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Arteriolar Dilation (arteriolar + dilation)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Hydrogen Peroxide-Dependent Arteriolar Dilation in Contracting Muscle of Rats Fed Normal and High Salt Diets

MICROCIRCULATION, Issue 8 2007
Paul J. Marvar
ABSTRACT Objective: High dietary salt intake decreases the arteriolar dilation associated with skeletal muscle contraction. Because hydrogen peroxide (H2O2) can be released from contracting muscle fibers, this study was designed to assess the possible contribution of H2O2 to skeletal muscle functional hyperemia and its sensitivity to dietary salt. Methods: The authors investigated the effect of catalase treatment on arteriolar dilation and hyperemia in contracting spinotrapezius muscle of rats fed a normal salt (0.45%, NS) or high salt (4%, HS) diet for 4 weeks. Catalase-sensitive 2,,7,-dichlorofluorescein (DCF) fluorescence was measured as an index of H2O2 formation, and the mechanism of arteriolar dilation to H2O2 was probed in each group using pharmacological inhibitors. Results: DCF fluorescence increased with muscle contraction, but not if catalase was present. Catalase also reduced arteriolar dilation and hyperemia during contraction in both dietary groups. Exogenous H2O2 dilated arterioles in both groups, with greater responses in HS rats. Guanylate cyclase inhibition did not affect arteriolar responses to H2O2 in either group, but KCa or KATP channel inhibition equally reduced these responses, and KATP channel inhibition equally reduced functional hyperemia in both groups. Conclusions: These results indicate that locally produced H2O2 contributes to arteriolar dilation and hyperemia in contracting skeletal muscle, and that the effect of H2O2 on arteriolar tone in this vascular bed is mediated largely through K+ channel activation. High dietary salt intake does not reduce the contribution of H2O2 to active hyperemia, or alter the mechanism through which H2O2 relaxes arteriolar smooth muscle. [source]

Regulation of In Situ Skeletal Muscle Arteriolar Tone: Interactions Between Two Parameters

MICROCIRCULATION, Issue 6 2002
JEFFERSON C. FRISBEEArticle first published online: 26 JAN 2010
ABSTRACT Objective: The growing understanding of the complexity of mechanisms regulating arteriolar tone demands that a systematic determination of how these processes interact to alter diameter be undertaken. This study examined how five mediators of skeletal muscle distal arteriolar tone [adenosine concentration, oxygen content, ,-adrenergic activation (norepinephrine), intravascular pressure and wall shear rate], taken two parameters at a time, interact to regulate vessel diameter. Methods: The reactivity of distal arterioles of in situ rat cremaster muscle after alterations in each of the above mediators was assessed. In addition, arteriolar responses to all two-parameter combinations were evaluated to determine the effect of altered environment on vascular reactivity to stimuli. Results: Arteriolar dilation to adenosine was unaltered by changes in other parameters. In contrast, wall shear rate-induced arteriolar dilation was impaired by 60,88% after increases in the other parameters. Myogenic reactivity was reduced by 28% with elevated O2 and by 65% with norepinephrine (because of vessel closure) and was impaired by 89% with elevated adenosine. O2 -induced arteriolar reactivity was impaired by 56% with increased adenosine and by 44% with increased norepinephrine concentration but was largely unaffected by elevated intravascular pressure. Adrenergic reactivity was attenuated with elevated intravascular pressure (by 69%) and O2 (by 54%) because of vessel closure but was unaltered with elevated adenosine. Conclusions: These data suggest that (1) individual mediators contributing to the regulation of arteriolar tone exist within a hierarchy of importance and (2) mechanisms regulating arteriolar tone can be impacted by unidentified alterations in other processes. Ongoing investigation into interactions between multiple processes regulating arteriolar tone will allow for a more integrated understanding of how microvessels regulate their diameter. [source]

Functional and molecular evidence of adenosine A2A receptor in coronary arteriolar dilation to adenosine

DRUG DEVELOPMENT RESEARCH, Issue 1-2 2001
Lih Kuo
Abstract Adenosine is a potent vasodilator implicated in the regulation of coronary microvascular diameter during metabolic stress. However, the specific adenosine receptors and underlying mechanism responsible for the dilation of coronary microvessels to adenosine remains to be elucidated. Thus, pig subepicardial coronary arterioles (<100 ,m) were isolated, cannulated, and pressurized without flow for in vitro study. All vessels developed basal tone and dilated concentration-dependently to adenosine. Disruption of endothelium and inhibition of nitric oxide (NO) synthase by L-NAME produced identical attenuation of adenosine-induced dilation. KATP channel inhibitor glibenclamide further reduced the dilation of denuded vessels. cAMP antagonist Rp-8-Br-cAMP blocked vasodilation to forskolin, but failed to inhibit vasodilation to adenosine. Coronary dilation to adenosine was blocked by a selective adenosine A2A receptor antagonist ZM241385, but was not altered by an A1 receptor antagonist, DPCPX. Reverse transcription-polymerase chain reaction study revealed that A2A receptor mRNA was expressed in microvessels but not in cardiac myocytes; A1 receptor expression was observed only in cardiac myocytes. These results suggest that adenosine-induced dilation of coronary arterioles is mediated predominantly by A2A receptors. Activation of these receptors elicits vasodilation by endothelial release of NO and by smooth muscle opening of KATP channels in a cAMP-independent manner. Drug Dev. Res. 52:350,356, 2001. © 2001 Wiley-Liss, Inc. [source]

