Identification of adenosine triphosphate in human plasma and the concentration in the venous effluent of forearm muscles before, during and after sustained contractions

Forrester, T; Lind, A. R.

doi:10.1113/jphysiol.1969.sp008917

Cited by 126 publications

(74 citation statements)

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“…2011). During exercise in normal environmental conditions, plasma ATP also increases in the forearm and leg circulations (Forrester & Lind, 1969; Forrester, 1972; González‐Alonso et al . 2002; Mortensen et al .…”

Section: Introductionmentioning

confidence: 99%

Blood temperature and perfusion to exercising and non‐exercising human limbs

González‐Alonso

Calbet

Boushel

et al. 2015

Experimental Physiology

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New Findings What is the central question of this study? Temperature‐sensitive mechanisms are thought to contribute to blood‐flow regulation, but the relationship between exercising and non‐exercising limb perfusion and blood temperature is not established. What is the main finding and its importance? The close coupling among perfusion, blood temperature and aerobic metabolism in exercising and non‐exercising extremities across different exercise modalities and activity levels and the tight association between limb vasodilatation and increases in plasma ATP suggest that both temperature‐ and metabolism‐sensitive mechanisms are important for the control of human limb perfusion, possibly by activating ATP release from the erythrocytes. Temperature‐sensitive mechanisms may contribute to blood‐flow regulation, but the influence of temperature on perfusion to exercising and non‐exercising human limbs is not established. Blood temperature (T B), blood flow and oxygen uptake (trueV˙O2) in the legs and arms were measured in 16 healthy humans during 90 min of leg and arm exercise and during exhaustive incremental leg or arm exercise. During prolonged exercise, leg blood flow (LBF) was fourfold higher than arm blood flow (ABF) in association with higher T B and limb trueV˙O2. Leg and arm vascular conductance during exercise compared with rest was related closely to T B (r 2 = 0.91; P < 0.05), plasma ATP (r 2 = 0.94; P < 0.05) and limb V˙normalO2 (r 2 = 0.99; P < 0.05). During incremental leg exercise, LBF increased in association with elevations in T B and limb trueV˙O2, whereas ABF, arm T B and V˙normalO2 remained largely unchanged. During incremental arm exercise, both ABF and LBF increased in relationship to similar increases in trueV˙O2. In 12 trained males, increases in femoral T B and LBF during incremental leg exercise were mirrored by similar pulmonary artery T B and cardiac output dynamics, suggesting that processes in active limbs dominate central temperature and perfusion responses. The present data reveal a close coupling among perfusion, T B and aerobic metabolism in exercising and non‐exercising extremities and a tight association between limb vasodilatation and increases in plasma ATP. These findings suggest that temperature and V˙normalO2 contribute to the regulation of limb perfusion through control of intravascular ATP.

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Section: Introductionmentioning

confidence: 99%

Blood temperature and perfusion to exercising and non‐exercising human limbs

González‐Alonso

Calbet

Boushel

et al. 2015

Experimental Physiology

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“…First, since indomethacin inhibits prostaglandin synthetase (Ferreira, Moncada & Vane, 1971;Vane, 1971) the results could be ascribed to supersensitivity; secondly, indomethacin inhibits prostaglandin dehydrogenase in the dose-range used (Flower, 1974), so retarded break-down of PGE1 was feasible. been detected in vasoactive quantities in the venous effluent from exercising human forearm muscle (Forrester & Lind, 1969;Forrester, 1972) and has recently been identified in the blood stream after whole-body exercise (Parkinson, 1973).…”

Section: Pmentioning

confidence: 99%

Communications

1974

The Journal of Physiology

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When muscles shorten they produce heat faster than during isometric contraction. This extra heat production is the shortening heat (Hill, 1938). In a series of closely spaced tetanic contractions of frog sartorius muscle at O0 C, the shortening heat is less in the second and subsequent contractions than in the first. Fig. 1 A shows records of the heat rate during the first and second contractions of a series at 5 sec intervals. Fig. 1B shows how the average value of the shortening heat falls during such series, to 66 + 4 % (mean+ s.E.) of the initial value by the third contraction. By the 10th contraction the shortening heat was found to be only 15 + 18 % of the initial value (3 observations). The reduction in the shortening heat is less when the interval between the tetani is greater, and is hardly evident when this interval is 40 sec.The reduction in shortening heat might be due to previous activation, metabolic activity, or shortening. If either activation or metabolic activity were the cause, an isometric contraction should also reduce the shortening heat in subsequent contractions. The results in Fig. 1B show that this is not the case; thus it can be concluded that the reduction in shortening heat is a specific consequence of previous shortening.The isometric tension developed falls during a series of contractions but the tension exerted during shortening at speeds of 10, 20 and 30 mm/sec 98P

