed

PubMed · 6143771

Other pharmacologic agents that may affect bronchial hyperreactivity.

C T Furukawa

View original source ↗Export metadata ↓

Abstract

Although most asthmatic athletes can be adequately controlled by beta-adrenergic agents, sodium cromolyn, and/or theophylline, a few do not tolerate these medications or have suboptimal results. Cromolyn-like antiallergic drugs, newer antihistamine, antiserotonin, and antileukotriene agents as well as calcium channel blockers, antimuscarinics , alpha-adrenergic blockers, and new steroid preparations may be suitable for these individuals. Although efficacy has been demonstrated for a number of these new agents, much work remains to be done to evaluate thoroughly their potential pharmacologic effectiveness in exercise-induced asthma.

Explore related subjects

Adrenergic alpha-Antagonists Asthma Asthma, Exercise-Induced Benzothiazoles Budesonide Calcium Channel Blockers Carbazoles Chromones Cyproheptadine Humans Ketotifen Parasympatholytics Piperazines Pregnenediones Promethazine Thioxanthenes Xanthines Xanthones Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

C T Furukawa. 1984. Other pharmacologic agents that may affect bronchial hyperreactivity.. https://doi.org/10.1016/0091-6749(84)90308-7

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Differential effects of urapidil and doxazosin on heart rate.

OBJECTIVE: Although alpha-blockers are effective in lowering blood pressure, they may increase heart rate, an unwanted effect that could negatively affect outcome. However, the alpha-blocker urapidil might not increase heart rate due to its additional effect on 5-HT1A receptors. Therefore, we compared the effects of urapidil on heart rate with those of another alpha-blocker, doxazosin. METHODS: We performed a randomised, double-blind, placebo-controlled, cross-over study in 12 healthy males who received single oral doses of 60 mg urapidil, 4 mg doxazosin and placebo. Four hours following drug intake, heart rate and blood pressure were measured at rest and during exercise. RESULTS: Both doxazosin and urapidil decreased blood pressure to the same extent. Compared to placebo, resting heart rate was significantly increased by doxazosin (+25%, P < 0.05) but not by urapidil (+12%, n.s.). Resting heart rate with doxazosin was significantly higher than with urapidil (P < 0.05). Similarly, the rate pressure product (RPP) at rest was increased by doxazosin (+17%, P < 0.05) but not by urapidil (+6%, n.s.). CONCLUSIONS: We conclude that the increase in heart rate caused by urapidil is less pronounced than that with doxazosin, a property that might favour urapidil in the treatment of arterial hypertension. In addition, only doxazosin (but not urapidil) increased the RPP at rest, a finding that might be helpful to explain why this drug was never shown to improve outcome in the treatment of arterial hypertension.

Adrenergic alpha-Antagonists↗

PubMed2007

The synthetic TRH analogue taltirelin exerts modality-specific antinociceptive effects via distinct descending monoaminergic systems.

BACKGROUND AND PURPOSE: Exogenously administered thyrotropin-releasing hormone (TRH) is known to exert potent but short-acting centrally-mediated antinociceptive effects. We sought to investigate the mechanisms underlying these effects using the synthetic TRH analogue taltirelin, focusing on the descending monoaminergic systems in mice. EXPERIMENTAL APPROACH: The mice received systemic or local injections of taltirelin combined with either central noradrenaline (NA) or 5-hydroxytryptamine (5-HT) depletion by 6-hydroxydopamine (6-OHDA) or DL-p-chlorophenylalanine (PCPA), respectively, or blockade of their receptors. The degree of antinociception was determined using the tail flick and tail pressure tests. KEY RESULTS: Subcutaneously (s.c.) administered taltirelin exhibited dose-dependent antinociceptive effects in the tail flick and tail pressure tests. These effects appeared to be primarily supraspinally mediated, since intracerebroventricularly (i.c.v.) but not intrathecally (i.t.) injected taltirelin generated similar effects. Depletion of central NA abolished only the analgesic effect of taltirelin (s.c. and i.c.v.) on mechanical nociception. By contrast, depletion of central 5-HT abolished only its analgesic effect on thermal nociception. Intraperitoneal (i.p.) and i.t. injection of the alpha2-adrenoceptor antagonist yohimbine respectively reduced the analgesic effect of taltirelin (s.c. and i.c.v.) on mechanical nociception. By contrast, the 5-HT1A receptor antagonist WAY-100635 (i.p. and i.t.) reduced the effect of taltirelin (s.c. and i.c.v.) on thermal nociception. Neither the 5-HT2 receptor antagonist ketanserin nor the opioid receptor antagonist naloxone altered the antinociceptive effect of taltirelin. CONCLUSIONS AND IMPLICATIONS: These findings suggest that taltirelin activates the descending noradrenergic and serotonergic pain inhibitory systems, respectively, to exert its analgesic effects on mechanical and thermal nociception.

Adrenergic alpha-Antagonists↗

PubMed2007

Characteristics and mechanisms of locomotion induced by intraspinal microstimulation and dorsal root stimulation in spinal cats.

Intraspinal microstimulation (ISMS) through a single microelectrode can induce locomotion in cats spinalized at T(13) 1 wk before (untrained) or after 3-5 wk of treadmill training. Here we study the optimal parameters of ISMS and the characteristics of locomotion evoked. ISMS was applied in the dorsal region of segments L(3)-S(1) at different lateralities (midline to 2.5 mm) and after an intravenous injection of clonidine (noradrenergic agonist). Kinematics and electromyographic recordings were used to characterize locomotion. ISMS could induce a bilateral locomotor pattern similar to that obtained with perineal stimulation, and the characteristics of locomotion varied according to the spinal segment stimulated. Mechanisms by which ISMS could evoke locomotion were then investigated by stimulating, inactivating, or lesioning different spinal structures. Dorsal root stimulation (DRS), just like ISMS, could evoke a variety of ipsi- and bilateral nonlocomotor movements as well as locomotor responses. This suggests that sensory afferent pathways are involved in the production of locomotion by ISMS. Microinjections of yohimbine (noradrenergic antagonist) in L(3) and L(4) segments or a complete second spinal lesion at L(3)-L(4) abolished all locomotor activity evoked by ISMS applied at more caudal segments. Progressive dorsoventral spinal lesions at L(3) or L(4) and restricted ventral lesions at L(4) further suggest that the integrity of the ventral or ventrolateral funiculi as well as the L(3)-L(4) segments are critical for the induction of locomotion by ISMS at L(5) to S(1) or by DRS at these caudal segments.

Adrenergic alpha-Antagonists↗