ArticleThe Journal of physiology2012
Effects of chronic heart failure on neuronal nitric oxide synthase-mediated control of microvascular O2 pressure in contracting rat skeletal muscle.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Edward F. Adolph Distinguished Lecture. Contemporary model of muscle microcirculation: gateway to function and dysfunction.Journal of applied physiology (Bethesda, Md. : 1985) · 2019Review
- Neuronal nitric oxide synthase regulation of skeletal muscle functional hyperemia: exercise training and moderate compensated heart failure.Nitric oxide : biology and chemistry · 2018Article
- Effect of sodium nitrite on local control of contracting skeletal muscle microvascular oxygen pressure in healthy rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- Critical Power: An Important Fatigue Threshold in Exercise Physiology.Medicine and science in sports and exercise · 2016Review
- Dietary nitrate supplementation: impact on skeletal muscle vascular control in exercising rats with chronic heart failure.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Exercise training in chronic heart failure: improving skeletal muscle O2 transport and utilization.American journal of physiology. Heart and circulatory physiology · 2015Review
- ROS and endothelial nitric oxide synthase (eNOS)-dependent trafficking of angiotensin II type 2 receptor begets neuronal NOS in cardiac myocytes.Basic research in cardiology · 2015Article
- Skeletal muscle microvascular oxygenation dynamics in heart failure: exercise training and nitric oxide-mediated function.American journal of physiology. Heart and circulatory physiology · 2014Article
- Muscle fibre-type dependence of neuronal nitric oxide synthase-mediated vascular control in the rat during high speed treadmill running.The Journal of physiology · 2013Article
- Neuronal nitric oxide synthase inhibition and regional sympathetic nerve discharge: implications for peripheral vascular control.Respiratory physiology & neurobiology · 2013Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
unlabelledChronic heart failure (CHF) impairs nitric oxide (NO)-mediated regulation of the skeletal muscle microvascular O(2) delivery/V(O(2)) ratio (which sets the microvascular O(2) pressure, PO(2)mv). Given the pervasiveness of endothelial dysfunction in CHF, this NO-mediated dysregulation is attributed generally to eNOS. It is unknown whether nNOS-mediated PO(2)mv regulation is altered in CHF. We tested the hypothesis that CHF impairs nNOS-mediated PO(2)mv control. In healthy and CHF (left ventricular end diastolic pressure (LVEDP): 6 ± 1 versus 14 ± 1 mmHg, respectively, P < 0.05) rats spinotrapezius muscle blood flow (radiolabelled microspheres), PO(2)mv (phosphorescence quenching), and V(O(2)) (Fick calculation) were measured before and after 0.56 mg kg(-1)i.a. of the selective nNOS inhibitor S-methyl-l-thiocitrulline (SMTC). In healthy rats, SMTC increased baseline PO(2)mv ( CONTROL: 29.7 ± 1.4, SMTC: 34.4 ± 1.9 mmHg, P < 0.05) by reducing V(O(2)) (↓20%) without any effect on blood flow and speeded the mean response time (MRT, time to reach 63% of the overall kinetics response, CONTROL: 24.2 ± 2.0, SMTC: 18.5 ± 1.3 s, P < 0.05). In CHF rats, SMTC did not alter baseline PO(2)mv ( CONTROL: 25.7 ± 1.6, SMTC: 28.6 ± 2.1 mmHg, P > 0.05), V(O(2)) at rest, or the MRT (CONTROL: 22.8 ± 2.6, SMTC: 21.3 ± 3.0 s, P > 0.05). During the contracting steady-state, SMTC reduced blood flow (↓15%) and V(O(2)) (↓15%) in healthy rats such that PO(2)mv was unaltered ( CONTROL: 19.8 ± 1.7, SMTC: 20.7 ± 1.8 mmHg, P > 0.05). In marked contrast, in CHF rats SMTC did not change contracting steady-state blood flow, V(O(2)), or PO(2)mv ( CONTROL: 17.0 ± 1.4, SMTC: 17.7 ± 1.8 mmHg, P > 0.05). nNOS-mediated control of skeletal muscle microvascular function is compromised in CHF versus healthy rats. Treatments designed to ameliorate microvascular dysfunction in CHF may benefit by targeting improvements in nNOS function.
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