Vascular Patterns and Active Vasomotion as Determiners of Flow Through Minute Vessels

Nicoll, Paul A.; Webb, Richard L.

doi:10.1177/000331975500600403

Cited by 143 publications

(39 citation statements)

References 7 publications

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“…The circulation was highly anastomotic with many interarteriolar, intercapillary and intervenular connections. A similar anastomotic circulation has been described in the bat's wing (9,10), in the subcutaneous tissue of mice (11), in voluntary muscle (12) and in intestinal wall (13). Since pressures at either end of the anastomosis were similar, flow was sluggish in the anastomosis.…”

Section: Resultssupporting

confidence: 61%

Rapid and Slow Components of the Circulation in the Human Forearm1

Freis¹,

Schnaper²,

Lilienfield³

1957

J. Clin. Invest.

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Section: Resultssupporting

confidence: 61%

Rapid and Slow Components of the Circulation in the Human Forearm1

Freis¹,

Schnaper²,

Lilienfield³

1957

J. Clin. Invest.

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“…3 ± 5 The vasomotion has been observed directly only in the vessels of the mesentery 15,16 and the wing of the bat. 17 The vasomotion in the spinal cord, however, can be more accurately determined when observed stereoscopically using vascular corrosion casts and a scanning electron microscope, 6 ± 9,14 and it is becoming better understood through immunohistochemical studies. 18 The vasomotion at the arteriolar level was found to consist of two types: Type I vasomotion may represent the peristaltic movement by the arteriolar vessels that is hypothesized to have a pumping e ect.…”

Section: Discussionmentioning

confidence: 99%

Regulation of vasomotion of arterioles and capillaries in the cat spinal cord: role of α actin and endothelin-1

et al. 1997

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Ring-shaped vasoconstrictions of arterioles at their branching sites have often been reported in vascular corrosion casts of the brain and spinal cord in rats and cats. It is surmised that smooth muscle cells in arteriolar walls could regulate the blood¯ow by changing the diameter of the lumen (ie vasomotion). However, few reports have described vasomotion at the capillary (capillaries have no smooth muscle cells). Also, there have been no reports on endothelin-1 in the arterioles and capillaries of the spinal cord. This study was designed to determine (1) the electron microscopic architecture of vasomotion; (2) the immunohistochemical identi®cation of a actin and endothelin-1 in the arterioles and capillaries of the spinal cord. Twenty-seven adult mongrel cats were used to study vascular corrosion casts at the lumbosacral spinal cord segments immunohistologically and through scanning electron microscopic observations. Sections of the spinal cord were stained with monoclonal anti-a actin and endothelin-1 antibodies.Vascular corrosion casts demonstrated two types of vasomotion: a sausage-like peristalsis and a ring-shaped vasoconstriction at the arteriole and capillary levels. In the immunohistological study, a actin and endothelin-1 were identi®able in the vascular wall at the bifurcation, and pericytes were found to contain micro®laments of a actin. The ringshaped vasoconstriction might be regulated by smooth muscle cells in arterioles and by pericytes in capillaries by releasing endothelin-1.

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“…Arterial vasomotion is believed to originate within the smooth muscle cell layer of the artery wall because it can occur independently of endothelium (6,8) or innervation (1,3,6,52). Although AVP has been reported to stimulate vasomotion in several arterial preparations (3,9,10), the biochemical mechanisms underlying this effect have not been elucidated.…”

Section: Pyk2 and Ca 2ϩ Spiking In A7r5 Cellsmentioning

confidence: 99%

“…Periodic or oscillatory increases in cytosolic free [Ca 2ϩ ] ( [Ca 2ϩ ] i ) 1 in vascular smooth muscle cells are believed to underlie arterial vasomotion. These rhythmic contractions of resistance arteries and arterioles are important for local perfusion of tissues (1) as well as a determinant of blood pressure and peripheral resistance (2).…”

mentioning

confidence: 99%

Signal Transduction of Physiological Concentrations of Vasopressin in A7r5 Vascular Smooth Muscle Cells

Byron

Lucchesi

2002

Journal of Biological Chemistry

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The signal transduction pathway linking physiological concentrations of [Arg 8 ]vasopressin (AVP) to an increase in frequency of Ca 2؉ spiking was examined in confluent cultures of A7r5 vascular smooth muscle cells. Immunoprecipitation/Western blot studies revealed a robust increase in tyrosine phosphorylation of the nonreceptor tyrosine kinase, PYK2, in A7r5 cells treated with 4␤-phorbol 12-myristate 13-acetate or ionomycin. 100 pM AVP also induced PYK2 tyrosine phosphorylation, and this effect was inhibited by protein kinase C inhibitors Ro-31-8220 (1-10 M) or chelerythrine chloride (1-20 M). In fura-2-loaded A7r5 cells, the stimulation of Ca 2؉ spiking by 100 pM AVP or 1 nM 4␤-phorbol 12-myristate 13-acetate was completely blocked by PP2 (10 M, a Src family kinase inhibitor). Salicylate (20 mM, recently identified as a PYK2 inhibitor) and the tyrosine kinase inhibitor, tyrphostin A47 (50 M), but not its inactive analog, tyrphostin A63, also blocked AVP-stimulated Ca 2؉ spiking. PYK2 phosphorylation was inhibited by both PP2 and salicylate, whereas tyrphostin A47 failed to inhibit PYK2 tyrosine phosphorylation. ERK1/2 kinases did not appear to be involved because 1) 100 pM AVP did not appreciably increase ERK1/2 phosphorylation and U-0126 (2.5 M) did not inhibit AVP-stimulated Ca 2؉ spiking; and 2) epidermal growth factor (10 nM) robustly stimulated ERK1/2 phosphorylation but did not induce Ca 2؉ spiking. It remains to be elucidated how activation of PKC ultimately produces Ca 2ϩ spiking. One possibility is that PKC activation leads to membrane depolarization and consequently to activation of L-type voltage-sensitive Ca 2ϩ channels. We have preliminary data that suggest that inhibition of delayed rectifier K ϩ channels (K v channels) may provide the trigger for L-type Ca 2ϩ channel activation (16). The present study examines the possibility that one or more tyrosine kinases may serve as intermediary links in this signaling cascade. In particular, we focus on the non-receptor tyrosine kinase PYK2 (proline-rich tyrosine kinase 2, also known as RAFTK or CADTK), a member of the focal adhesion kinase (p125 FAK ) family, which is acti-

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Vascular Patterns and Active Vasomotion as Determiners of Flow Through Minute Vessels

Cited by 143 publications

References 7 publications

Rapid and Slow Components of the Circulation in the Human Forearm1

Rapid and Slow Components of the Circulation in the Human Forearm1

Regulation of vasomotion of arterioles and capillaries in the cat spinal cord: role of α actin and endothelin-1

Signal Transduction of Physiological Concentrations of Vasopressin in A7r5 Vascular Smooth Muscle Cells

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