Exogenous NO administration and α-adrenergic vasoconstriction in human limbs

2003 ◽  
Vol 95 (6) ◽  
pp. 2370-2374 ◽  
Author(s):  
Jaya B. Rosenmeier ◽  
Sandy J. Fritzlar ◽  
Frank A. Dinenno ◽  
Michael J. Joyner
Keyword(s):  
Blood Flow ◽  
Skeletal Muscles ◽  
Forearm Blood Flow ◽  
Norepinephrine Release ◽  
Vascular Conductance ◽  
No Donor ◽  
Exercise Hyperemia ◽  
Functional Sympatholysis ◽  
Human Forearm ◽  
Forearm Vascular Conductance

Nitric oxide (NO) is capable of blunting α-adrenergic vasoconstriction in contracting skeletal muscles of experimental animals (functional sympatholysis). We therefore tested the hypothesis that exogenous NO administration can blunt α-adrenergic vasoconstriction in resting human limbs by measuring forearm blood flow (FBF; Doppler ultrasound) and blood pressure in eight healthy males during brachial artery infusions of three α-adrenergic constrictors (tyramine, which evokes endogenous norepinephrine release; phenylephrine, an α1-agonist; and clonidine, an α2-agonist). To simulate exercise hyperemia, the vasoconstriction caused by the α-agonists was compared during adenosine-mediated (>50% NO independent) and sodium nitroprusside-mediated (SNP; NO donor) vasodilation of the forearm. Both adenosine and SNP increased FBF from ∼35–40 to ∼200–250 ml/min. All three α-adrenergic constrictor drugs caused marked reductions in FBF and calculated forearm vascular conductance ( P < 0.05). The relative reductions in forearm vascular conductance caused by the α-adrenergic constrictors during SNP infusion were similar (tyramine, –74 ± 3 vs. –65 ± 2%; clonidine, –44 ± 6 vs. –44 ± 6%; P > 0.05) or slightly greater (phenylephrine, –47 ± 6 vs. –33 ± 6%; P < 0.05) compared with the responses during adenosine. In conclusion, these results indicate that exogenous NO sufficient to raise blood flow to levels simulating those seen during exercise does not blunt α-adrenergic vasoconstriction in the resting human forearm.

Evidence for sympatholysis at the onset of forearm exercise

2002 ◽  
Vol 93 (2) ◽  
pp. 555-560 ◽  
Author(s):  
Darren S. DeLorey ◽  
Simon S. Wang ◽  
J. Kevin Shoemaker
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Lower Body Negative Pressure ◽  
Voluntary Contraction ◽  
Dependent Manner ◽  
Vascular Conductance ◽  
Exercise Hyperemia ◽  
Forearm Vascular Conductance ◽  
Forearm Exercise ◽  
Handgrip Contractions

The effect of augmented sympathetic outflow on forearm vascular conductance after single handgrip contractions of graded intensity was examined to determine whether sympatholysis occurs early in exercise ( n = 7). While supine, subjects performed contractions that were 1 s in duration and 15, 30, and 60% of maximal voluntary contraction (MVC) in intensity. The contractions were repeated during control and lower body negative pressure (LBNP) (−40 mmHg) sessions. Forearm blood flow (FBF; Doppler ultrasound) and mean arterial pressure were measured continuously for 30 s before and 60 s after the single contractions. Vascular conductance (VC) was calculated. Total postcontraction blood flow increased in an exercise intensity-dependent manner. Compared with control, LBNP caused a reduction in baseline and postexercise FBF ( P < 0.05), VC ( P < 0.01), as well as total excess flow ( P < 0.01). Specifically, during LBNP, baseline FBF and VC were reduced by 29 and 34% of control, respectively ( P < 0.05). After the 15% MVC contraction, peak VC during LBNP was reduced by a magnitude similar to that during baseline (i.e., ∼30%), but it was only reduced by 15% during both the 30 and 60% MVC trials ( P < 0.01). It was concluded that the stimuli for exercise hyperemia during moderate and heavy, but not mild, handgrip exercise intensities, diminish the vasoconstrictor effects of LBNP. Furthermore, these data demonstrate that this sympatholysis occurs early in exercise.

