Trial reportBritish journal of clinical pharmacology2004
The I1-imidazoline agonist moxonidine decreases sympathetic tone under physical and mental stress.
Trial report in British journal of clinical pharmacology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Effects of moxonidine on sympathetic nervous system activity: An update on metabolism, cardio, and other target-organ protection.Journal of pharmacy & bioallied sciences · 2013Review
- Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsMoxonidine is an I1-imidazoline receptor agonist that reduces blood pressure by inhibition of central sympathetic activity. The effects of the drug under physical and mental stress have not been studied in detail.
methodsWe investigated the effects of 0.4 mg moxonidine orally on sympathetic activity, blood pressure and heart rate in a double-blind, placebo-controlled crossover study in 12 healthy volunteers. The subjects underwent physical exercise test using bicycle ergometry and a mental stress test using an adaptive reaction test device. Potential association of parameters with the GNB3 C825T polymorphism was also assessed.
resultsUnder resting conditions, moxonidine decreased plasma noradrenaline (NA: -66.1 +/- 12 pg ml(-1); P < 0.01 vs placebo) and adrenaline (A: -18.8 +/- 6 pg ml(-1); P < 0.05 vs placebo). Physical exercise evoked a significant increase in plasma NA and A (NA: 760 +/- 98 pg ml(-1); A: 97 +/- 9 pg ml(-1); P < 0.001 vs baseline), which was significantly reduced after pretreatment with moxonidine (NA: 627 +/- 68 pg ml(-1); P < 0.05 vs placebo; A: 42.8 +/- 4 pg ml(-1); P < 0.01 vs placebo). Maximal physical exercise capacity was not limited by moxonidine (NS). During the mental stress test, increases in NA (placebo: 146 +/- 24 pg ml(-1), moxonidine: 84 +/- 26 pg ml(-1); P < 0.01 vs placebo) and A (placebo: 22.8 +/- 9 pg ml(-1), moxonidine: 8.0 +/- 8 pg ml(-1); P < 0.01 vs placebo) were significantly reduced after pretreatment with moxonidine. Increases in blood pressure during mental stress were significantly lower after pretreatment with moxonidine (P < 0.05 vs placebo). There was no association of the response to moxonidine with GNB3 genotypes (NS).
conclusionsMoxonidine decreases total sympathetic tone under basal conditions as well as during physical exercise and mental stress without limiting absolute exercise capacity. Thus, moxonidine appears suitable for the treatment of patients with high SNS activity and hypertension induced by physical or mental stress. As the drug does not reduce exercise capacity, it may be considered as an alternative to beta-adrenoceptor blockers in selected patients.
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