DOES NITRIC OXIDE-MEDIATED, SYMPATHETIC VASODILATION OCCUR DURING ISCHEMIC HANDGRIP EXERCISE IN HUMANS? 1042

1996 ◽  
Vol 28 (Supplement) ◽  
pp. 175
Author(s):  
K A Engelke ◽  
N M Dietz ◽  
R T Fix ◽  
T T Samuel ◽  
M M Williams ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Handgrip Exercise ◽  
Ischemic Handgrip Exercise ◽  
Exercise In Humans

scholarly journals Tetrahydrobiopterin ameliorates the exaggerated exercise pressor response in patients with chronic kidney disease: a randomized controlled trial

2016 ◽  
Vol 310 (10) ◽  
pp. F1016-F1025 ◽  
Author(s):  
Ann M. Lin ◽  
Peizhou Liao ◽  
Erin C. Millson ◽  
Arshed A. Quyyumi ◽  
Jeanie Park
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Pressor Response ◽  
Controlled Trial ◽  
Treated Group ◽  
Handgrip Exercise ◽  
Significant Difference ◽  
Double Blinded ◽  
Oxide Synthase

Chronic kidney disease (CKD) patients have an exaggerated increase in blood pressure (BP) during rhythmic handgrip exercise (RHG 20%) and static handgrip exercise (SHG 30%). Nitric oxide levels increase during exercise and help prevent excessive hypertension by both increasing vasodilation and reducing sympathetic nerve activity (SNA). Therefore, we hypothesized that tetrahydrobiopterin (BH4), an essential cofactor for nitric oxide synthase, would ameliorate the exaggerated exercise pressor response in CKD patients. In a randomized, double-blinded, placebo-controlled trial, we tested the effects of 12 wk of sapropterin dihydrochloride (6 R-BH4; n = 18) versus placebo ( n = 14) treatement on BP and muscle SNA (MSNA) responses during RHG 20% and SHG 30% in CKD patients. The 6 R-BH4-treated group had a significantly lower systolic BP (+6 ± 1 vs. +13 ± 2 mmHg, P = 0.002) and mean arterial pressure response (+5 ± 1 vs. +10 ± 2 mmHg, P = 0.020) during RHG 20% and a significantly lower systolic BP response (+19 ± 3 vs. +28 ± 3 mmHg, P = 0.043) during SHG 30%. Under baseline conditions, there was no significant difference in MSNA responses between the groups; however, when the BP response during exercise was equalized between the groups using nitroprusside, the 6 R-BH4-treated group had a significantly lower MSNA response during RHG 20% (6R-BH4 vs. placebo, +12 ± 1 vs. +21 ± 2 bursts/min, P = 0.004) but not during SHG 30%. These findings suggest that 6 R-BH4 ameliorates the augmented BP response during RHG 20% and SHG 30% in CKD patients. A reduction in reflex activation of SNA may contribute to the decreased exercise pressor response during RHG 20% but not during SHG 30% in CKD patients.

Repeated increases in blood flow, independent of exercise, enhance conduit artery vasodilator function in humans

2011 ◽  
Vol 300 (2) ◽  
pp. H664-H669 ◽  
Author(s):  
Louise H. Naylor ◽  
Howard Carter ◽  
Matthew G. FitzSimons ◽  
N. Timothy Cable ◽  
Dick H. J. Thijssen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Complex Stimulus ◽  
Artery Blood Flow ◽  
Handgrip Exercise ◽  
Repeated Heating ◽  
Conduit Artery ◽  
Pressure Cuff ◽  
Ischemic Handgrip Exercise ◽  
Bilateral Heating

This study aimed to determine the importance of repeated increases in blood flow to conduit artery adaptation, using an exercise-independent repeated episodic stimulus. Recent studies suggest that exercise training improves vasodilator function of conduit arteries via shear stress-mediated mechanisms. However, exercise is a complex stimulus that may induce shear-independent adaptations. Nine healthy men immersed their forearms in water at 42°C for three 30-min sessions/wk across 8 wk. During each session, a pneumatic pressure cuff was inflated around one forearm to unilaterally modulate heating-induced increases in shear. Forearm heating was associated with an increase in brachial artery blood flow ( P < 0.001) and shear rate ( P < 0.001) in the uncuffed forearm; this response was attenuated in the cuffed limb ( P < 0.005). Repeated episodic exposure to bilateral heating induced an increase in endothelium-dependent vasodilation in response to 5-min ischemic ( P < 0.05) and ischemic handgrip exercise ( P < 0.005) stimuli in the uncuffed forearm, whereas the 8-wk heating intervention did not influence dilation to either stimulus in the cuffed limb. Endothelium-independent glyceryl trinitrate responses were not altered in either limb. Repeated heating increases blood flow to levels that enhance endothelium-mediated vasodilator function in humans. These findings reinforce the importance of the direct impacts of shear stress on the vascular endothelium in humans.