scholarly journals Effect of PDE5 inhibition on the modulation of sympathetic α-adrenergic vasoconstriction in contracting skeletal muscle of young and older recreationally active humans

2015 ◽  
Vol 309 (11) ◽  
pp. H1867-H1875 ◽  
Author(s):  
Michael Nyberg ◽  
Peter Piil ◽  
Jon Egelund ◽  
Randy S. Sprague ◽  
Stefan P. Mortensen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Subjects ◽  
Pde5 Inhibitor ◽  
Knee Extensor ◽  
No Donor ◽  
Pde5 Inhibition ◽  
Exercise Hyperemia ◽  
Functional Sympatholysis ◽  
Venous Plasma

Aging is associated with an altered regulation of blood flow to contracting skeletal muscle; however, the precise mechanisms remain unclear. We recently demonstrated that inhibition of cGMP-binding phosphodiesterase 5 (PDE5) increased blood flow to contracting skeletal muscle of older but not young human subjects. Here we examined whether this effect of PDE5 inhibition was related to an improved ability to blunt α-adrenergic vasoconstriction (functional sympatholysis) and/or improved efficacy of local vasodilator pathways. A group of young (23 ± 1 yr) and a group of older (72 ± 1 yr) male subjects performed knee-extensor exercise in a control setting and following intake of the highly selective PDE5 inhibitor sildenafil. During both conditions, exercise was performed without and with arterial tyramine infusion to evoke endogenous norepinephrine release and consequently stimulation of α1- and α2-adrenergic receptors. The level of the sympatholytic compound ATP was measured in venous plasma by use of the microdialysis technique. Sildenafil increased ( P < 0.05) vascular conductance during exercise in the older group, but tyramine infusion reduced ( P < 0.05) this effect by 38 ± 9%. Similarly, tyramine reduced ( P < 0.05) the vasodilation induced by arterial infusion of a nitric oxide (NO) donor by 54 ± 9% in the older group, and this effect was not altered by sildenafil. Venous plasma [ATP] did not change with PDE5 inhibition in the older subjects during exercise. Collectively, PDE5 inhibition in older humans was not associated with an improved ability for functional sympatholysis. An improved efficacy of the NO system may be one mechanism underlying the effect of PDE5 inhibition on exercise hyperemia in aging.

Hypohydration affects forearm vascular conductance independent of heart rate during exercise

1992 ◽  
Vol 73 (4) ◽  
pp. 1232-1237 ◽  
Author(s):  
C. G. Tankersley ◽  
D. H. Zappe ◽  
T. G. Meister ◽  
W. L. Kenney
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Forearm Blood Flow ◽  
Body Core Temperature ◽  
Esophageal Temperature ◽  
Vascular Conductance ◽  
Cutaneous Vasodilation ◽  
Forearm Vascular Conductance ◽  
Body Core

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.

Augmented Muscle Vasodilatory Responses in Obese Children with Glu27 β2-Adrenoceptor Polymorphism

2008 ◽  
Vol 20 (2) ◽  
pp. 157-168 ◽  
Author(s):  
Alexandre G. da Silva ◽  
Mauricio M. Ribeiro ◽  
Ivani C. Trombetta ◽  
Christiane Nicolau ◽  
Eliana Frazzatto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow ◽  
Color Word ◽  
Isometric Exercise ◽  
Obese Children ◽  
Vascular Conductance ◽  
Word Test ◽  
Forearm Vascular Conductance ◽  
Stroop Color Word Test

This study examined forearm vasodilatation during mental challenge and exercise in 72 obese children (OC; age = 10 ± 0.1 years) homozygous with polymorphism in the allele 27 of the β2-adrenoceptors: Gln27 (n = 61) and Glu27 (n = 11). Forearm blood flow was recorded during 3 min of each using the Stroop color-word test (MS) and handgrip isometric exercise. Baseline hemodynamic and vascular measurements were similar. During the MS, peak forearm vascular conductance was significantly greater in group Glu27 (Δ = 0.35 ± 0.4 vs. 0.12 ± 0.1 units, respectively, p = .042). Similar results were found during exercise (Δ = 0.64 ± 0.1 vs. 0.13 ± 0.1 units, respectively, p = .035). Glu27 OC increased muscle vasodilatory responsiveness upon the MS and exercise.

