Diameter changes in arteriolar networks of contracting skeletal muscle

The effect of muscular contraction on vessel diameter was studied in the arteriolar network of the exteriorized cat sartorius muscle during normal and elevated vascular tone. Dilation during 4 Hz motor-nerve stimulation was proportionately greatest in the third-order (transverse) arterioles and in vessels immediately upstream and downstream (P less than 0.01). This pattern of dilation was maintained with increased contraction frequency (30 Hz) and during concurrent sympathetic nerve stimulation (8 Hz). The pattern of constriction with sympathetic nerve stimulation alone showed a similar trend with the greatest response in the third-order and adjacent vessels. A model developed to estimate the resistance distribution in the arteriolar network, using data from earlier micropressure and vascular architecture studies in the sartorius muscle, allowed calculation of the resistance change during muscle contraction and sympathetic stimulation. Model predictions indicate that the third-order and adjacent vessels are the greatest site of resistance with both normal and elevated vascular tone. Thus these vessels were the site of greatest resistance change during muscle contraction. The more proximal, arcade vessels made lesser contributions to overall resistance changes, whereas the most distal, fifth-, and sixth-order arterioles appear not to be important in this regard. These findings indicate the third-order, transverse, arterioles are of special importance in regulating blood flow in the sartorius muscle.

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Arteriolar network response to pressure reduction during sympathetic nerve stimulation in cat skeletal muscle

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.3.h1251 ◽

1994 ◽

Vol 266 (3) ◽

pp. H1251-H1259 ◽

Cited By ~ 2

Author(s):

P. Ping ◽

P. C. Johnson

Keyword(s):

Blood Flow ◽

Shear Stress ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Similar Degree ◽

Sartorius Muscle ◽

Pressure Reduction ◽

Third Order ◽

Sympathetic Nerve Stimulation ◽

Resistance Change

Previous studies in this laboratory have shown that autoregulation of blood flow and dilation of midsized (second-order) arterioles were significantly enhanced during sympathetic nerve stimulation of cat sartorius muscle apparently because of a greater myogenic response of the arterioles. Quite typically, blood flow increased with arterial pressure reduction to 80, 60, and 40 mmHg (superregulation) during sympathetic nerve stimulation. To determine the contribution of the various orders of arterioles to the enhanced autoregulation, we measured diameters in all orders of arterioles and measured red cell velocity in first-, second-, and third-order arterioles. Without sympathetic nerve stimulation, all orders of arterioles except the first order dilated to pressure reduction, but flow autoregulation was weak. With sympathetic nerve stimulation, arteriolar dilation to pressure reduction was significantly enhanced in all six orders of arterioles, and flow rose significantly. The resistance change in the arteriolar network during pressure reduction as calculated from diameter changes was greatest in third- and fourth-order arterioles. Experimentally determined flow changes to pressure reduction and to sympathetic nerve stimulation were quantitatively similar to those predicted from diameter changes in a model of the arteriolar network. Calculated wall shear stress (from viscosity and shear rate) for first-, second-, and third-order arterioles decreased during pressure reduction with and without sympathetic nerve stimulation. We concluded that endothelium-mediated dilation due to shear stress would tend to oppose autoregulation of blood flow to a similar degree under both circumstances.

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Antagonism of vasoconstriction by muscle contraction differs with alpha-adrenergic subtype

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.264.3.h892 ◽

1993 ◽

Vol 264 (3) ◽

pp. H892-H900 ◽

Cited By ~ 3

Author(s):

L. R. Dodd ◽

P. C. Johnson

Keyword(s):

Muscle Contraction ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Sympathetic Nerves ◽

Second Order ◽

Sartorius Muscle ◽

Receptor Subtypes ◽

Sympathetic Nerve Stimulation ◽

Adrenergic Antagonist ◽

Prejunctional Inhibition

It has been suggested that muscle contraction causes prejunctional inhibition of transmitter release from sympathetic nerves. In accordance with this, we found that second-order (50 microns ID) arterioles of the cat sartorius muscle dilate 40-80% more with muscle contraction during 2-, 4-, or 8-Hz sympathetic nerve stimulation than during equivalent constriction produced by intravenous norepinephrine injection. However, when constriction was to the selective alpha 1-agonist phenylephrine, the magnitude of dilation induced by muscle contraction was similar to that seen with sympathetic nerve stimulation, suggesting that prejunctional inhibition is not involved. Alternatively, different receptor subtypes may be activated by sympathetic nerve stimulation and exogenous norepinephrine. In support of this explanation, we found that approximately 50% of the vasoconstrictor effect of sympathetic nerve stimulation (8 Hz) was blocked by prazosin, an alpha 1-adrenergic antagonist, but no further diminution of tone was seen with addiction of yohimbine, an alpha 2-adrenergic antagonist. In contrast, the vasoconstrictor response to exogenous norepinephrine was not affected by prazosin, while addition of yohimbine almost completely blocked the response. These findings suggest that muscle contraction selectively attenuates vasoconstriction mediated by junctional receptors in second-order arterioles.

