Hostname: page-component-78c5997874-s2hrs Total loading time: 0 Render date: 2024-11-05T05:05:04.837Z Has data issue: false hasContentIssue false
  • English
  • Français

Effects of nitric oxide synthase inhibition on vascular conductance during high speed treadmill exercise in rats

Published online by Cambridge University Press:  19 November 2001

Timothy I. Musch ,
Richard M. McAllister ,
J. David Symons ,
Charles L. Stebbins ,
Tadakazu Hirai ,
K. Sue Hageman  and
David C. Poole
Timothy I. Musch
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
Richard M. McAllister
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
J. David Symons
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
Charles L. Stebbins
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
Tadakazu Hirai
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
K. Sue Hageman
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
David C. Poole
Affiliation:
Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA and The Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Toyama 930-01, Japan
Get access

Abstract

To determine the functional role of nitric oxide (NO) in regulating vascular conductance during high intensity dynamic exercise in skeletal muscles composed of all major fibre types, female Wistar rats (277 ± 4 g; n = 7) were run on a motor-driven treadmill at a speed and gradient (60 m min-1, 10 % gradient) established to yield maximal oxygen uptake (V˙O2,max). Vascular conductance (ml min-1 (100 g)-1 mmHg-1), defined as blood flow normalised to mean arterial pressure (MAP), was determined using radiolabelled microspheres during exercise before and after NO synthase (NOS) inhibition with N G-nitro-L-arginine methyl ester (L-NAME; 10 mg kg-1, I.A.). The administration of L-NAME increased MAP from pre-L-NAME baseline values, demonstrating that NOS activity is reduced. The administration of L-NAME also reduced vascular conductance in 20 of the 28 individual hindlimb muscles or muscle parts examined during high speed treadmill exercise. These reductions in vascular conductance correlated linearly with the estimated sum of the percentage of slow twitch oxidative (SO) and fast twitch oxidative glycolytic (FOG) types of fibres in each muscle (Δconductance = -0.0082(%SO + %FOG) - 0.0105; r = 0.66; P < 0.001). However, if the reduction in vascular conductance found in the individual hindquarter muscles or muscle parts was expressed as a percentage decrease from the pre-L-NAME value (%Δ = (pre-L-NAME conductance - post-L-NAME conductance)/ pre-L-NAME conductance × 100), then the reduction in vascular conductance was similar in all muscles examined (average %Δ = -23 ± 2 %). These results suggest that NO contributes substantially to the regulation of vascular conductance within and among muscles of the rat hindquarter during high intensity exercise. When expressed in absolute terms, the results suggest that the contribution of NO to the regulation of vascular conductance during high intensity exercise is greater in muscles that possess a high oxidative capacity. In contrast, if results are expressed in relative terms, then the contribution of NO to the regulation of vascular conductance during high intensity exercise is similar across the different locomotor muscles located in the rat hindlimb and independent of the fibre type composition. Experimental Physiology (2001) 86.6, 749-757.

Type
Full Length Papers
Information
Experimental Physiology , Volume 86 , Issue 6 , November 2001 , pp. 749 - 757
Copyright
© The Physiological Society 2001

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)