scholarly journals Rapid vasodilation in response to passive leg movement with age: the role of nitric oxide and the impact of perfusion pressure (546.6)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
H Groot ◽  
Joel Trinity ◽  
Gwenael Layec ◽  
Matthew Rossman ◽  
Stephen Ives ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Perfusion Pressure ◽  
Leg Movement ◽  
The Impact

scholarly journals Passive leg movement and nitric oxide-mediated vascular function: the impact of age

2015 ◽  
Vol 308 (6) ◽  
pp. H672-H679 ◽  
Author(s):  
Joel D. Trinity ◽  
H. Jonathan Groot ◽  
Gwenael Layec ◽  
Matthew J. Rossman ◽  
Stephen J. Ives ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Function ◽  
Area Under The Curve ◽  
The Elderly ◽  
Novel Approach ◽  
Leg Movement ◽  
The Impact ◽  
Male Subjects ◽  
Peak Increase

In young healthy men, passive leg movement (PLM) elicits a robust nitric oxide (NO)-dependent increase in leg blood flow (LBF), thus providing a novel approach to assess NO-mediated vascular function. While the magnitude of the LBF response to PLM is markedly reduced with age, the role of NO in this attenuated response in the elderly is unknown. Therefore, this study sought to determine the contribution of NO in the PLM-induced LBF with age. Fourteen male subjects (7 young, 24 ± 1 yr; and 7 old, 75 ± 3 yr) underwent PLM with and without NO synthase (NOS) inhibition achieved by intra-arterial infusion of NG-monomethyl-l-arginine (l-NMMA). LBF was determined second-by-second by Doppler ultrasound, and central hemodynamics were measured by finger photoplethysmography. NOS inhibition blunted the PLM-induced peak increase in LBF in the young (control: 668 ± 106; l-NMMA: 431 ± 95 Δml/min; P = 0.03) but had no effect in the old (control: 266 ± 98; l-NMMA: 251 ± 92 Δml/min; P = 0.59). Likewise, the magnitude of the reduction in the overall (i.e., area under the curve) PLM-induced LBF response to NOS inhibition was less in the old (LBF: −31 ± 18 ml) than the young (LBF: −129 ± 21 ml; P < 0.01). These findings suggest that the age-associated reduction in PLM-induced LBF in the elderly is primarily due to a reduced contribution to vasodilation from NO and therefore support the use of PLM as a novel approach to assess NO-mediated vascular function across the lifespan.

scholarly journals Passive leg movement-induced vasodilation in women: the impact of age

2015 ◽  
Vol 309 (5) ◽  
pp. H995-H1002 ◽  
Author(s):  
H. Jonathan Groot ◽  
Matthew J. Rossman ◽  
Joel D. Trinity ◽  
Gwenael Layec ◽  
Stephen J. Ives ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Function ◽  
Heart Rate Response ◽  
Perfusion Pressure ◽  
Female Population ◽  
Novel Method ◽  
Seated Posture ◽  
Leg Movement ◽  
The Impact ◽  
Hemodynamic Measurements

Passive leg movement (PLM), an assessment of predominantly nitric oxide-dependent vasodilation, is decreased with age and cannot be augmented by posture-induced increases in femoral perfusion pressure in older men. However, this novel method of assessing vascular function has yet to be used to evaluate alterations in nitric oxide-dependent vasodilation with age in females. PLM was performed in 10 young (20 ± 1 yr) and 10 old (73 ± 2 yr) women in both the supine and upright-seated postures, whereas central and peripheral hemodynamic measurements were acquired second by second using noninvasive techniques (finger photoplethysmography and Doppler ultrasound, respectively). The heart rate response to PLM was attenuated in the old compared with the young in both the supine (young, 10 ± 1; and old, 5 ± 1 beats/min; P < 0.05) and upright-seated posture (young, 10 ± 2; and old, 5 ± 1 beats/min; P < 0.05), leading to a blunted cardiac output response in the old in the upright-seated posture (young, 1.0 ± 0.2; and old, 0.3 ± 0.1 l/min; P < 0.05). The PLM-induced peak change in leg vascular conductance was lower in the old compared with the young in both postures (young supine, 5.7 ± 0.5; old supine, 2.6 ± 0.3; young upright, 9.2 ± 0.7; and old upright, 2.2 ± 0.4 ml·min−1·mmHg−1; P < 0.05) and was significantly augmented by the upright-seated posture in the young only, revealing a vasodilatory reserve capacity in the young (3.5 ± 0.6 ml·min−1·mmHg−1, P < 0.05) that was absent in the old (−0.5 ± 0.3 ml·min−1·mmHg−1, P = 0.18). These data support previous literature demonstrating attenuated PLM-induced vasodilation with age and extend these findings to include the female population, thus bolstering the utility of PLM as a novel assessment of vascular function across the life span in humans.