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Response of arteriolar network of skeletal muscle to sympathetic nerve stimulation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.254.5.h919 ◽

1988 ◽

Vol 254 (5) ◽

pp. H919-H928 ◽

Cited By ~ 10

Author(s):

M. A. Boegehold ◽

P. C. Johnson

Keyword(s):

Skeletal Muscle ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Vascular Tone ◽

Volume Flow ◽

Sartorius Muscle ◽

Sympathetic Stimulation ◽

Sympathetic Nerve Stimulation ◽

Calculated Volume ◽

Arteriolar Diameter

The influence of vessel location on arteriolar responses to sympathetic nerve stimulation was systematically studied in a skeletal muscle arteriolar network under normal and altered tissue O2 levels. The exteriorized cat sartorius muscle was exposed to 0, 5, and 10% ambient O2 during sympathetic chain stimulation at 8 pulses/s. Under 0% O2, stimulation initially caused a 25-45% constriction that was faster and more pronounced in distal arterioles. Ninety-one percent of vessels showed a secondary dilation (sympathetic escape), which was largest in distal arterioles. Escape had little effect on calculated volume flow, which, after a large initial fall, showed a modest secondary increase. Under 5 and 10% O2, resting arteriolar diameter was reduced by 12 and 17%, respectively, and escape was reduced by 60 and 73%. Escape was not attenuated in proximal arterioles preconstricted with vasopressin, suggesting that O2 did not attenuate escape through increased vascular tone. Therefore, the arteriolar response to sympathetic stimulation depends largely on location within the network and is modulated to varying degrees by metabolic influences.

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Mechanism of enhanced myogenic response in arterioles during sympathetic nerve stimulation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.4.h1185 ◽

1992 ◽

Vol 263 (4) ◽

pp. H1185-H1189 ◽

Cited By ~ 13

Author(s):

P. Ping ◽

P. C. Johnson

Keyword(s):

Nerve Stimulation ◽

Sympathetic Nerve ◽

Similar Degree ◽

Sartorius Muscle ◽

Myogenic Response ◽

Pressure Reduction ◽

Sympathetic Nerve Stimulation ◽

Norepinephrine Infusion ◽

Cell Velocity ◽

Significant Mechanism

In a previous study we found that the arteriolar myogenic response was enhanced during sympathetic nerve stimulation in the cat sartorius muscle. In this study we determined whether the enhancement was unique to sympathetic nerve stimulation. Changes of arteriolar diameter and red cell velocity during femoral arterial pressure reduction from 110 to 60 mmHg were examined. Arterioles of 40 microns diameter were constricted by norepinephrine infusion to a similar degree as sympathetic nerve stimulation. Arteriolar dilation to pressure reduction was significantly enhanced during norepinephrine infusion and was not significantly different from that during sympathetic nerve stimulation. This indicates that junctional release of transmitters is not essential and rules out prejunctional inhibition of neurotransmitter release during pressure reduction as a significant mechanism in the enhanced dilation. Arteriolar dilation to pressure reduction was also enhanced during vasopressin or BAY K 8644 (a calcium channel agonist) infusion. In all instances, autoregulation of flow was significantly enhanced. These results demonstrate that modulation of the myogenic response occurs at postreceptor sites in the smooth muscle cell.

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Responses of muscles of cat small intestine to autonomic nerve stimulation

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1963.204.2.352 ◽

1963 ◽

Vol 204 (2) ◽

pp. 352-358 ◽

Cited By ~ 19

Author(s):

Gordon L. Van Harn

Keyword(s):

Small Intestine ◽

Muscle Contraction ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Longitudinal Muscle ◽

Muscle Layer ◽

Slow Waves ◽

Intraluminal Pressure ◽

Sympathetic Nerve Stimulation ◽

Longitudinal Muscle Layer

The externally recorded slow waves from the cat small intestine originate in the longitudinal muscle layer. In vitro the slow waves are recorded from all layers of the intestine if the segment is not immersed in a saline bath. When the longitudinal layer is removed from one region, the magnitude of the slow-wave potential in the other intestinal layers decreases as the distance from the intact longitudinal muscle layer is increased. An active intestine, in vivo, responds to sympathetic nerve stimulation by a hyperpolarization, cessation of spikes, and inhibition of muscle contraction. During inactivity of the intestine, either vagus or sympathetic nerve stimulation results in a depolarization, initiation of spikes, and muscle contraction. The nature of the response is influenced by the frequency of nerve stimulation and by the level of activity of the intestinal muscle, which is altered by intraluminal pressure changes. The effect of drugs on the response of the intestine to vagal and sympathetic nerve stimulation is such as to indicate that both inhibitory and excitatory nerve fibers are present in each of the autonomic nerves. The duration of the latent period of the response is long and highly variable, and a response requires 50–100 nerve volleys.

