scholarly journals Hindlimb unweighting does not alter vasoconstrictor responsiveness and nitric oxide-mediated inhibition of sympathetic vasoconstriction

2015 ◽  
Vol 593 (9) ◽  
pp. 2213-2224 ◽  
Author(s):  
Timothy P. Just ◽  
Nicholas G. Jendzjowsky ◽  
Darren S. DeLorey
Keyword(s):  
Nitric Oxide ◽  
Hindlimb Unweighting ◽  
Sympathetic Vasoconstriction

Arteriolar wall Po 2 and nitric oxide release during sympathetic vasoconstriction in the rat intestine

2000 ◽  
Vol 279 (2) ◽  
pp. H484-H491 ◽  
Author(s):  
Bryan A. Sauls ◽  
Matthew A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Rat Intestine ◽  
Nerve Activity ◽  
Sympathetic Nerve Stimulation ◽  
Nitric Oxide Release ◽  
Sympathetic Vasoconstriction ◽  
Arteriolar Wall

Endothelium-derived nitric oxide (NO) attenuates arteriolar constriction in the rat small intestine during periods of increased sympathetic nerve activity. This study was undertaken to test the hypothesis that a flow-dependent fall in arteriolar wall Po 2 serves as the stimulus for endothelial NO release under these conditions. Sympathetic nerve stimulation at 3–16 Hz induced frequency-dependent arteriolar constriction, with arteriolar wall O2 tension (Po 2) falling from 67 ± 3 mmHg to as low as 41 ± 6 mmHg. Arteriolar responses to nerve stimulation were enhanced after inhibition of NO synthase with N G-monomethyl-l-arginine (l-NMMA). Under a high-O2 (20%) superfusate, the fall in wall Po 2 was significantly attenuated, arteriolar constrictions were increased by 57 ± 9 to 66 ± 12%, and these responses were no longer sensitive tol-NMMA. The high-O2 superfusate had no effect on vascular smooth muscle responsiveness to NO (as judged by arteriolar responses to sodium nitroprusside) or on arteriolar wall oxidant activity (as determined by the reduction of tetranitroblue tetrazolium dye). These results indicate that a flow-dependent fall in arteriolar wall Po 2 may serve as a stimulus for the release of endothelium-derived NO during periods of increased sympathetic nerve activity.

scholarly journals Effect of acute dietary nitrate supplementation on sympathetic vasoconstriction at rest and during exercise

2019 ◽  
Vol 127 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Christopher J. de Vries ◽  
Darren S. DeLorey
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Skeletal Muscle ◽  
Beetroot Juice ◽  
Total Plasma ◽  
Dietary Nitrate ◽  
Arterial Blood ◽  
Sympathetic Vasoconstriction ◽  
Nitrate Supplementation ◽  
Healthy Males

Dietary nitrate ([Formula: see text]) supplementation has been shown to reduce resting blood pressure. However, the mechanism responsible for the reduction in blood pressure has not been identified. Dietary [Formula: see text] supplementation may increase nitric oxide (NO) bioavailability, and NO has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle. Therefore, the purpose of this study was to investigate the hypothesis that acute dietary [Formula: see text] supplementation would attenuate sympathetic vasoconstrictor responsiveness at rest and during exercise. In a double-blind randomized crossover design, 12 men (23 ± 5 yr) performed a cold-pressor test (CPT) at rest and during moderate- and heavy-intensity alternate-leg knee-extension exercise after consumption of [Formula: see text] rich beetroot juice (~12.9 mmol [Formula: see text]) or a [Formula: see text]-depleted placebo (~0.13 mmol [Formula: see text]). Venous blood was sampled before and 2.5 h after the consumption of beetroot juice for the measurement of total plasma nitrite/[Formula: see text] [NOx]. Beat-by-beat blood pressure was measured by Finometer. Leg blood flow was measured at the femoral artery via Doppler ultrasound, and leg vascular conductance (LVC) was calculated. Sympathetic vasoconstrictor responsiveness was calculated as the percentage decrease in LVC in response to the CPT. Total plasma [NOx] was greater ( P < 0.001) in the [Formula: see text] (285 ± 120 µM) compared with the placebo (65 ± 30 µM) condition. However, mean arterial blood pressure and plasma catecholamines were not different ( P > 0.05) between [Formula: see text] and placebo conditions at rest or during moderate- and heavy-intensity exercise. Sympathetic vasoconstrictor responsiveness (Δ% LVC) was not different ( P > 0.05) between [Formula: see text] and placebo conditions at rest ([Formula: see text]: −33 ± 10%; placebo: −35 ± 11%) or during moderate ([Formula: see text]: −18 ± 8%; placebo: −20 ± 10%)- and heavy ([Formula: see text]: −12 ± 8%; placebo: −11 ± 9%)-intensity exercise. These data demonstrate that acute dietary [Formula: see text] supplementation does not alter sympathetic vasoconstrictor responsiveness at rest or during exercise in young healthy males. NEW & NOTEWORTHY Dietary nitrate may increase nitric oxide bioavailability, and nitric oxide has been shown to attenuate sympathetic vasoconstriction in resting and contracting skeletal muscle and enhance functional sympatholysis. However, the effect of dietary nitrate on sympathetic vasoconstrictor responsiveness is unknown. Acute dietary nitrate supplementation did not alter blood pressure or sympathetic vasoconstrictor responsiveness at rest or during exercise in young healthy males.

scholarly journals Adenosine linking reduced O2 to arteriolar NO release in intestine is not formed from extracellular ATP

