scholarly journals ENDOTHELIAL CONTRACTION INDUCED BY HISTAMINE-TYPE MEDIATORS

1969 ◽  
Vol 42 (3) ◽  
pp. 647-672 ◽  
Author(s):  
Guido Majno ◽  
Stephen M. Shea ◽  
Monika Leventhal
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Blood Vessels ◽  
Venous Congestion ◽  
Cremaster Muscle ◽  
Satisfactory Explanation ◽  
To Receive ◽  
Intercellular Gaps ◽  
Chemical Mediators

Previous work has shown that endogenous chemical mediators, of which histamine is the prototype, increase the permeability of blood vessels by causing gaps to appear between endothelial cells. In the present paper, morphologic and statistical evidence is presented, to suggest that endothelial cells contract under the influence of mediators, and that this contraction causes the formation of intercellular gaps. Histamine, serotonin, and bradykinin were injected subcutaneously into the scrotum of the rat, and the vessels of the underlying cremaster muscle were examined by electron microscopy. To eliminate the vascular collapse induced by routine fixation, in one series of animals (including controls) the root of the cremaster was constricted for 2–4 min prior to sacrifice, and the tissues were fixed under conditions of mild venous congestion. Electron micrographs were taken of 599 nuclei from the endothelium of small blood vessels representing the various experimental situations. Nuclear deformations were classified into four types of increasing tightness (notches, foldsl closing folds, and pinches. In the latter the apposed surfaces of the nuclear membrane are in contact). It was found that: (1) venous congestion tends to straighten the nuclei in al groups; (2) mediators cause a highly significant increase in the number of pinches (P < 0.001), also if the vessels are distended by venous congestion; (3) fixation without venous congestion causes vascular collapse. The degree of endothelial recoil, as measured by nuclear pinches, is very different from that caused by mediators (P < 0.001). (4) Pinched nuclei are more frequent in leaking vessels, and in cells adjacent to gaps (P < 0.001); (5) mediators also induce, in the endothelium, cytoplasmic changes suggestive of contraction, and similar to those of contracted smooth muscle; (6) there is no evidence of pericyte contraction under the conditions tested. Occasional pericytes appeared to receive fine nerve endings. Various hypotheses to explain nuclear pinching are discussed; the only satisfactory explanation is that which requires endothelial contraction.

ADENINE NUCLEOTIDES AND THEREGULATION OF VASCULAR TONE

1987 ◽  
Author(s):  
J L Gordon
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Vascular Tone ◽  
Adenine Nucleotides ◽  
Muscle Cells ◽  
Vascular Endothelial ◽  
Atp Analogs ◽  
Vascular Beds

ATP, although known mainly as an intracellular energy source, is also capable of acting extracellularly as a vasoactive agent of great potency, at concentrations around lμM or less. ADP is approximately equipotent with ATP in its actions on extracellular receptors in the vasculature.ATP and ADP can arise extracellularly through release from the cytoplasm of cellsexposed to damaging stimuli or by degranulation of platelets. The concentration of the nucleotides in the cytoplasm of most cells (including vascular endothelial and smooth muscle cells) is more than ImM, and the concentration in the dense storage granules of platelets approaches 1M. Thus, there is potential for very high localised concentrations of ATP and ADP in the plasma following platelet degranulation or damageto cells of the vessel well. Release from vascular endothelial and smooth muscle cells can occur with no loss of cell viability or leakage of cytoplasmic proteins.The vasoactivity of ATP and ADP is mediated via P2 purinoceptors. Vasodilation can be induced through the release of EDRF from endothelial cells or through stimulation of PGI2 production (PGI2 is a vasodilator in many, althoughnot all, arterial beds). Purinoceptor-mediated prostacyclin production can be stimulated from perfused vascular beds (e.g. theheart andthe lung), from isolated blood vessels or from cultured endothelial cells.In some blood vessels, purinoceptor-mediated vasoconstriction can be induced by direct actionon the vascular smooth muscle cells. The receptors responsible are sub-classified as P2X (which induce vasoconstriction) and P2Y (whichinduce vasodilation). The P2Y purinoceptor that mediates EDRF production is very similar to that which is responsible for PGI2 production, although there are some intriguing differences inthe potency of ATP analogs at stimulating these two responses, even on the same cells. The intracellular mechanisms responsible have not yet been fully elucidated, but it appears that elevation of intracellular calcium is likely to play a causal role.Adenosine, which is the product of ATP and ADP metabolism by nucleotidases, can also induce vasodilation in many blood vessels, acting via P1] purinoceptors on the smooth muscle cells, but its potency is often less than that of ATP and ADP.The fate of adenine nucleotides released into the plasma is determined by ectonucleotidases on the luminal surface of the endothelial cells, not by enzymes in the blood itself (the half-life of ATP in samples of blood or plasma is many minutes, while in the microcirculation the half-life isless than one second). Endothelial ectonucleotidases have been detected in several vascular beds, and many of their characteristics are now known. These enzymes are distinct entities from the P2 purinoceptors on endothelium, as shown by the marked differences in potency of several ATP analogs as P2 receptor stimulants and as substrates for the nucleotidases.In summary, vascular endothelial and smooth muscle cells respond to extracellularATP and ADP, and can also metabolise thesenucleotides extracellularly by ectonucleotidases. In addition, ATP and ADP can be selectively released from the cells of the vessel wall and from activated platelets. Thus, the endothelial pericellular environment can be the site of complex interactions by which vascular tone is regulated through the release, actions and metabolism ofextracellular nucleotides.