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“…This protection from ischemic insult was suggested to occur through inhibition of ATP release from Panx1 channels, by a negative feedback mechanism involving the P2X 7 purinergic receptor [156]. Prolonged activation of P2X 7 receptors results in the opening of a large pore permeable to divalent cations such as Ca 2+ that eventually leads to cell death [170][171][172]. This study revealed that ischemic insult to cultured cortical astrocytes resulted in initial ATP release from Panx1 channels that in turn activated P2X 7 receptors, inducing closure of Panx1 channels, which prevented loss of integral intracellular constituents and averted cell death.…”

Section: Pannexin Channelsmentioning

confidence: 99%

“…The effects of ATP signaling have been observed throughout the vasculature in both homeostatic and pathological conditions, including: reactive hyperemia [7,8], hypoxiainduced vasodilation [9,10], alpha-adrenergic receptor mediated vasoconstriction [11], hypertension [12], VSMC proliferation in atherosclerosis and vascular inflammation [13][14][15][16][17]. Elucidation of the mechanisms regulating purine nucleotide release in the cells comprising the vascular wall is critical for both understanding the pathogenesis of vascular diseases and the identification of novel drug interventions.…”

Section: Purinergic Signaling In the Vasculaturementioning

confidence: 99%

“…The role of extracellular purines, including ATP, in the systemic circulation has been shown to be important for several vascular functions including the regulation of vascular tone [12,60], reactive hyperemia during contraction of skeletal muscle [7,8] and hypoxiainduced vasodilation [9,10,19]. Although there are well-described reports of ATP release occurring from both circulating erythrocytes and sympathetic nerves innervating vascular smooth muscle cells [10,[24][25][26][27][28][29][30]54], there is accumulating evidence indicating that endothelial and smooth muscle cells of the vascular wall can also release ATP [11,[19][20][21]84,114,168].…”

Section: Introductionmentioning

confidence: 99%

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Function and Regulation of Pannexin 1 Channels in the Vascular Endothelium

Lohman¹

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The nucleotide adenosine 5'-triphosphate (ATP) has classically been considered the cell's primary energy currency; however, a novel role for ATP as an extracellular autocrine/paracrine signaling molecule has evolved over the past century. Purinergic signaling is now known to regulate a plethora of physiological and pathophysiological processes in almost every organ system. In the vasculature, ATP and its metabolites elicit dual control over blood vessel tone and tissue perfusion, and purinergic signaling events have been implicated in vascular pathologies including atherosclerosis and inflammation.While the importance of extracellular ATP in the vascular system is well recognized, the mechanism(s) mediating the regulated release of the purine from vascular cells are less well understood and are a key target of current investigation. One such ATP-liberation mechanism has been ascribed to the recently identified pannexin (Panx) channels, namely Panx1. Initially, we characterized the expression and localization profiles of Panx isoforms across the systemic vasculature, identifying predominant representation by the Panx1 isoform in both smooth muscle (SMC) and endothelial cells (EC) comprising the blood vessel wall, with more heterogeneous expression profiles observed in specialized vascular systems including the heart, lung and kidney. In particular, the Panx1 isoform is highly expressed in ECs regardless of blood vessel type or size, while Panx1 expression is limited to SMCs of small arteries and arterioles. Panx1 forms hexameric channels in the plasma membrane of ECs, functioning to release ATP in response to a number of stimuli. However, prolonged Panx1 channel activity is extremely detrimental to cell viability. Here we report a novel negative regulatory mechanism that may govern the activity of Panx1 channels in ECs, by which the bioactive gas nitric oxide (NO) covalently modifies two cysteine (Cys) residues in the channel by a process termed S- reinforce the dual effect of purines on peripheral resistance and blood pressure. Purinergic Control of Vascular InflammationWhile the foundation for purinergic control of vascular functions was initially characterized extensively in the context of vascular reactivity and overall blood flow and pressure regulation, it has become increasingly clear that extracellular ATP also plays important regulatory roles in the vascular inflammatory response. Vascular inflammation can be characterized as acute (physiological) or chronic (pathological) in nature.The acute vascular inflammatory response is an innate process of inflammatory cell homing to infected or damaged tissues resulting from integrated cross-talk between circulating leukocytes and the vascular endothelium, primarily at the level of postcapillary venules [61]. This process has been highly studied and is now known to occur in a step-wise manner beginning with local recruitment, rolling (fast and slow), adhesion and final extravasation into the surrounding tissue (reviewed in [62...

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Identification of adenosine triphosphate in human plasma and the concentration in the venous effluent of forearm muscles before, during and after sustained contractions

Cited by 126 publications

References 11 publications

Blood temperature and perfusion to exercising and non‐exercising human limbs

Blood temperature and perfusion to exercising and non‐exercising human limbs

Communications

Function and Regulation of Pannexin 1 Channels in the Vascular Endothelium

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