scholarly journals The role of nitric oxide in passive leg movement-induced vasodilatation with age: insight from alterations in femoral perfusion pressure

2015 ◽  
Vol 593 (17) ◽  
pp. 3917-3928 ◽  
Author(s):  
H. Jonathan Groot ◽  
Joel D. Trinity ◽  
Gwenael Layec ◽  
Matthew J. Rossman ◽  
Stephen J. Ives ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Perfusion Pressure ◽  
Leg Movement

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

Release of nitric oxide and prostaglandin H2 to acetylcholine in skeletal muscle venules

1997 ◽  
Vol 272 (6) ◽  
pp. H2541-H2546 ◽  
Author(s):  
G. Dornyei ◽  
G. Kaley ◽  
A. Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Thromboxane A2 ◽  
No Synthase ◽  
Gracilis Muscle ◽  
Vasoactive Agents ◽  
Before And After ◽  
Higher Doses

The role of endothelium in regulating venular resistance is not well characterized. Thus we aimed to elucidate the endothelium-derived factors involved in the mediation of responses of rat gracilis muscle venules to acetylcholine (ACh) and other vasoactive agents. Changes in diameter of perfusion pressure (7.5 mmHg)- and norepinephrine (10(-6) M)-constricted venules (approximately 225 microns in diam) to cumulative doses of ACh (10(-9) to 10(-4) M) and sodium nitroprusside (SNP, 10(-9) to 10(-4) M), before and after endothelium removal or application of various inhibitors, were measured. Lower doses of ACh elicited dilations (up to 42.1 +/- 4.7%), whereas higher doses of ACh resulted in smaller dilations or even constrictions. Endothelium removal abolished both ACh-induced dilation and constriction. In the presence of indomethacin (2.8 x 10(-5) M), a cyclooxygenase blocker, or SQ-29548 (10(-6) M), a thromboxane A2-prostaglandin H2 (PGH2) receptor antagonist, higher doses of ACh caused further dilation (up to 72.7 +/- 7%) instead of constriction. Similarly, lower doses of arachidonic acid (10(-9) to 10(-6) M) elicited dilations that were diminished at higher doses. These reduced responses were, however, reversed to substantial dilation by SQ-29548. The nitric oxide (NO) synthase blocker, N omega-nitro-L-arginine (L-NNA, 10(-4) M), significantly reduced the dilation to ACh (from 30.6 +/- 5.5 to 5.4 +/- 1.4% at 10(-6) M ACh). In contrast, L-NNA did not affect dilation to SNP. Thus ACh elicits the release of both NO and PGH2 from the venular endothelium.

scholarly journals The role of the endothelium in the hyperemic response to passive leg movement: looking beyond nitric oxide

2020 ◽  
Author(s):  
Joel D. Trinity ◽  
Oh Sung Kwon ◽  
Ryan M. Broxterman ◽  
Jayson R. Gifford ◽  
Andrew C. Kithas ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Vascular Function ◽  
No Synthase ◽  
Ketorolac Tromethamine ◽  
Arterial Infusion ◽  
Healthy Men ◽  
Leg Movement ◽  
Hyperemic Response