Hydrogen Peroxide-Dependent Arteriolar Dilation in Contracting Muscle of Rats Fed Normal and High Salt Diets

MICROCIRCULATION, Issue 8 2007
Paul J. Marvar
ABSTRACT Objective: High dietary salt intake decreases the arteriolar dilation associated with skeletal muscle contraction. Because hydrogen peroxide (H2O2) can be released from contracting muscle fibers, this study was designed to assess the possible contribution of H2O2 to skeletal muscle functional hyperemia and its sensitivity to dietary salt. Methods: The authors investigated the effect of catalase treatment on arteriolar dilation and hyperemia in contracting spinotrapezius muscle of rats fed a normal salt (0.45%, NS) or high salt (4%, HS) diet for 4 weeks. Catalase-sensitive 2,,7,-dichlorofluorescein (DCF) fluorescence was measured as an index of H2O2 formation, and the mechanism of arteriolar dilation to H2O2 was probed in each group using pharmacological inhibitors. Results: DCF fluorescence increased with muscle contraction, but not if catalase was present. Catalase also reduced arteriolar dilation and hyperemia during contraction in both dietary groups. Exogenous H2O2 dilated arterioles in both groups, with greater responses in HS rats. Guanylate cyclase inhibition did not affect arteriolar responses to H2O2 in either group, but KCa or KATP channel inhibition equally reduced these responses, and KATP channel inhibition equally reduced functional hyperemia in both groups. Conclusions: These results indicate that locally produced H2O2 contributes to arteriolar dilation and hyperemia in contracting skeletal muscle, and that the effect of H2O2 on arteriolar tone in this vascular bed is mediated largely through K+ channel activation. High dietary salt intake does not reduce the contribution of H2O2 to active hyperemia, or alter the mechanism through which H2O2 relaxes arteriolar smooth muscle. [source]

Regulation of In Situ Skeletal Muscle Arteriolar Tone: Interactions Between Two Parameters

MICROCIRCULATION, Issue 6 2002
JEFFERSON C. FRISBEEArticle first published online: 26 JAN 2010
ABSTRACT Objective: The growing understanding of the complexity of mechanisms regulating arteriolar tone demands that a systematic determination of how these processes interact to alter diameter be undertaken. This study examined how five mediators of skeletal muscle distal arteriolar tone [adenosine concentration, oxygen content, ,-adrenergic activation (norepinephrine), intravascular pressure and wall shear rate], taken two parameters at a time, interact to regulate vessel diameter. Methods: The reactivity of distal arterioles of in situ rat cremaster muscle after alterations in each of the above mediators was assessed. In addition, arteriolar responses to all two-parameter combinations were evaluated to determine the effect of altered environment on vascular reactivity to stimuli. Results: Arteriolar dilation to adenosine was unaltered by changes in other parameters. In contrast, wall shear rate-induced arteriolar dilation was impaired by 60,88% after increases in the other parameters. Myogenic reactivity was reduced by 28% with elevated O2 and by 65% with norepinephrine (because of vessel closure) and was impaired by 89% with elevated adenosine. O2 -induced arteriolar reactivity was impaired by 56% with increased adenosine and by 44% with increased norepinephrine concentration but was largely unaffected by elevated intravascular pressure. Adrenergic reactivity was attenuated with elevated intravascular pressure (by 69%) and O2 (by 54%) because of vessel closure but was unaltered with elevated adenosine. Conclusions: These data suggest that (1) individual mediators contributing to the regulation of arteriolar tone exist within a hierarchy of importance and (2) mechanisms regulating arteriolar tone can be impacted by unidentified alterations in other processes. Ongoing investigation into interactions between multiple processes regulating arteriolar tone will allow for a more integrated understanding of how microvessels regulate their diameter. [source]

Decreased Arteriolar Sensitivity to Shear Stress in Adult Rats is Reversed by Chronic Exercise Activity

MICROCIRCULATION, Issue 2 2002
Dong Sun M.D., Ph.D.
Objective: We tested the hypothesis that the decline in endothelium-dependent arteriolar dilation in adult rats is reversed by chronic exercise activity. Methods: Rats were divided into young (8,10 weeks)-sedentary (SEDY), adult (29,32 weeks)-sedentary (SEDA), and adult-exercised (EXA, treadmill exercise for 18,20 weeks) groups. Responses of isolated arterioles (,50 µm at 80 mm Hg) of gracilis muscle were assessed to increases in perfusate flow and vasoactive agents. Results: With no differences in basal tone, maximal flow-induced dilations were not different between arterioles of SEDY and SEDA rats (71 ± 2 and 72 ± 2% of passive diameter, respectively), yet the sensitivity of arterioles to shear stress (WSS50) was significantly less in SEDA than in SEDY rats (35 ± 4 vs. 23 ± 3 dyne/cm2, respectively). In vessels of EXA rats, maximal flow-induced dilation was significantly augmented (88 ± 2% of passive diameter) and WSS50 (15 ± 1 dyn/cm2) was significantly reduced. Dilation to acetylcholine was enhanced in arterioles of EXA, whereas dilation to sodium nitroprusside was not different in vessels of the three groups. Conclusion: Chronic exercise activity reverses age related reduction in sensitivity of arterioles to increases in wall shear stress. [source]