scholarly journals Ascorbic acid improves brachial artery vasodilation during progressive handgrip exercise in the elderly through a nitric oxide-mediated mechanism

2016 ◽  
Vol 310 (6) ◽  
pp. H765-H774 ◽  
Author(s):  
Joel D. Trinity ◽  
D. Walter Wray ◽  
Melissa A. H. Witman ◽  
Gwenael Layec ◽  
Zachary Barrett-O'Keefe ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Ascorbic Acid ◽  
Free Radical ◽  
Brachial Artery ◽  
Vascular Function ◽  
The Elderly ◽  
Voluntary Contraction ◽  
Dependent Manner ◽  
Handgrip Exercise ◽  
Age Related

The proposed mechanistic link between the age-related attenuation in vascular function and free radicals is an attractive hypothesis; however, direct evidence of free radical attenuation and a concomitant improvement in vascular function in the elderly is lacking. Therefore, this study sought to test the hypothesis that ascorbic acid (AA), administered intra-arterially during progressive handgrip exercise, improves brachial artery (BA) vasodilation in a nitric oxide (NO)-dependent manner, by mitigating free radical production. BA vasodilation (Doppler ultrasound) and free radical outflow [electron paramagnetic resonance (EPR) spectroscopy] were measured in seven healthy older adults (69 ± 2 yr) during handgrip exercise at 3, 6, 9, and 12 kg (∼13–52% of maximal voluntary contraction) during the control condition and nitric oxide synthase (NOS) inhibition via NG-monomethyl-l-arginine (l-NMMA), AA, and coinfusion of l-NMMA + AA. Baseline BA diameter was not altered by any of the treatments, while l-NMMA and l-NMMA + AA diminished baseline BA blood flow and shear rate. AA improved BA dilation compared with control at 9 kg (control: 6.5 ± 2.2%, AA: 10.9 ± 2.5%, P = 0.01) and 12 kg (control: 9.5 ± 2.7%, AA: 15.9 ± 3.7%, P < 0.01). NOS inhibition blunted BA vasodilation compared with control and when combined with AA eliminated the AA-induced improvement in BA vasodilation. Free radical outflow increased with exercise intensity but, interestingly, was not attenuated by AA. Collectively, these results indicate that AA improves BA vasodilation in the elderly during handgrip exercise through an NO-dependent mechanism; however, this improvement appears not to be the direct consequence of attenuated free radical outflow from the forearm.

Endogenous nitric oxide in expired air: Effects of acute exercise in humans

Life Sciences ◽  
1994 ◽  
Vol 55 (24) ◽  
pp. 1903-1909 ◽  
Author(s):  
John Anthony Bauer ◽  
Jeffrey A. Wald ◽  
Shawn Doran ◽  
David Soda
Keyword(s):  
Nitric Oxide ◽  
Acute Exercise ◽  
Endogenous Nitric Oxide ◽  
Exercise In Humans ◽  
Expired Air

Exhaled nitric oxide during exercise: site of release and modulation by ventilation and blood flow

1996 ◽  
Vol 80 (6) ◽  
pp. 1865-1871 ◽  
Author(s):  
C. R. Phillips ◽  
G. D. Giraud ◽  
W. E. Holden
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Exhaled Nitric Oxide ◽  
Balloon Occlusion ◽  
Dobutamine Infusion ◽  
Exhaled No ◽  
Increased Blood Flow ◽  
Exercise In Humans

To define the site of release and factors modulating exhaled nitric oxide (NO) during exercise in humans, we measured exhaled NO output during exercise, during exercise after balloon occlusion of the nasopharynx (to exclude nasal NO), and at rest with isocapneic hyperventilation or dobutamine infusion. Exhaled NO output increased from rest to exercise (57 +/- 10 to 171 +/- 30 nl.min-1.m-2; P < 0.003; n = 8). Exclusion of nasal NO reduced exhaled NO at rest and during exercise. Calculated nasal contribution at rest (53 +/- 5%) decreased during exercise (29 +/- 6%; P < 0.05), whereas nonnasal contribution increased (47 +/- 5 to 71 +/- 6%; P < 0.05). Isocapneic hyperventilation at rest increased exhaled NO output (51 +/- 8 to 94 +/- 22 nl.min-1.m-2; P = 0.05). Dobutamine infusion did not increase exhaled NO output. We conclude that nasal exhaled NO decreases (and nonnasal exhaled NO increases) with exercise. We also conclude that, under the conditions of this study, increased exhaled NO output during exercise is more closely related to increased ventilation than to increased blood flow.

scholarly journals Blood pressure predicts endothelial function and the effects of ethinyl estradiol exposure in young women

2018 ◽  
Vol 315 (4) ◽  
pp. H925-H933 ◽  
Author(s):  
Tessa E. Adler ◽  
Charlotte W. Usselman ◽  
Akira Takamata ◽  
Nina S. Stachenfeld
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Young Women ◽  
Pressure Range ◽  
Ethinyl Estradiol ◽  
Flow Mediated Dilation ◽  
Handgrip Exercise ◽  
Endothelial Impairment ◽  
Ischemic Handgrip Exercise

