Inhibitory effects of clonidine on the allergen-induced wheal-and-flare reactions in patients with extrinsic asthma

Lindgren, Bjiirn R.; Brundin, A; Andersson, Rolf G. G.

doi:10.1016/0091-6749(87)90244-2

Cited by 16 publications

(12 citation statements)

References 24 publications

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“…Our results are in accordance with the findings of Aceros et al, who reported that moxonidine (I1R agonist) reduces oxidative stress by increasing nischarin expression . Lindgren et al suggested that treatment with clonidine reduces allergen‐induced inflammatory reactions in subjects with extrinsic asthma . Zaitsev et al reported that imidazoline compounds protect against IL‐1β‐induced apoptosis in pancreatic β‐cells, possibly by inhibiting iNOS expression, a key element in this pathway …”

Section: Discussionsupporting

confidence: 92%

Effect of imidazoline‐1 receptor agonists on renal dysfunction in rats associated with chronic, sequential fructose and ethanol administration

Elkomy

Ibrahim

El-Fayoumi

et al. 2020

Clin Exp Pharma Physio

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Insulin resistance and chronic alcoholism are risk factors for renal dysfunction. This study investigated the therapeutic effects of two imidazoline‐1 receptor (I1R) agonists on renal dysfunction in rats after chronic, sequential fructose and ethanol administration. Daily drinking water was supplemented with fructose (10%, w/v) for 12 weeks and then with ethanol (20%, v/v) for another 8 weeks. Rats were treated with rilmenidine and clonidine in the last two weeks of the study. Blood glucose and serum insulin (sIns) levels, lipid profiles, kidney function and renal histopathology were evaluated at the end of the experiment. Additionally, renal gene expression of nischarin, phosphatidylcholine‐specific phospholipase C (PC‐PLC) and prostaglandin E2 (PGE2) were measured. Renal levels of superoxide dismutase (SOD), malondialdehyde (MDA), myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and total NO (tNO) were detected, and we determined the relative renal gene expression levels of alpha smooth muscle actin (α‐SMA), hydroxyproline, interleukin 10 (IL‐10), tumour necrosis factor alpha (TNF‐α) and caspase‐3. The results showed significant deterioration of blood glucose, sIns, lipid profiles, kidney function and renal histopathology in fructose/ethanol‐fed rats. Additionally, markers of inflammation, fibrosis, apoptosis and oxidative stress were upregulated. The administration of rilmenidine or clonidine significantly improved blood glucose and sIns levels and reduced renal dysfunction. Our work showed that chronic, sequential fructose and ethanol administration induced fasting hyperglycaemia and renal impairment, and these effects were ameliorated by I1R agonists.

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Section: Discussionsupporting

confidence: 92%

Effect of imidazoline‐1 receptor agonists on renal dysfunction in rats associated with chronic, sequential fructose and ethanol administration

Elkomy

Ibrahim

El-Fayoumi

et al. 2020

Clin Exp Pharma Physio

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“…However, intravenous phenylephrine in a dose which has significant cardiovascular effects, does not suppress the flare response (Kram et al, 1975) and this does not fit the hypothesis that adrenaline inhibits flare by o-adrenoceptor stimulation. In contrast, clonidine, an a2adrenoceptor agonist that decreases central sympathetic outflow, does inhibit both the weal and flare response to antigen in patients with asthma (Lindgren et al, 1987). It was argued that cr2-adrenoceptor stimulation of sensory C fibres in the skin explained this observation (Lindgren et al, 1987) and therefore adrenaline may inhibit flare by c2-adrenoceptor rather than a1-adrenoceptor stimulation.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, clonidine, an a2adrenoceptor agonist that decreases central sympathetic outflow, does inhibit both the weal and flare response to antigen in patients with asthma (Lindgren et al, 1987). It was argued that cr2-adrenoceptor stimulation of sensory C fibres in the skin explained this observation (Lindgren et al, 1987) and therefore adrenaline may inhibit flare by c2-adrenoceptor rather than a1-adrenoceptor stimulation. The inhibition of weal formation by adrenaline with the higher dose of antigen was blocked by pretreatment with ICI-118,551 suggesting that this is mediated via 132-adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

Importance of beta 2‐adrenoceptor stimulation in the suppression of intradermal antigen challenge by adrenaline.

Warren

Pixley

Dollery

1989

Brit J Clinical Pharma

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1 Seven atopic subjects received two injections of antigen and one of saline intradermally in the back on each of 4 separate days. They were pretreated with four different drug combinations: (a) adrenaline 0.3 mg subcutaneously over the deltoid muscle (b) subcutaneous adrenaline preceded by 5 mg of the specific ,32-adrenoceptor antagonist ICI 118,551 orally (c) 8 mg of salbutamol orally (d) placebo. Tablets were given 2 h before and subcutaneous injections 15 min before the intradermal injections of saline and antigen. 2 The median flare response to intradermal low dose antigen and high dose antigen after pretreatment with adrenaline was 4% and 49% of the response seen following pretreatment with placebo (P < 0.001). When adrenaline was preceded by ICI-118,551, the corresponding median flare responses were 2% and 44% (P < 0.001) of the placebo response. The flare response after pretreatment with salbutamol was not significantly different from placebo.3 Adrenaline suppressed the median weal response to the higher dose of antigen to 52% of the response after pretreatment with placebo (P < 0.05). This suppression by adrenaline was blocked by pretreatment with ICI 118,551. The median weal response after the highest dose of antigen was suppressed by salbutamol to 66% of the response seen after placebo, although this was not significant even when a further three subjects were studied with either salbutamol or placebo. 4 These results confirm that a small dose of systemic adrenaline attenuates the weal and flare response to intradermal antigen. This suppression of the weal response is blocked by a P2-adrenoceptor antagonist although it is only partially mimicked by high dose oral salbutamol. The suppression of the flare response may involve a-adrenoceptor stimulation.

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“…The effects of clonidine on airway diameter are controversial with studies demonstrating both bronchodilation and bronchoconstriction. Clonidine has been shown to attenuate bronchoconstriction in patients with asthma (102) and inhibit allergen‐induced wheal/flare reactions in patients with extrinsic asthma (103). To our knowledge, however, no articles on the use of clonidine in children with asthma have been published.…”

Section: Application Of Clonidine In Paediatric Anaesthesiamentioning

confidence: 99%

Clonidine in paediatric anaesthesia

Nishina

Mikawa

Shiga

et al. 1999

Pediatric Anesthesia

114

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Inhibitory effects of clonidine on the allergen-induced wheal-and-flare reactions in patients with extrinsic asthma

Cited by 16 publications

References 24 publications

Effect of imidazoline‐1 receptor agonists on renal dysfunction in rats associated with chronic, sequential fructose and ethanol administration

Effect of imidazoline‐1 receptor agonists on renal dysfunction in rats associated with chronic, sequential fructose and ethanol administration

Importance of beta 2‐adrenoceptor stimulation in the suppression of intradermal antigen challenge by adrenaline.

Clonidine in paediatric anaesthesia

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