2001 ◽  
Vol 281 (3) ◽  
pp. H1193-H1200 ◽  
Author(s):  
Bryan A. Sauls ◽  
Matthew A. Boegehold
Keyword(s):  
Nitric Oxide ◽  
Direct Application ◽  
Rat Intestine ◽  
Sympathetic Nerve Stimulation ◽  
First Order ◽  
Vascular Bed ◽  
Sympathetic Vasoconstriction ◽  
No Release ◽  
Endothelial Nitric Oxide ◽  
Dose Dependent

We have previously reported that adenosine formed in response to reduced arteriolar and/or tissue Po 2 preserves endothelial nitric oxide (NO) synthesis during sympathetic vasoconstriction in the rat intestine. To more precisely identify the site and mechanism of adenosine formation under these conditions, we tested the hypothesis that ATP released in response to reduced O2 levels serves as a source of adenosine. Direct application of ATP to the wall of first-order arterioles elicited dose-dependent dilations of 15–33% above resting diameter that were reduced by 71–80% by the 5′-ectonucleotidase inhibitor α,β-methyleneadenosine 5′-diphosphate (AOPCP, 4.5 × 10−5 M) and completely abolished by N G-monomethyl-l-arginine (l-NMMA, 10−4 M). Under control conditions, sympathetic nerve stimulation at 3 and 8 Hz induced arteriolar constrictions of 11 ± 1 and 19 ± 1 μm, respectively. These responses were enhanced by 58–69% in the presence ofl-NMMA or when local Po 2 was maintained at resting levels. However, in the presence of AOPCP, the enhancing effects of l-NMMA and the high O2superfusate on sympathetic constriction were preserved. These results suggest that, although exogenously applied ATP can stimulate arteriolar NO release in the intestine largely through its sequential extracellular hydrolysis to adenosine, this process does not contribute to adenosine formation and sustained NO release during sympathetic constriction in this vascular bed.

Role of neuronal nitric oxide in the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of healthy rats

2013 ◽  
Vol 115 (1) ◽  
pp. 97-106 ◽  
Author(s):  
Nicholas G. Jendzjowsky ◽  
Darren S. DeLorey
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Muscle Contraction ◽  
Triceps Surae ◽  
Sympathetic Stimulation ◽  
Sprague Dawley ◽  
Sympathetic Vasoconstriction ◽  
In Series ◽  
Nnos Inhibition

Isoform-specific nitric oxide (NO) synthase (NOS) contributions to NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle are incompletely understood. The purpose of the present study was to investigate the role of neuronal NOS (nNOS) in the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of healthy rats. We hypothesized that acute pharmacological inhibition of nNOS would augment sympathetic vasoconstriction in resting and contracting skeletal muscle, demonstrating that nNOS is primarily responsible for NO-mediated inhibition of sympathetic vasoconstriction. Sprague-Dawley rats ( n = 13) were anesthetized and instrumented with an indwelling brachial artery catheter, femoral artery flow probe, and lumbar sympathetic chain stimulating electrodes. Triceps surae muscles were stimulated to contract rhythmically at 60% of maximal contractile force. In series 1 ( n = 9), the percent change in femoral vascular conductance (%FVC) in response to sympathetic stimulations delivered at 2 and 5 Hz was determined at rest and during muscle contraction before and after selective nNOS blockade with S-methyl-l-thiocitrulline (SMTC, 0.6 mg/kg iv) and subsequent nonselective NOS blockade with Nω-nitro-l-arginine methyl ester (l-NAME, 5 mg/kg iv). In series 2 ( n = 4), l-NAME was injected first, and then SMTC was injected to determine if the effect of l-NAME on constrictor responses was influenced by selective nNOS inhibition. Sympathetic stimulation decreased FVC at rest (−25 ± 7 and −44 ± 8%FVC at 2 and 5 Hz, respectively) and during contraction (−7 ± 3 and −19 ± 5%FVC at 2 and 5 Hz, respectively). The decrease in FVC in response to sympathetic stimulation was greater in the presence of SMTC at rest (−32 ± 6 and −49 ± 8%FVC at 2 and 5 Hz, respectively) and during contraction (−21 ± 4 and −28 ± 4%FVC at 2 and 5 Hz, respectively). l-NAME further increased ( P < 0.05) the sympathetic vasoconstrictor response at rest (−47 ± 4 and −60 ± 6%FVC at 2 and 5 Hz, respectively) and during muscle contraction (−33 ± 3 and −40 ± 6%FVC at 2 and 5 Hz, respectively). The effect of l-NAME was not altered by the order of nNOS inhibition. These data demonstrate that NO derived from nNOS and endothelial NOS contribute to the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.

Nitric oxide and muscle blood flow in exercise

2008 ◽  
Vol 33 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Michael E. Tschakovsky ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Integrated Control ◽  
Muscle Blood Flow ◽  
Dynamic Adjustment ◽  
Resistance Vessels ◽  
Sympathetic Vasoconstriction ◽  
Exercise Hyperemia ◽  
Blood Flow Control

Despite being the subject of investigation for well over 100 years, the nature of exercising muscle blood flow control remains, in many respects, poorly understood. In this review we focus on the potential role of nitric oxide in vasodilation of muscle resistance vessels during a bout of exercise. Its contribution is explored in the context of whether it contributes to steady-state exercise hyperemia, the dynamic adjustment of muscle blood flow to exercise, or the modulation of sympathetic vasoconstriction in exercising muscle. It appears that the obligatory role of nitric oxide in all three of these categories is modest at best. The elucidation of the integrated nature of exercise hyperemia control in terms of synergy and redundancy of mechanism interaction remains in its infancy, and much more remains to be learned about the role of nitric oxide in this type of integrated control.

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