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Integrative Biology of Exercise 2004 APS Intersociety Meeting
October 6-9, 2004 Austin, Texas
4.14
Role
of vascular ATP-sensitive potassium channels in exercise hyperemia
Jason J Hamann. John B Buckwalter. Zoran Valic. Philip S Clifford. Anesthesiology, Medical College of Wisconsin,
VA Medical Center, 5000 W. National Ave, Milwaukee, Wl, 53295
Previously, we have shown that katp channel blockade attenuates vasodilation during steady-state
exercise. To assess whether reductions in blood flow are the direct effect of vascular KATp channel inhibition or an indirect effect of impaired muscle
function, mongrel dogs (n=7) were instrumented with flow probes on the external iliac arteries. During steady-state exercise at 6 miles/hr (moderate intensity), the katp
channel antagonist glibenclamide was infused into the femoral artery to elicit a 20% reduction in blood flow. Arterial and venous blood samples were obtained
simultaneously to calculate hindlimb Vo2. On a separate day, the effects on Vo2 were determined with a similar decrease in iliac blood flow via inflation of a terminal aortic occluder. Infusion of glibenclamide during exercise decreased iliac blood flow from 616 33 to 479 29 ml/min and decreased Vo2 by 10%. When blood flow was reduced to the same extent with vascular occlusion Vo2 was also reduced by 10%. The similar reductions in Vo2 by both interventions suggest that muscle function was not directly affected by glibenclamide. This finding supports the idea that metabolic vasodilation is dependent on activation of vascular smooth muscle katp channels. (Supported by NHLBI and VA)
6.1
Effects of Acute Exhausting Exercise and Acute Psychological Stress on the Hemodynamics
of the Rat Small Intestine: Role of Endothelin-A (ET-A) and Endothelin-B (ET-B) Receptors
Salah Gandur1. Berrak Yegen2. Hizir Kurtel2. 'Physiology, Marmara Medical
School, Tibbiye Cad, Haydarpasa, Istanbul, 34668, Turkey, 2Physiology, Marmara Medical School
Although the hemodynamic alterations have been implicated in the gastrointestinal responses following the acute
exhausting exercise (AEx) or acute psychological stress (APS), the mechanisms of these alterations are not well understood. The aim of the present study was to assess the
role of ET-A and ET-B receptors on AEx and APS induced changes in superior mesenteric artery (SMA) hemodynamics. METHODS: The study was approved by institutional Animal
Use and Care Committee. AEx and APS were induced by 2 h of forced swimming and water avoidance stress in Wistar Albino rats of both sexes, respectively. Blood flow in the
SMA was measured by the ultrasonic transit time technique. The mean arterial pressure (MAP) was recorded simultaneously and the resistance of SMA calculated. All
measurements were obtained immediately after induction of AEx or APS. ET-A or ET-B receptor antagonists (BQ-485;60 ug/kg,ip and BQ-788; 60 ug/kg,ip respectively) were
administered 20 min before AEx or APS. Data from groups (n=5-7) were analyzed using ANOVA. RESULTS: Both AEx and APS increased the MAP and SMA resistance values
(p<0.01) and decreased the SMA blood flow (p<0.01). APS-induced hemodynamic alterations were more profound than AEx (p<0.05). Pretreatments with ET-A or ET-B
receptor antagonists significantly inhibited the AEx and APS-induced hemodynamic changes (p<0.01). CONCLUSIONS: Our results suggest psychological stress is a more
powerful stimulator of mesenteric hemodynamic changes than the stress caused by acute exercise. Moreover, both ET-A and ET-B receptors are involved in mesenteric
hemodynamic alterations observed after inductions of AEx and APS. Supported by Scientific and Technical Research Council of Turkey (TUBITAK, SBAG-2605)
20.16
Influence of progesterone on hemodynamics during treadmill locomotion in rats
Jennifer Rogers, Don sheriff, Exercise Science, The University of Iowa, 424 FH, Iowa City, Iowa, 52242
Previously we have shown that estrogen modulates the response of hindlimb blood flow, vascular conductance, and
arterial pressure to mild-intensity tradmilll locomotion in rats. The purpose of this study was to determine of progesterone (and/or testosterone) also exerts
cardiovascular influences at trest and during exercise. Hindlimb blood flow (ultrasonic transit time flow probe), arterial pressure, and vascular conductance
(calculated as the ratio of blood flow and arterial pressure) were determined in male (N=4), female (N=5), ovariectomized female (N=3), and ovariectomized female with
chronic progesterone replacement (n=4) Sprague-Dawley rats at rest and during treadmill locomotion at 7.5 and 15 m/min. Blood samples were obtained for immunoassay
measurement of plasma progesterone and testosterone concentrations. Regression analysis revealed that female gender was associated with higher blood flow and conductance
and lower blood pressure (all p <0.05). Neither progesterone nor testosterone modulated hindlimb blood flow or vascular conductance. However, progesterone was
associated with a significant increase in arterial pressure (regression coefficient = +0.20 mmHg/ng/ml; p < 0.05) while testosterone was associated with a significant
decrease in arterial pressure (-0.29 mmHg/ng/dl; p < 0.05). These results suggest that sex hormones influence cardiovascular function at rest and during exercise.
Supported byNIHHL46314.
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