Arteriolar diameter and tissue oxygen tension during muscle contraction in hypertensive rats.

Boegehold, Matthew A.; Bohlen, H. G.

doi:10.1161/01.hyp.12.2.184

Cited by 43 publications

(53 citation statements)

References 28 publications

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“…However, the role of H 2 O 2 in this dilation is not diminished by high-salt intake, suggesting that the salt-induced decrease in functional dilation must be due to a reduction in the influence of some other dilator stimulus. A decrease in local oxygen levels can also contribute to arteriolar dilation during muscle contraction (7,17,41), either directly if there is a fall in arteriolar wall PO 2 or indirectly via vasoactive mediators produced when PO 2 declines in nearby parenchymal cells or paired venules (27,43). Because the blunting of functional dilation in salt-fed rats could reflect a reduced arteriolar responsiveness to such changes in PO 2 , one aim of this study was to examine the effects of a high-salt diet on arteriolar responses to oxygen.…”

Section: Discussionmentioning

confidence: 99%

“…Throughout the surgery and subsequent experimental period, the muscle was continuously superfused with an electrolyte solution (119 mM NaCl, 25 mM NaHCO 3, 6 mM KCl, and 3.6 mM CaCl2) warmed to 35°C and equilibrated with 95% N2-5% CO2 (pH 7.35-7.40). Superfusate flow rate was maintained at 4 -6 ml/min to minimize equilibration with atmospheric oxygen (7).…”

Section: Surgical Preparation and Intravital Microscopymentioning

confidence: 99%

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High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

Marvar

Falck²,

Boegehold

2007

American Journal of Physiology-Heart and Circulatory Physiology

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coupling of tissue blood flow to cellular metabolic demand involves oxygen-dependent adjustments in arteriolar tone, and arteriolar responses to oxygen can be mediated, in part, by changes in local production of 20-HETE. In this study, we examined the long-term effect of dietary salt on arteriolar oxygen responsiveness in the exteriorized, superfused rat spinotrapezius muscle and the role of 20-HETE in this responsiveness. Rats were fed either a normal-salt (NS, 0.45%) or high-salt (HS, 4%) diet for 4 -5 wk. There was no difference in steady-state tissue PO 2 between NS and HS rats, and elevation of superfusate oxygen content from 0% to 10% caused tissue PO 2 to increase by the same amount in both groups. However, the resulting reductions in arteriolar diameter and blood flow were less in HS rats than NS rats. Inhibition of 20-HETE formation with or 17-octadecynoic acid (17-ODYA) attenuated oxygen-induced constriction in NS rats but not HS rats. Exogenous 20-HETE elicited arteriolar constriction that was greatly reduced by the large-conductance Ca 2ϩ -activated potassium (K Ca) channel inhibitors tetraethylammonium chloride (TEA) and iberiotoxin (IbTx) in NS rats and a smaller constriction that was less sensitive to TEA or IbTx in HS rats. Arteriolar responses to exogenous angiotensin II were similar in both groups but more sensitive to inhibition with DDMS in NS rats. Norepinephrine-induced arteriolar constriction was similar and insensitive to DDMS in both groups. We conclude that 20-HETE contributes to oxygen-induced constriction of skeletal muscle arterioles via inhibition of K Ca channels and that a high-salt diet impairs arteriolar responses to increased oxygen availability due to a reduction in vascular smooth muscle responsiveness to 20-HETE. 20-hydroxyeicosatetraenoic acid; vascular control; blood flow; NaCl LOCAL OXYGEN AVAILABILITY is an important determinant of microvascular resistance and tissue blood flow (10,17,22,41), and consumption of a high-salt diet can lead to changes in resistance vessel function that alter the relationship between oxygen and vascular tone. For example, small gracilis muscle feed arteries from rats fed high salt for as little as 3 days consistently show an impaired dilator response to reduced oxygen levels (47, 48). However, the effect of oxygen on the tone of smaller arterioles in rat cremaster muscle is unchanged after 3 days on a high-salt diet (13). This suggests that either a longer period of high-salt intake is required to alter the oxygen responsiveness of these more distal resistance vessels or that there is a fundamental difference between extraparenchymal arteries and intramuscular arterioles in the susceptibility of oxygen-sensitive tone to dietary salt. The first aim of this study was to distinguish between these possibilities by determining whether a prolonged period of high-salt intake can change the relationship between oxygen and vascular tone in the arteriolar network of skeletal muscle.The mechanisms through which oxygen can influence resistance vessel to...

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Section: Discussionmentioning

confidence: 99%

Section: Surgical Preparation and Intravital Microscopymentioning

confidence: 99%

High dietary salt reduces the contribution of 20-HETE to arteriolar oxygen responsiveness in skeletal muscle

Marvar

Falck²,

Boegehold

2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…Measurements made with oxygen microelectrodes indicate that at this flow rate, suffusate PO 2 immediately above the muscle surface averages 14 mm Hg. 14 The muscle was transilluminated with a 150 W halogen fiber-optic light source (American Volpi, Auburn, New York), and its microvasculature was observed with an Olympus BHMJ intravital microscope (Hyde Park, New York) fitted with a Panasonic Newvicon video camera (Secaucus, New Jersey). Video images were displayed on a Panasonic high resolution television monitor and stored on videocassette tape for off-line analysis.…”

Section: Methodsmentioning

confidence: 99%

Effect of dietary salt on the skeletal muscle microvasculature in Dahl rats.

Boegehold

1990

Hypertension

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The purpose of this study was to identify microvascular alterations that could contribute to increased peripheral vascular resistance in the Dahl salt-sensitive rat with salt-induced hypertension. Intravital microscopy was used to study the spinotrapezius muscle arteriolar network in anesthetized salt-sensitive rats fed either a high salt (7% sodium chloride) or low-normal salt (0.45% sodium chloride) diet for 4 weeks. Age-matched Dahl salt-resistant rats on high and low-normal salt diets served as controls. The high salt diet had no effect on arterial pressure in salt-resistant rats but increased arterial pressure in salt-sensitive rats. Mean resting diameter of arcade arterioles in salt-sensitive rats on high salt diet was reduced by 25% compared with salt-sensitive rats on low salt or salt-resistant rats on either diet. After abolition of vascular tone with 10~3 M adenosine, arcade diameters were comparable in all groups. No difference among groups was found in either resting or passive diameter of the more distal transverse arterioles. Measurement of vessel lengths and numbers in cleared muscle specimens revealed no differences among groups in the anatomic density of either arcade or transverse arterioles. These data suggest that a reduction in the resting diameter of arcade, but not transverse, arterioles may increase spinotrapezius muscle vascular resistance in hypertensive salt-sensitive rats. The similarity in vascular densities among groups indicates that structural rarefaction of arterioles does not contribute to any increase in spinotrapezius muscle resistance at this stage of salt-induced hypertension. {Hypertension 1990;15:420-426)

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“…Circumstantial evidence along this line comes from measurements of tissue partial pressure of oxygen in rat models of hypertension, where relative hypoxia occurred in the cremaster, 76,77 a muscle in which rarefaction was consistently demonstrated, 30,31 but not the spinotrapezius, 78 a muscle in which no rarefaction was found. 79 The theoretical impact of rarefaction on tissue oxygenation was investigated by modeling the spatial distribution of partial pressure of oxygen with a finite element method; in that simulation, suppression of 25% of microvessels generated extended areas of profound hypoxia, especially in the presence of high cellular demand for oxygen.…”

Section: Consequences Of Microvascular Rarefactionmentioning

confidence: 99%