The role of myogenic relaxation, adenosine and prostaglandins in human forearm reactive hyperaemia.

Abstract

SUMMARY1. Forearm blood flow was measured bilaterally in healthy young male and female volunteers, in the basal state and after upper-arm occlusion of arterial or venous blood flow for 1-20 min. The investigations were repeated after pre-treatment with drugs affecting vascular prostaglandins and/or adenosine.2. Simultaneous arterial occlusion in one arm and venous occlusion in the contralateral arm for up to 20 min elicited a considerable reactive hyperaemia in the arm subjected to arterial occlusion, but completely failed to elevate the post-occlusive flow in the arm subjected to venous occlusion above the pre-occlusive level.3. When the arterial occlusion was increased from 1 to 20 min there was a progressive increase in the subsequent reactive hyperaemia, up to 30 ml 100 ml tissue-1. The time dependence following 1-3 min of arterial occlusion was based on a facilitation of the peak post-occlusive flow, while prolongation of the arterial occlusion from 3 to 20 min augmented the reactive hyperaemia mainly by increasing its duration.4. Inhibition of prostaglandin synthesis with ibuprofen reduced the total reactive hyperaemia following 3-5 min of arterial occlusion by up to 70 %. This attenuation was due both to a reduction of peak post-occlusive flow and to a shortening of the duration of the post-occlusive hyperaemia.5. The adenosine receptor antagonist theophylline reduced the reactive hyperaemia following 5 min of arterial occlusion by about 35 %. Combined treatment with ibuprofen and theophylline did not reduce the reactive hyperaemia more than either drug alone.6. Infusion of dipyridamole, a drug which inhibits the elimination of adenosine, reinforced the reactive hyperaemia by about 45 %. This effect of dipyridamole was completely inhibited by administration of theophylline, and also by ibuprofen.7. Plasma levels of adenosine, hypoxanthine and uric acid were maintained during the reactive hyperaemia, indicating increased production of purines during or immediately after the ischaemia.

Blockade of vascular ATP-sensitive potassium channels reduces the vasodilator response to ischaemia in humans

“…Indeed, several reports have suggested that only the initial cellular potassium efflux after ischaemia is mediated by activation of K ATP channels [36,37]. The delayed vasodilator response to ischaemia seems predominantly to be mediated by other mechanisms, including the endothelial release of endothelium-derived nitric oxide [38] and prostaglandins [39,40]. This may explain why total flow debt repayment can be inhibited by N G -monomethyl-l-arginine (a specific inhibitor of nitric oxide-synthase) [38] or by ibuprofen (a prostaglandin synthase inhibitor) [39], but not by the K ATP channel blocker glibenclamide.…”

Impaired endothelium mediated vascular reactivity in endogenous Cushing's syndrome

“…Transient arterial occlusion results in vasodilation of the resistance vessels and a decrease in the tone of both the resistance and conduit vessels due to metabolic and myogenic mechanisms [28][29][30]. Restoration of perfusion pressure at the release of arterial occlusion is followed by an increase in blood flow to the ischaemic tissues and a flow mediated vasodilatory response in the proximal conduit vessels [31].…”

Anestesia na população negra

“…Hiperemia reativa no negro envolve mecanismos complexos através de mediadores como prostaciclina e adenosina na vasodilatação simpá-tica, incluindo a redução do efeito vasodilatador do NO no músculo liso. A reatividade diferenciada ao estresse pode contribuir para diferenças raciais na etiopatogenia, prevalência e complicações da HAS 46,47 . Diferente do hipertenso caucasiano, o negro hipertenso com insuficiência cardíaca congestiva apresenta menor resposta ao anti-hipertensivo inibidor da enzima de conversão de angiotensina I (IECA ), como captopril e enalapril, antagonistas do receptor AT 1 e β bloqueadores 13,14,22,[47][48][49][50][51] .…”

“…Reactive hyperemia in blacks involves complex mechanisms through mediators such as prostacyclin and adenosine in sympathetic vasodilation, including a decreased vasodilating effect in smooth muscles of NO. Differentiated reactivity to stress may contribute to racial differences in SAH ethiopathogeny, prevalence and complications 46,47 . Differently from hypertensive Caucasians, hypertensive blacks with congestive heart failure show a poorer response to angiotensin converting enzyme (ACE) inhibitors, such as captopril and enalapril, AT 1 receptor antagonists and β-blockers 13,14,22,[47][48][49][50][51] .…”