ArticleClinical autonomic research : official journal of the Clinical Autonomic Research Society1998
The effect of noradrenaline, angiotensin II and vasopressin on blood flow and sensitivity to heat in capsaicin-treated skin.
Article in Clinical autonomic research : official journal of the Clinical Autonomic Research Society, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 25 citations in OpenAlex.
- Repeated local administration of noradrenaline or saline inhibits thermal hyperalgesia in pain-sensitized human skin.British journal of clinical pharmacology · 2001Trial
- Angiotensin receptors and neuropathic pain.Pain reports · 2021Review
- Article
- The sympathetic nervous system and pain.Neuromolecular medicine · 2008Review
Corrections and comments
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1 author at 1 institution in 1 country.
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Abstract
The effect of iontophoretically applied noradrenaline, angiotensin II and vasopressin on blood flow and sensitivity to heat was investigated in the capsaicin-treated forearms of 52 healthy volunteers. Non-specific effects of a 4-min saline iontophoresis were investigated in another 19 subjects. Pretreatment with phentolamine inhibited vasoconstriction and thermal hyperalgesia to noradrenaline, indicating that alpha-adrenoceptors mediated these responses. The intensity of thermal hyperalgesia differed significantly across the following treatments: saline (heat pain threshold 1.1 degrees C lower than at control sites), angiotensin II (3.4 degrees C), noradrenaline (6.4 degrees C) and vasopressin (9.0 degrees C). Decreases in skin blood flow were significantly greater after the iontophoresis of noradrenaline (65% reduction from baseline) and vasopressin (68%) than after the iontophoresis of angiotensin II (45%). In contrast to the other two drugs, angiotensin II induced thermal hyperalgesia in proportion to the intensity of vasoconstriction. The findings suggest that iontophoretic currents induce minor non-specific thermal hyperalgesia. Angiotensin II appears to increase sensitivity to heat by an ischaemic mechanism, whereas an additional non-vascular influence contributes to thermal hyperalgesia induced by noradrenaline and vasopressin. These mechanisms could contribute to hyperalgesia in chronic inflammatory or neuropathic pain syndromes.
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