Gly16 + Glu27 β2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

2005 ◽  
Vol 98 (3) ◽  
pp. 787-794 ◽  
Author(s):  
Ivani C. Trombetta ◽  
Luciana T. Batalha ◽  
Maria U. P. B. Rondon ◽  
Mateus C. Laterza ◽  
Eliana Frazzatto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Forearm Blood Flow ◽  
Muscle Sympathetic Nerve Activity ◽  
Isometric Exercise ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Forearm Vascular Conductance

We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

Abstract P172: Endothelial Function In The Early Years After Delivery: Effect Of Adverse Pregnancy Outcomes And Activity Behaviors

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Abbi D Lane-Cordova ◽  
Erin O'Connor ◽  
Janet M Catov ◽  
Bo Fernhall ◽  
Jihong Liu ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Function ◽  
Pregnancy Outcomes ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Adverse Pregnancy Outcomes ◽  
Early Years ◽  
Vascular Conductance ◽  
Forearm Vascular Conductance ◽  
Adverse Pregnancy

Introduction: Adverse pregnancy outcomes (APOs) are independently associated with cardiovascular disease (CVD). Endothelial dysfunction may indicate early CVD and can be influenced by physical activity (PA) and sedentary behavior (SED). Hypothesis: We hypothesized women with a past APO would have worse endothelial function versus controls and that mid-pregnancy and current PA would be directly related while SED would be inversely related to endothelial function in the years soon after delivery. Methods: We used venous occlusion plethysmography to measure baseline forearm blood flow, reactive hyperemia, and vascular conductance (forearm blood flow/mean arterial pressure) in a case control study of 53 women 6 mo to 3 yrs after a singleton birth; 26% with past APO, 21% African American, mean age=33±1 yrs, mean BMI=27.4±0.9 kg/m 2 . Current and mid-pregnancy leisure time PA and weekday SED were assessed with validated questionnaires. We evaluated differences in endothelial function by APO exposure with t-tests and relations of endothelial function with PA and SED with Spearman correlations. Results: Baseline forearm blood flow (APO: 1.6±0.2; non-APO: 1.8±0.1 ml*min -1 *100 ml -1 tissue, p=0.3) and reactive hyperemia (APO: 13.2±2; non-APO: 11.4±1 ml*min -1 *100 ml -1 , p=0.8) were similar between groups. Vascular conductance was non-significantly lower in women with a past APO: 1.7x10 -2 versus 2.1x10 -2 ml*min -1 *100 ml -1 mmHg -1 in women without a past APO, p<0.10. Vascular conductance was related to current and mid-pregnancy SED (figure) but not PA (r=0.2 and r=0.06, p>0.05 for mid-pregnancy and current PA). Associations of mid-pregnancy and current SED with vascular conductance after delivery persisted after adjustment for age and BMI. Conclusions: Forearm vascular conductance tended to be lower soon after delivery in women with an APO. Mid-pregnancy and current SED were inversely related to forearm vascular conductance and may represent targets for interventions aimed at improving endothelial function after delivery.

Thermoregulatory reflexes and cutaneous active vasodilation during heat stress in hypertensive humans

1998 ◽  
Vol 85 (1) ◽  
pp. 175-180 ◽  
Author(s):  
D. L. Kellogg ◽  
S. R. Morris ◽  
S. B. Rodriguez ◽  
Y. Liu ◽  
M. Grossmann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Skin Blood Flow ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Doppler Flowmetry ◽  
Forearm Vascular Conductance ◽  
Normotensive Subjects ◽  
Cutaneous Vascular Conductance