Studies of the innervation of rabbit myometrium and cervix

1989 ◽  
Vol 67 (8) ◽  
pp. 837-844 ◽  
Author(s):  
R. Bulat ◽  
M. S. Kannan ◽  
R. E. Garfield
Keyword(s):  
Electron Microscopy ◽  
Smooth Muscle ◽  
Blood Vessels ◽  
Spontaneous Activity ◽  
Isometric Contraction ◽  
Glyoxylic Acid ◽  
Adrenergic Innervation ◽  
Significant Inhibition ◽  
Adrenergic Nerves ◽  
Field Stimulation

We characterized the innervation of isolated circular and longitudinal-oriented muscle strips from the nulliparous rabbit uterus and cervix by field stimulation (FS). FS with increasing frequency (2.5–50 pps) and voltage (2.5–70 V) caused graded increases in isometric contraction with no relaxation or inhibition of spontaneous activity. Tetrodotoxin(TTX, 3.1 × 10−6 M) significantly reduced the FS response by 75% in all strips at higher stimulus frequencies. Contractile responses to FS were also significantly inhibited by atropine (3.5 × 10−6 M) in circular uterus and in longitudinal cervix. Guanethidine (5 × 10−6 M) reduced the response in all strips, as did phentolamine (3.6 × 10−6 M) in longitudinal uterus and circular cervix. Propranolol (3.9 × 10−6 M) did not significantly change the response in longitudinal uterus or circular cervix. In longitudinal uterus, combined guanethidine and atropine produced significant inhibition, but not statistically different from either drug alone. Similar results were seen in circular uterus. Electron microscopy and glyoxylic acid histofluorescence indicate that both blood vessels and smooth muscle in rabbit uterus are supplied with adrenergic nerves. The results suggest the presence of TTX-sensitive adrenergic and cholinergic excitatory innervation of rabbit uterus and cervix.Key words: uterus, myometrium, cervix, adrenergic innervation.

Electron microscopy of the glio-vascular organization of the brain of octopus

1969 ◽  
Vol 255 (797) ◽  
pp. 13-32 ◽  
Keyword(s):  
Electron Microscopy ◽  
Smooth Muscle ◽  
Blood Vessels ◽  
Light And Electron Microscopy ◽  
Muscle Cells ◽  
Medium Size ◽  
Muscle Fibres ◽  
Special Importance ◽  
Form Complex ◽  
Large Neurons

The glio-vascular organization of the octopus brain has been studied by light and electron microscopy. The structure of the walls of the blood vessels has been described. Two types of neuroglia can be recognized, the fibrous and protoplasmic glia; also enigmatic dark cells. Most blood vessels in the neuropil are surrounded by extracellular zones containing collagen. These zones give off glio-vascular tunnels (strands) that penetrate the neuropil in a complex network. The extracellular zones and tunnels contain in addition to collagen, smooth muscle cells and fibrocytes. Glial processes surround the extracellular zones and incompletely partition them from the neuropil. The small neuronal perikarya have no glial folds around them. The medium-size cells have thin glial sheets or finger processes related to their surfaces, which may indent the cells to form small trophospongia. The large neurons of the suboesophageal lobe have complex glial sheaths interspersed with extracellular channels. Both penetrate the neurons to form complex trophospongia. A new form of extracellular material has been observed in these extracellular channels. The occurrence of trophospongia in vertebrate and invertebrate neurons may be correlated with the absence of dendrites. Special problems discussed include the nature of the trophospongial function, the question of fluid-filled extracellular zones and their possible function as lymph channels, and the presence in some of them of haemocyanin molecules identical with those in the blood vessels. Perhaps of special importance is the observation that the lobes of the octopus brain are permeated with extracellular tunnels containing smooth muscle fibres, but it still needs to be determined whether or not the muscle cells in the tunnels of the neuropil actively contract and massage the neuropil to facilitate metabolic and other exchanges.

