Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm

Engelke, K. A.; Halliwill, John R.; Proctor, David N.; Dietz, Niki M.; Joyner, Michael J.

doi:10.1152/jappl.1996.81.4.1807

Cited by 229 publications

(258 citation statements)

References 24 publications

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“…Regardless of the initiating event, the relaxation of vascular smooth muscle in the resistance vessels appears to be due in part to activation of inwardly rectifying potassium channels (K IR ) (9). The results of most (8,11,27,32) but not all (10, 23) studies have found that endothelium signaling pathways make little or no contribution to peak reactive hyperemia in humans. In isolated vessels, endothelium removal or inhibition of nitric oxide synthase partially blocked both peak reactive dilation and the duration of dilation (17,18).…”

Section: Discussionmentioning

confidence: 99%

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Jasperse

Shoemaker

Gray

et al. 2015

Journal of Applied Physiology

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Jasperse JL, Shoemaker JK, Gray EJ, Clifford PS. Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia. J Appl Physiol 119: 569 -575, 2015. First published July 2, 2015; doi:10.1152/japplphysiol.01253.2013.-Studies have reported a greater blood flow response to muscle contractions when the limb is below the heart compared with above the heart, and these results have been interpreted as evidence for a skeletal muscle pump contribution to exercise hyperemia. If limb position affects the blood flow response to other vascular challenges such as reactive hyperemia, this interpretation may not be correct. We hypothesized that the magnitude of reactive hyperemia would be greater with the limb below the heart. Brachial artery blood flow (Doppler ultrasound) and blood pressure (finger-cuff plethysmography) were measured in 10 healthy volunteers. Subjects lay supine with one arm supported in two different positions: above or below the heart. Reactive hyperemia was produced by occlusion of arterial inflow for varying durations: 0.5 min, 1 min, 2 min, or 5 min in randomized order. Peak increases in blood flow were 77 Ϯ 11, 178 Ϯ 24, 291 Ϯ 25, and 398 Ϯ 33 ml/min above the heart and 96 Ϯ 19, 279 Ϯ 62, 550 Ϯ 60, and 711 Ϯ 69 ml/min below the heart (P Ͻ 0.05). Thus a standard stimulus (vascular occlusion) elicited different responses depending on limb position. To determine whether these differences were due to mechanisms intrinsic to the arterial wall, a second set of experiments was performed in which acute intraluminal pressure reduction for 0.5 min, 1 min, 2 min, or 5 min was performed in isolated rat soleus feed arteries (n ϭ 12). The magnitude of dilation upon pressure restoration was greater when acute pressure reduction occurred from 85 mmHg (mimicking pressure in the arm below the heart; 28.3 Ϯ 7.9, 37.5 Ϯ 5.9, 55.1 Ϯ 9.9, and 68.9 Ϯ 8.6% dilation) than from 48 mmHg (mimicking pressure in the arm above the heart; 20.8 Ϯ 4.8, 22.6 Ϯ 4.4, 31.2 Ϯ 5.8, and 49.2 Ϯ 7.1% dilation). These data support the hypothesis that arm position differences in reactive hyperemia are at least partially mediated by mechanisms intrinsic to the arterial wall. Overall, these results suggest the need to reevaluate studies employing positional changes to examine muscle pump influences on exercise hyperemia. muscle blood flow; muscle contraction; skeletal muscle pump; functional hyperemia AT THE ONSET OF DYNAMIC EXERCISE, there is a rapid increase in blood flow [30,31,41, and see Fig. 2 in Clifford and Hellsten (5)]. In fact, even a single muscle contraction produces a prompt increase in blood flow (1,7,14,26,36,39). There has been a debate over the last few decades about whether this rapid hyperemia is due to the muscle pump mechanism or to rapid vasodilation (5, 35).The muscle pump, as described by Laughlin (20), depends on an increased pressure gradient across the skeletal muscle vascular bed. Muscle contraction compresses the veins within the contracting muscle, expelling blood from the veins. ...

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Section: Discussionmentioning

confidence: 99%

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Jasperse

Shoemaker

Gray

et al. 2015

Journal of Applied Physiology

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“…Taken together, it seems reasonable to conclude that PGs do not play an essential role in skeletal muscle vasodilation during dynamic exercise under normoxic conditions. However, available evidence in humans suggests that PGs contribute to the rise in skeletal muscle blood flow following periods of limb ischemia (2,10,14,20). Moreover, COX inhibition has been shown to attenuate muscle vasodilation evoked by systemic hypoxia in rats (25).…”

Section: Discussionmentioning

confidence: 99%

“…These findings are based on little to no change in muscle blood flow following PG synthesis inhibition. However, PGs have been reported to be involved in the regulation of skeletal muscle blood flow following periods of ischemia (2,10,14,20) and during systemic hypoxia (25). Therefore, it is possible that the PGs may become a more important vasodilator signal during exercise under conditions of reduced oxygen availability.…”