During dynamic exercise in the heat, increases in skin blood flow are attenuated in hypertensive subjects when compared with normotensive subjects. We studied responses to passive heat stress (water-perfused suits) in eight hypertensive and eight normotensive subjects. Forearm blood flow was measured by venous-occlusion plethysmography, mean arterial pressure (MAP) was measured by Finapres, and forearm vascular conductance (FVC) was calculated. Bretylium tosylate (BT) iontophoresis was used to block active vasoconstriction in a small area of skin. Skin blood flow was indexed by laser-Doppler flowmetry at BT-treated and untreated sites, and cutaneous vascular conductance was calculated. In normothermia, FVC was lower in hypertensive than in normotensive subjects ( P < 0.01). During heat stress, FVC rose to similar levels in both groups ( P > 0.80); concurrent cutaneous vascular conductance increases were unaffected by BT treatment ( P > 0.60). MAP was greater in hypertensive than in normotensive subjects during normothermia ( P < 0.05, hypertensive vs. normotensive subjects). During hyperthermia, MAP fell in hypertensive subjects but showed no statistically significant change in normotensive subjects ( P < 0.05, hypertensive vs. normotensive subjects). The internal temperature at which vasodilation began did not differ between groups ( P> 0.80). FVC is reduced during normothermia in unmedicated hypertensive subjects; however, they respond to passive heat stress in a fashion no different from normotensive subjects.

Sex differences in sympathetic neural and limb vascular reactivity to mental stress in humans

2013 ◽  
Vol 304 (3) ◽  
pp. H436-H443 ◽  
Author(s):  
Huan Yang ◽  
Thomas D. Drummer ◽  
Jason R. Carter
Keyword(s):  
Blood Flow ◽  
Mental Stress ◽  
Vascular Reactivity ◽  
Sympathetic Nerve Activity ◽  
Forearm Blood Flow ◽  
Muscle Sympathetic Nerve Activity ◽  
Vascular Conductance ◽  
Nerve Activity ◽  
Men And Women ◽  
Forearm Vascular Conductance

Mental stress elicits a robust and consistent forearm vasodilation, but vascular reactivity in the calf remains inconsistent. It has been reported that calf vascular responses to MS may be sex dependent. Muscle sympathetic nerve activity (MSNA) is an important contributor to calf blood flow (CBF), yet the relations between sex, limb blood flow, and MSNA reactivity to mental stress have not been explored. We hypothesized that mental stress would elicit more dramatic vasodilation of the limbs in women and that this might be explained by reduced MSNA reactivity and/or blunted sympathetic vascular transduction. We measured heart rate (HR), mean arterial pressure (MAP), CBF, calf vascular conductance (CVC), forearm blood flow (FBF), forearm vascular conductance (FVC), and MSNA concurrently in 18 men (age: 23 ± 2 yr) and 16 women (age: 24 ± 2 yr) during 5 min of supine baseline and 5 min of mental stress. Mental stress elicited similar increases in MAP (Δ10 ± 1 vs. Δ11 ± 1 mmHg), HR (Δ16 ± 2 vs. Δ17 ± 2 beats/min), FBF (Δ81 ± 16% vs. Δ83 ± 15%), and FVC (Δ62 ± 13% vs. Δ65 ± 13%) in men and women, respectively. In contrast, CBF (Δ16 ± 8% vs. Δ37 ± 9%, P = 0.036) and CVC (Δ4 ± 7% vs. Δ24 ± 8%, P = 0.036) responses were exaggerated in women compared with men. Changes in FVC were significantly correlated with changes in CVC in women ( r = 0.681, P = 0.004) but not in men. MSNA reactivity to mental stress was not different between men and women; however, changes in CVC were negatively correlated with increases of MSNA in men ( r = −0.411, P = 0.045) but not in women. In conclusion, our data suggest different patterns of calf vascular reactivity to mental stress in men and women that might relate, in part, to altered vascular transduction of MSNA.

Selective α2-adrenergic properties of dexmedetomidine over clonidine in the human forearm

2005 ◽  
Vol 99 (2) ◽  
pp. 587-592 ◽  
Author(s):  
Shizue Masuki ◽  
Frank A. Dinenno ◽  
Michael J. Joyner ◽  
John H. Eisenach
Keyword(s):  
Blood Flow ◽  
Young Adults ◽  
Brachial Artery ◽  
Forearm Blood Flow ◽  
Adrenergic Blockade ◽  
Norepinephrine Release ◽  
Similar Extent ◽  
Human Forearm ◽  
Before And After