Passive leg movement (PLM) evokes a robust and predominantly nitric oxide (NO)-mediated increase in blood flow that declines with age and disease. Consequently, PLM is becoming increasingly accepted as a sensitive assessment of endothelium-mediated vascular function. However, a substantial PLM-induced hyperemic response is still evoked despite NO synthase (NOS) inhibition. Therefore, in 9 young healthy men (25±4 yrs), this investigation aimed to determine if the combination of two potent endothelium-dependent vasodilators, specifically prostaglandin (PG) and endothelium-derived hyperpolarizing factor (EDHF), account for the remaining hyperemic response to the two variants of PLM, PLM (60 movements) and single PLM (sPLM, 1 movement) when NOS is inhibited. The leg blood flow (LBF, Doppler ultrasound) response to PLM and sPLM following the intra-arterial infusion of NG-monomethyl L-arginine (L-NMMA), to inhibit NOS, was compared to the combined inhibition of NOS, cyclooxygenase (COX), and cytochrome P450 (CYP450) by L-NMMA, ketorolac tromethamine (KET), and fluconazole (FLUC), respectively. NOS inhibition attenuated the overall LBF (LBFAUC) response to both PLM (control: 456±194, L-NMMA: 168±127 ml, p<0.01) and sPLM (control: 185±171, L-NMMA: 62±31 ml, p=0.03). The combined inhibition of NOS, COX, and CYP450 (i.e. L-NMMA+KET+FLUC) did not further attenuate the hyperemic responses to PLM (LBFAUC: 271±97 ml, p>0.05) or sPLM (LBFAUC: 72±45 ml, p>0.05). Therefore, PG and EDHF do not collectively contribute to the non-NOS-derived NO-mediated, endothelium-dependent, hyperemic response to either PLM or sPLM in healthy young men. These findings add to the mounting evidence and understanding of the vasodilatory pathways assessed by the PLM and sPLM vascular function tests.

scholarly journals The Nitrate-Nitrite-Nitric Oxide Pathway on Healthy Ageing: A Review of Pre-clinical and Clinical Data on the Impact of Dietary Nitrate in the Elderly

2021 ◽  
Vol 2 ◽  
Author(s):  
Bárbara S. Rocha
Keyword(s):  
Nitric Oxide ◽  
Free Radicals ◽  
Clinical Data ◽  
The Elderly ◽  
Healthy Ageing ◽  
Leafy Vegetables ◽  
Metabolic Effects ◽  
Radical Theory ◽  
The Impact

We are living longer. Are we living healthier? As we age, cellular and molecular damage reshape our physiological responses towards environmental and endogenous stimuli. The free radical theory of ageing has been proposed long before ageing has been considered a “scientific discipline” and, since then, has been discussed and upgraded as a major contributor to aberrant ageing. Assuming that ageing results merely from the accumulation of oxidative modifications of biomolecules is not only a simplistic and reductive view of such a complex and dynamic process, but also free radicals and related oxidants are now considered pivotal signalling molecules. The fine modulation of critical signalling pathways by redox compounds demands a novel approach to tackle the role of free radicals in ageing. Nitric oxide (⋅NO) is a paradigmatic example given its biological functions in cardiovascular, neurologic and immune systems. In addition to the canonical ⋅NO synthesis by a family of enzymes, nitrate from green leafy vegetables, is reduced to nitrite in the oral cavity which is further reduced to ⋅NO in the stomach. Boosting this nitrate-nitrite-NO pathway has been shown to improve gastrointestinal, cardiovascular, metabolic and cognitive performance both in humans and in animal models of disease. In the elderly, nitrate-derived ⋅NO has been shown improve several physiological functions that typically decline during ageing. In this paper, the role of nitrate and derived nitrogen oxides will be discussed while reviewing pre-clinical and clinical data on the cardiovascular, neuronal, musculoskeletal and metabolic effects of nitrate during healthy ageing.