mentioning

confidence: 99%

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Casey

Joyner

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Casey DP, Joyner MJ. Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle. Am J Physiol Heart Circ Physiol 301: H261-H268, 2011. First published May 2, 2011; doi:10.1152/ajpheart.00222.2011.-We tested the hypothesis that 1) prostaglandins (PGs) contribute to compensatory vasodilation in contracting human forearm subjected to acute hypoperfusion, and 2) the combined inhibition of PGs and nitric oxide would attenuate the compensatory vasodilation more than PG inhibition alone. In separate protocols, subjects performed forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included baseline, exercise before inflation, exercise with inflation, and exercise after deflation. Forearm blood flow (FBF; ultrasound) and local (brachial artery) and systemic arterial pressure [mean arterial pressure (MAP); Finometer] were measured. In protocol 1 (n ϭ 8), exercise was repeated during cyclooxygenase (COX) inhibition (Ketorolac) alone and during Ke-In protocol 2 (n ϭ 8), exercise was repeated during L-NMMA alone and during L-NMMA-Ketorolac. Forearm vascular conductance (FVC; ml·min Ϫ1 · 100 mmHg Ϫ1 ) was calculated from FBF (ml/min) and local MAP (mmHg). The percent recovery in FVC during inflation was calculated as (steady-state inflation ϩ exercise value Ϫ nadir)/ [steady-state exercise (control) value Ϫ nadir] ϫ 100. In protocol 1, COX inhibition alone did not reduce the %FVC recovery compared with the control (no drug) trial (92 Ϯ 11 vs. 100 Ϯ 10%, P ϭ 0.83). However, combined COX-nitric oxide synthase (NOS) inhibition caused a substantial reduction in %FVC recovery (54 Ϯ 8%, P Ͻ 0.05 vs. Ketorolac alone). In protocol 2, the percent recovery in FVC was attenuated with NOS inhibition alone (69 Ϯ 9 vs. 107 Ϯ 10%, P Ͻ 0.01) but not attenuated further during combined NOS-COX inhibition (62 Ϯ 10%, P ϭ 0.74 vs. L-NMMA alone). Our data indicate that PGs are not obligatory to the compensatory dilation observed during forearm exercise with hypoperfusion.prostaglandins; blood flow; nitric oxide; vasodilation; exercise; hypoperfusion DURING ACUTE EXPERIMENTAL hypoperfusion, skeletal muscle blood flow is partially restored in the exercising forearm through local dilator mechanisms and/or a myogenic response (4, 5). Along these lines, nitric oxide synthase (NOS) inhibition blunts the magnitude of restoration of forearm blood flow (FBF) and vascular conductance (FVC) during exercise with acute hypoperfusion by 10 -20% (4). The fact that a substantial flow restoration still occurs despite NOS inhibition suggests that additional vasodilator signals are likely involved in this response.In general, prostaglandins (PGs) do not appear to contribute significantly to the exercise hyperemic response to dynamic contractions (9,16,20,29,31). These findings are based on little to no change in muscle blood flow following PG synthesis inhibition. However, PGs have been reported to be involved in the regulation of skeletal muscle ...

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“…In humans, moreover, insulin has been shown to stimulate vasodilatory effects by inducing endothelial nitric oxide (NO) production [21]. The idea that NO plays a part in intramuscular reactive hyperaemia is supported by most [22,23,24], but not all studies [25] using venous occlusion plethysmography. Therefore, in the present study, enhanced endothelial NO production might have contributed to insulin-mediated changes in intramuscular reactive hyperaemia.…”

Section: Discussionmentioning

confidence: 99%

Physiological hyperinsulinaemia increases intramuscular microvascular reactive hyperaemia and vasomotion in healthy volunteers

et al. 2004

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Aims/hypothesis. Insulin possesses vasodilatory actions that may be important in regulating its access to insulin-sensitive tissues. Our study aims to directly measure changes in response to insulin in the human skeletal muscle microcirculation. Measurement was by an implanted laser Doppler probe. Methods. We investigated changes in intramuscular and skin microvascular perfusion in 12 healthy individuals during a hyperinsulinaemic and a control clamp. We determined leg blood flow with plethysmography, finger skin functional capillary recruitment with capillaroscopy, endothelium-(in)dependent vasodilation by iontophoresis of acetylcholine and sodium nitroprusside, and leg intramuscular reactive hyperaemia and vasomotion with laser Doppler measurements. Results. Compared to the control study, hyperinsulinaemia (416±82 pmol/l) caused: (i) an increase in leg blood flow (1.0±1.0 vs 0.1±0.6 ml·min −1 ·100 ml, p<0.05); (ii) an increase in finger skin capillary recruitment (14.9±10.1 vs -5.6±11.0%, p<0.01); (iii) no change in baseline laser Doppler perfusion either in finger skin or leg muscle; (iv) a tendency to increase acetylcholine-mediated vasodilation (475±534 vs 114±337%, p=0.07) with no change in sodiumnitroprusside-mediated vasodilation (p=0.2) in finger skin; (v) an increase in intramuscular reactive hyperaemia (423±507 vs 0±220%, p<0.01); and (vi) a decrease in time needed to reach peak intramuscular perfusion (−3.6±3.0 vs 1.1±3.1 s, p<0.01). In addition, hyperinsulinaemia induced an increase in intramuscular vasomotion by increasing the contribution of frequencies between 0.01 and 0.04 Hz (p<0.05 for all), which probably represents increased endothelial and neurogenic activity. Conclusions/interpretation. Physiological hyperinsulinaemia not only stimulates total blood flow and skin microvascular perfusion, but also augments human skeletal muscle microvascular recruitment and vasomotion as detected directly by laser Doppler measurements.

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Contribution of nitric oxide and prostaglandins to reactive hyperemia in the human forearm

Cited by 229 publications

References 24 publications

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Positional differences in reactive hyperemia provide insight into initial phase of exercise hyperemia

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Physiological hyperinsulinaemia increases intramuscular microvascular reactive hyperaemia and vasomotion in healthy volunteers

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