We tested the hypothesis that dexmedetomidine (Dex) has greater α2- vs. α1 selectivity than clonidine and causes more α2-selective vasoconstriction in the human forearm. After local β-adrenergic blockade with propranolol, forearm blood flow (plethysmography) responses to brachial artery administration of Dex, clonidine, and phenylephrine (α1-agonist) were determined in healthy young adults before and after α2-blockade with yohimbine ( n = 10) or α1-blockade with prazosin ( n = 9). Yohimbine had no effect on phenylephrine-mediated vasoconstriction but blunted Dex-mediated vasoconstriction (mean ± SE: −41 ± 5 vs. −11 ± 2%; before vs. after yohimbine) more than clonidine-mediated vasoconstriction (−39 ± 5 vs. −28 ± 4%; before vs. after yohimbine) ( P < 0.02). Prazosin blunted phenylephrine-mediated vasoconstriction (−39 ± 4 vs. −8 ± 2%; before vs. after prazosin) but had similar effects on both Dex- (−30 ± 4 vs. −39 ± 6%; before vs. after prazosin) and clonidine-mediated vasoconstriction (−29 ± 3 vs. −41 ± 7%; before vs. after prazosin) ( P > 0.7). Both Dex and clonidine reduced deep forearm venous norepinephrine concentrations to a similar extent (−59 ± 12 vs. −55 ± 10 pg/ml; Dex vs. clonidine, P > 0.6); this effect was abolished by yohimbine and blunted by prazosin. These results suggest that Dex causes more α2-selective vasoconstriction in the forearm than clonidine. The similar vasoconstrictor responses to both drugs after prazosin might be explained by the presynaptic effects on norepinephrine release.

scholarly journals Hyperbaric hyperoxia reduces exercising forearm blood flow in humans

2011 ◽  
Vol 300 (5) ◽  
pp. H1892-H1897 ◽  
Author(s):  
Darren P. Casey ◽  
Michael J. Joyner ◽  
Paul L. Claus ◽  
Timothy B. Curry
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Muscle Blood Flow ◽  
Hyperbaric Hyperoxia ◽  
Exercise Hyperemia ◽  
Forearm Vascular Conductance ◽  
Forearm Exercise ◽  
The Impact ◽  
Hyperemic Response

Hypoxia during exercise augments blood flow in active muscles to maintain the delivery of O2 at normoxic levels. However, the impact of hyperoxia on skeletal muscle blood flow during exercise is not completely understood. Therefore, we tested the hypothesis that the hyperemic response to forearm exercise during hyperbaric hyperoxia would be blunted compared with exercise during normoxia. Seven subjects (6 men/1 woman; 25 ± 1 yr) performed forearm exercise (20% of maximum) under normoxic and hyperoxic conditions. Forearm blood flow (FBF; in ml/min) was measured using Doppler ultrasound. Forearm vascular conductance (FVC; in ml·min−1·100 mmHg−1) was calculated from FBF and blood pressure (in mmHg; brachial arterial catheter). Studies were performed in a hyperbaric chamber with the subjects supine at 1 atmospheres absolute (ATA) (sea level) while breathing normoxic gas [21% O2, 1 ATA; inspired Po2 (PiO2) ≈ 150 mmHg] and at 2.82 ATA while breathing hyperbaric normoxic (7.4% O2, 2.82 ATA, PiO2 ≈ 150 mmHg) and hyperoxic (100% O2, 2.82 ATA, PiO2 ≈ 2,100 mmHg) gas. Resting FBF and FVC were less during hyperbaric hyperoxia compared with hyperbaric normoxia ( P < 0.05). The change in FBF and FVC (Δ from rest) during exercise under normoxia (204 ± 29 ml/min and 229 ± 37 ml·min−1·100 mmHg−1, respectively) and hyperbaric normoxia (203 ± 28 ml/min and 217 ± 35 ml·min−1·100 mmHg−1, respectively) did not differ ( P = 0.66–0.99). However, the ΔFBF (166 ± 21 ml/min) and ΔFVC (163 ± 23 ml·min−1·100 mmHg−1) during hyperbaric hyperoxia were substantially attenuated compared with other conditions ( P < 0.01). Our data suggest that exercise hyperemia in skeletal muscle is highly dependent on oxygen availability during hyperoxia.

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