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Periarteriolar and tissue PO2 during sympathetic escape in skeletal muscle

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.254.5.h929 ◽

1988 ◽

Vol 254 (5) ◽

pp. H929-H936 ◽

Cited By ~ 20

Author(s):

M. A. Boegehold ◽

P. C. Johnson

Keyword(s):

Skeletal Muscle ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Parenchymal Cell ◽

Vascular Wall ◽

Sartorius Muscle ◽

Sympathetic Nerve Stimulation ◽

Parenchymal Tissue ◽

Tissue Po2 ◽

High O2

The purpose of this study was to determine whether vascular escape from sympathetic nerve stimulation in skeletal muscle is caused by a fall in the tissue O2 level. O2 microelectrodes were used to measure PO2 at the wall of arterioles (periarteriolar PO2) and near the venous end of capillary networks (parenchymal tissue PO2) in the exteriorized cat sartorius muscle during sympathetic nerve stimulation. Measurements were made under a low O2 suffusate (equilibrated with 5% CO2-95% N2) and under a high O2 suffusate (10% O2-5% CO2-85% N2). During sympathetic stimulation under low O2, mean diameter of proximal (second-order) arterioles decreased from 55 to 32 micron before returning to 37 micron (sympathetic escape). Mean periarteriolar PO2 fell from 50 to 25 mmHg with no secondary increase. Distal (fifth-order) arterioles initially constricted from 7 to 4 micron before relaxing to 6 micron. Periarteriolar PO2 of these vessels fell from 40 to 13 mmHg with no secondary increase. During stimulation under high O2, periarteriolar PO2 levels of both proximal and distal arterioles were similar to those under low O2, yet escape was substantially reduced. The lack of relationship between periarteriolar PO2 and vascular escape argues against a role of vascular wall PO2 in this behavior. Parenchymal tissue PO2 fell to 9 mmHg during stimulation under low O2 but did not fall below 22 mmHg during stimulation under high O2. The attenuation of escape under conditions where tissue PO2 did not fall is consistent with the hypothesis that sympathetic escape in skeletal muscle is mediated through a fall in parenchymal cell PO2.

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Role of myogenic response in enhancing autoregulation of flow during sympathetic nerve stimulation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.4.h1177 ◽

1992 ◽

Vol 263 (4) ◽

pp. H1177-H1184 ◽

Cited By ~ 21

Author(s):

P. Ping ◽

P. C. Johnson

Keyword(s):

Nerve Stimulation ◽

Sympathetic Nerve ◽

Venous Pressure ◽

Volume Flow ◽

Sartorius Muscle ◽

Myogenic Response ◽

Pressure Reduction ◽

Sympathetic Nerve Stimulation ◽

Ambient Oxygen

The effect of sustained sympathetic nerve stimulation on autoregulation of blood flow was examined in the exteriorized cat sartorius muscle using intravital microscopy. Without sympathetic nerve stimulation (SNS), second-order arterioles showed insignificant dilation (3%) during arterial pressure reduction from 110 to 60 mmHg; volume flow fell coincident with pressure reduction. During SNS, these arterioles constricted significantly (25%), and their dilation during pressure reduction (20%) was significant and was significantly greater than that without SNS. Volume flow increased significantly (20-60%) during pressure reduction, a phenomenon termed superregulation of flow. Elevation of ambient oxygen in the suffusate from 0 to 20% caused arteriolar constriction but did not abolish arteriolar dilation during pressure reduction under sustained SNS. Arteriolar response to venous pressure elevation was also affected significantly by sustained SNS. Without SNS, third-order arterioles showed slight dilation (4%) when femoral venous pressure was elevated by 10 mmHg. During SNS, these arterioles constricted significantly and constricted further (20%) when venous pressure was elevated. Using a local anesthetic (lidocaine), we determined that a local venous-arteriolar reflex was not involved in the arteriolar constriction. Our data suggest that superregulation of flow during sustained sympathetic nerve stimulation is not due to metabolic factors but rather to an enhanced myogenic response.

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