scholarly journals Direct observations of sympathetic cholinergic vasodilatation of skeletal muscle small arteries in the cat.

1997 ◽  
Vol 500 (1) ◽  
pp. 213-225 ◽  
Author(s):  
K Matsukawa ◽  
T Shindo ◽  
M Shirai ◽  
I Ninomiya
2011 ◽  
Vol 300 (5) ◽  
pp. H1602-H1608 ◽  
Author(s):  
Adrian Gericke ◽  
Jan J. Sniatecki ◽  
Veronique G. A. Mayer ◽  
Evgeny Goloborodko ◽  
Andreas Patzak ◽  
...  

Acetylcholine regulates perfusion of numerous organs via changes in local blood flow involving muscarinic receptor-induced release of vasorelaxing agents from the endothelium. The purpose of the present study was to determine the role of M1, M3, and M5 muscarinic acetylcholine receptors in vasodilation of small arteries using gene-targeted mice deficient in either of the three receptor subtypes (M1R−/−, M3R−/−, or M5R−/− mice, respectively). Muscarinic receptor gene expression was determined in murine cutaneous, skeletal muscle, and renal interlobar arteries using real-time PCR. Moreover, respective arteries from M1R−/−, M3R−/−, M5R−/−, and wild-type mice were isolated, cannulated with micropipettes, and pressurized. Luminal diameter was measured using video microscopy. mRNA for all five muscarinic receptor subtypes was detected in all three vascular preparations from wild-type mice. However, M3 receptor mRNA was found to be most abundant. Acetylcholine produced dose-dependent dilation in all three vascular preparations from M1R−/−, M5R−/−, and wild-type mice. In contrast, cholinergic dilation was virtually abolished in arteries from M3R−/− mice. Deletion of either M1, M3, or M5 receptor genes did not affect responses to nonmuscarinic vasodilators, such as substance P and nitroprusside. These findings provide the first direct evidence that M3 receptors mediate cholinergic vasodilation in cutaneous, skeletal muscle, and renal interlobar arteries. In contrast, neither M1 nor M5 receptors appear to be involved in cholinergic responses of the three vascular preparations tested.


1981 ◽  
Vol 241 (2) ◽  
pp. H217-H223
Author(s):  
N. Skaug ◽  
R. Detar

Helical strips cut from small arteries taken from rabbit skeletal muscle were used to determine the steady-state effects of extracellular potassium concentration ([K]o) on the reactivity to epinephrine or norepinephrine. It was found that reactivity observed under the usual steady-state conditions (termed "usual reactivity") was depressed as steady-state [K]o was reduced from 8 to 1 mM. This depression reflected concurrent changes in two components of contraction: 1) a positive component (evaluated as reactivity during brief exposure to 10(-6) M ouabain) decreased when steady-state [K]o was reduced below approximately 5 mM, and 2) a negative component (evaluated indirectly as enhancement of reactivity produced by 10(-6) M ouabain) increased to a peak when steady-state [K]o was reduced from 8 to approximately 4-5 mM and decreased below this peak when steady-state [K]o was reduced below approximately 4-5 mM. It was also found that the magnitude of a reserve ouabain-sensitive negative component (demonstrated by abruptly increasing [K]o to 10.18 mM) increased from a minimum to a maximum level when steady-state [K]o was reduced from 6 to 3 mM. It is suggested that the effects of [K]o on the positive component of contraction, defined earlier as contractility, primarily involve some factor(s) other than transmembrane potential, whereas the effects on the negative component involve transmembrane potential exclusively and, in particular, the electrogenic potential. The latter suggestion constitutes the basis for use of the term electrogenesis in reference to this negative component.


1991 ◽  
Vol 260 (6) ◽  
pp. H1819-H1825 ◽  
Author(s):  
M. A. Boegehold

The purpose of this study was to determine the effect of salt-induced hypertension on the microvascular pressure profile in skeletal muscle. Measurements were made in the spinotrapezius muscle of anesthetized Dahl salt-sensitive (DS) rats fed either a high- (7%) or low-normal (0.45%)-NaCl diet for 4 wk. Age-matched Dahl salt-resistant (DR) rats on high- or low-normal salt diets were also studied. The high-salt diet had no effect on either arterial or microvascular pressures in DR rats. DS rats maintained on high salt developed arterial hypertension accompanied by a pressure increase of 49% in the feed arterioles and 31% in the transverse arterioles. Hypertensive DS rats exhibited a greater pressure drop across the small arteries, arcade arterioles, and distal arterioles, indicating that each of these segments contributes to increased whole organ resistance. Pressures in the collecting and draining venules were not elevated in DS on 7% NaCl, suggesting that increased precapillary resistance in salt-induced hypertension effectively shields the skeletal muscle capillary and venular networks from high hydrostatic pressures.


2003 ◽  
Vol 177 (2) ◽  
pp. 157-166 ◽  
Author(s):  
O. Tarasova ◽  
N. Sjöblom-Widfeldt ◽  
H. Nilsson

1965 ◽  
Vol 208 (3) ◽  
pp. 417-424 ◽  
Author(s):  
Lawrence D. Dorr ◽  
Michael J. Brody

The hypothesis that sympathetic innervation to skeletal muscle vasculature contains functionally distinct adrenergic and cholinergic fibers was investigated utilizing the dog isolated perfused gracilis muscle. The use of hemicholinium in an attempt to abolish cholinergic dilatation, but not adrenergic constriction, in response to intermittent nerve stimulation was not successful. Continuous nerve stimulation produced vasoconstriction which was maintained for the duration of stimulation. Conversely, when cholinergic vasodilatation was unmasked, continuous stimulation resulted in a dilator response which disappeared rapidly. These experiments suggested that release of the adrenergic transmitter could not be dependent upon an intermediate cholinergic link in the sympathetic nerve. This postulate was supported further by experiments utilizing electrical stimulation of medullary vasoconstrictor areas. Whereas cholinergic vasodilatation was unmasked routinely by peripheral stimulation following reserpine, guanethidine or ß-TM 10, this response was never seen when medullary vasoconstrictor neurons were activated following these agents. It was concluded that sympathetic cholinergic nerves to skeletal muscle vessels possess a purely vasodilator function, and do not play an intermediate role involving release of the adrenergic transmitter.


2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Kei Ishii ◽  
Kanji Matsukawa ◽  
Nan Liang ◽  
Kana Endo ◽  
Mitsuhiro Idesako ◽  
...  

2013 ◽  
Vol 1 (4) ◽  
Author(s):  
Kei Ishii ◽  
Kanji Matsukawa ◽  
Nan Liang ◽  
Kana Endo ◽  
Mitsuhiro Idesako ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document