scholarly journals Hypertension in Primary Open Angle Glaucoma

2014 ◽  
Vol 52 (194) ◽  
pp. 771-774
Author(s):  
Suprada Pokharel ◽  
Dakki Sherpa ◽  
Om Krishna Malla
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Odds Ratio ◽  
Perfusion Pressure ◽  
Open Angle Glaucoma ◽  
High Systolic Blood Pressure ◽  
Hypertensive Patients ◽  
The Impact

Introduction: The impact of vascular factors in POAG is well known and controversial. Some reports have shown high blood pressure in POAG, some low systolic blood pressure and some described no difference in blood pressure between POAG and controls. However decreased ocular perfusion pressure was found in most of the studies. Our study aims to assess the role of hypertension in POAG . Methods: It was cross-sectional case–control hospital based study carried out from 1st June 2012 to 1st June 2013. There were 40 cases and 100 controls included in the study. The role of hypertension were compared with those hypertensive patients with glaucoma (cases) and hypertensive patients without glaucoma (controls). Results: Age above 50 years (odds ratio: 4.827 with 95% CI 1.862-12.517), male genders (odds ratio: 3.10 with 95% CI 1.356-7.146) and low diastolic perfusion pressure (odds ratio: 3.857 with 95% CI 1.362-11.224) showed strongly positive association with POAG. High systolic blood pressure (odds ratio: 1.476 95% CI 0.627-3.476), high diastolic blood pressure (odds ratio: 1.348 95% CI 0.587-3.096) and low systolic perfusion pressure (odds ratio: 1.8661 with 95% CI 0.649- 5.335) were weakly associated with glaucoma in our study. Conclusions: Age above 50 years, male gender and low diastolic perfusion pressure were strong risk factor for the development of POAG. Keywords: diastolic blood pressure; diastolic perfusion pressure; POAG; systolic blood pressure; systolic perfusion pressure.

scholarly journals Augmented EDHF signaling in rat uteroplacental vasculature during late pregnancy

2010 ◽  
Vol 299 (5) ◽  
pp. H1642-H1652 ◽  
Author(s):  
N. I. Gokina ◽  
O. Y. Kuzina ◽  
A. M. Vance
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Combined Treatment ◽  
Late Pregnancy ◽  
Successful Pregnancy ◽  
High K ◽  
The Impact ◽  
Prostacyclin Production ◽  
In Pregnancy

A successful pregnancy outcome relies on extensive maternal cardiovascular adaptation, including enhanced uteroplacental vasodilator mechanisms. The objective of the present study was to determine the contribution of the endothelium-derived hyperpolarizing factor (EDHF) signaling in pregnancy-enhanced uterine vasodilation, to define the role of Ca2+-activated K+ channels in mediating EDHF effects, and to explore the impact of endothelial Ca2+ signaling in pregnancy-specific upregulation of EDHF. Fura 2-based measurements of smooth muscle cell (SMC) and endothelial cell cytosolic Ca2+ concentration ([Ca2+]i) were performed simultaneously with measurements of the diameter of uterine radial arteries from nonpregnant (NP) and late pregnant (LP) rats. Changes in SMC membrane potential of pressurized arteries from LP rats were assessed using glass microelectrodes. After blockade of nitric oxide and prostacyclin production, a cumulative application of ACh induced rapid and effective dilatation of uterine vessels from both NP and LP rats. This vasodilation was associated with SMC hyperpolarization and SMC [Ca2+]i reduction and was abolished by a high-K+ solution, demonstrating that NG-nitro-l-arginine (l-NNA)- and indomethacin-resistant responses are attributable to EDHF. Pregnancy significantly potentiates EDHF-mediated vasodilation in part due to enhanced endothelial Ca2+ signaling. l-NNA- and indomethacin-resistant responses were insensitive to iberiotoxin but abolished by a combined treatment with apamin and charybdotoxin, supporting the key role of small- and intermediate-conductance K+ channels in mediating EDHF signaling in the maternal uterine resistance vasculature.

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