Hypertension, obesity, and endothelial function predict cardiovascular disease in women, and these factors are interrelated. We hypothesized that hypertension and obesity are associated with endothelial dysfunction in young women and that short-term ethinyl estradiol exposure mitigates this dysfunction. We examined flow-mediated dilation (FMD) responses before and during 7 days of oral ethinyl estradiol (30 µg/day) in 19 women (25 ± 5, 18–35 yr). We divided our sample into two groups based on two criteria: blood pressure and obesity. Women were divided into normal blood pressure (NBP; mean arterial pressure range: 78–91 mmHg, n = 7) and high blood pressure (HBP; mean arterial pressure range: 95–113 mmHg, n = 9) groups. We also stratified our subjects by body composition (lean: 18–31%, n = 8; obese: 38–59%, n = 9). We evaluated brachial FMD after two distinct shear stress stimuli: occlusion alone and occlusion with ischemic handgrip exercise. Obesity was unrelated to both FMD responses. Before ethinyl estradiol administration, the HBP group had blunted ischemic exercise responses relative to the NBP group (8.0 ± 3.5 vs. 12.3 ± 3.2%, respectively, P = 0.05). However, during ethinyl estradiol administration, ischemic exercise responses increased in the HBP group (12.8 ± 6.1%, P = 0.04) but decreased in the NBP group (5.6 ± 2.4%, P = 0.01). Standard FMD did not reveal differences between groups. In summary, 1) moderate HBP predicted endothelial impairment, 2) ethinyl estradiol administration had divergent effects on FMD in women with NBP versus HBP, and 3) enhanced FMD (ischemic handgrip exercise) revealed differences in endothelial function, whereas standard FMD (occlusion alone) did not. NEW & NOTEWORTHY We are the first to show that mild hypertension is a stronger predictor of endothelial dysfunction than obesity in healthy women without overt cardiovascular dysfunction. Importantly, the standard 5-min flow-mediated vasodilation stimulus did not detect endothelial dysfunction in our healthy population; only an enhanced ischemic handgrip exercise shear stress stimulus detected endothelial impairment. Estradiol administration increased flow-mediated dilation in women with high blood pressure, so it may be a therapeutic intervention to improve endothelial function.

scholarly journals Elevated extracellular potassium prior to muscle contraction reduces onset and steady-state exercise hyperemia in humans

2018 ◽  
Vol 125 (2) ◽  
pp. 615-623 ◽  
Author(s):  
Janée D. Terwoord ◽  
Christopher M. Hearon ◽  
Gary J. Luckasen ◽  
Jennifer C. Richards ◽  
Michael J. Joyner ◽  
...  
Keyword(s):  
Steady State ◽  
Voluntary Contraction ◽  
Extracellular Potassium ◽  
Handgrip Exercise ◽  
Exercise Hyperemia ◽  
Forearm Vascular Conductance ◽  
Response To Exercise ◽  
Exercise In Humans ◽  
Hyperemic Response

The increase in interstitial potassium (K+) during muscle contractions is thought to be a vasodilatory signal that contributes to exercise hyperemia. To determine the role of extracellular K+ in exercise hyperemia, we perfused skeletal muscle with K+ before contractions, such that the effect of any endogenously-released K+ would be minimized. We tested the hypothesis that local, intra-arterial infusion of potassium chloride (KCl) at rest would impair vasodilation in response to subsequent rhythmic handgrip exercise in humans. In 11 young adults, we determined forearm blood flow (FBF) (Doppler ultrasound) and forearm vascular conductance (FVC) (FBF/mean arterial pressure) during 4 min of rhythmic handgrip exercise at 10% of maximal voluntary contraction during 1) control conditions, 2) infusion of KCl before the initiation of exercise, and 3) infusion of sodium nitroprusside (SNP) as a control vasodilator. Infusion of KCl or SNP elevated resting FVC similarly before the onset of exercise (control: 39 ± 6 vs. KCl: 81 ± 12 and SNP: 82 ± 13 ml·min−1·100 mmHg−1; both P < 0.05 vs. control). Infusion of KCl at rest diminished the hyperemic (ΔFBF) and vasodilatory (ΔFVC) response to subsequent exercise by 22 ± 5% and 30 ± 5%, respectively (both P < 0.05 vs. control), whereas SNP did not affect the change in FBF ( P = 0.74 vs. control) or FVC ( P = 0.61 vs. control) from rest to steady-state exercise. These findings implicate the K+ ion as an essential vasodilator substance contributing to exercise hyperemia in humans. NEW & NOTEWORTHY Our findings support a significant and obligatory role for potassium signaling in the local vasodilatory and hyperemic response to exercise in humans.

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