LRP: a new adhesion molecule for endothelial and smooth muscle cells

2001 ◽  
Vol 281 (4) ◽  
pp. F739-F750 ◽  
Author(s):  
Chuan Hu ◽  
Juan A. Oliver ◽  
Michael R. Goldberg ◽  
Qais Al-Awqati
Keyword(s):  
Monoclonal Antibody ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Adhesion Molecule ◽  
Kidney Development ◽  
Target Location ◽  
Muscle Cells ◽  
Laminin Receptor

We recently generated a monoclonal antibody that disrupted the association of endothelial cells with their target location during kidney development. Here, we purified the antigen of this monoclonal antibody to homogeneity using rat mesangial cell cytosol. Sequence revealed that it is a previously identified protein, termed the “laminin receptor precursor” (LRP). We found that this protein is expressed in most tissues, but immunocytochemistry revealed that it is present largely or entirely in blood vessels where it is located underneath endothelial cells and in between smooth muscle cells of the vascular wall. Vascular smooth muscle cells such as mesangial cells produce and secrete LRP into their extracellular matrix where it is present in several molecular weight forms. Endothelial cells produce very little if any of the protein, but they bind avidly to LRP-coated dishes. Anti-LRP antibodies prevent the binding of smooth muscle cells to uncoated plates, implying that cells that secrete it use it for attachment. In an assay for heterologous cell-to-cell interaction, antibodies to LRP inhibited the binding of smooth muscle cells to endothelial cells. Maturation and differentiation of blood vessels require interaction between endothelial and smooth muscle cells. LRP is a new component of the mesangial matrix, and we propose that it is an adhesion molecule that mediates an interaction between smooth muscle cells and endothelia.

Angiogenesis during human extraembryonic development involves the spatiotemporal control of PDGF ligand and receptor gene expression

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 749-754 ◽  
Author(s):  
L. Holmgren ◽  
A. Glaser ◽  
S. Pfeifer-Ohlsson ◽  
R. Ohlsson
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Receptor Gene ◽  
Muscle Cells ◽  
Receptor Mrna ◽  
Beta Receptor ◽  
Receptor Gene Expression

We have examined the role of platelet-derived growth factor (PDGF) ligand and receptor genes in the angiogenic process of the developing human placenta. In situ hybridization analysis of first trimester placentae showed that most microcapillary endothelial cells coexpress the PDGF-B and PDGF beta-receptor genes. This observation indicates that PDGF-B may participate in placental angiogenesis by forming autostimulatory loops in capillary endothelial cells to promote cell proliferation. Endothelial cells of macro blood vessels maintained high PDGF-B expression, whereas PDGF beta-receptor mRNA was not detectable. In contrast, PDGF beta-receptor mRNA was readily detectable in fibroblast-like cells and smooth muscle cells in the surrounding intima of intermediate and macro blood vessels. Taken together, these data suggest that the PDGF-B signalling pathway appears to switch from an autocrine to a paracrine mechanism to stimulate growth of surrounding PDGF beta-receptor-positive mesenchymal stromal cells. Smooth muscle cells of the blood vessel intima also expressed the PDGF-A gene, the protein product of which is presumably targeted to the fibroblast-like cells of the mesenchymal stroma as these cells were the only ones expressing the PDGF alpha-receptor. PDGF-A expression was also detected in columnar cytotrophoblasts where it may have a potential role in stimulating mesenchymal cell growth at the base of the growing placental villi. We discuss the possibility that the regulation of the PDGF-B and beta-receptor gene expression might represent the potential targets for primary angiogenic factors.

scholarly journals Intermediate-sized filaments of human endothelial cells.

1979 ◽  
Vol 81 (3) ◽  
pp. 570-580 ◽  
Author(s):  
W W Franke ◽  
E Schmid ◽  
M Osborn ◽  
K Weber
Keyword(s):  
Electron Microscopy ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Indirect Immunofluorescence ◽  
Immunofluorescence Microscopy ◽  
Major Protein ◽  
Human Endothelial Cells ◽  
Specific Antibodies ◽  
Indirect Immunofluorescence Microscopy ◽  
Polypeptide Band

Human endothelial cells prepared from unbilical cords are characterized in parallel by electron microscopy and indirect immunofluorescence microscopy using specific antibodies against different classes of intermediate-sized filaments. The strongly developed, loose bundles of intermediate-sized filaments typically found in these cells are not decorated by antibodies against prekeratin or antibodies against smooth muscle desmin. They are, however, strongly decorated by antibodies directed against murine "vimentin," i.e., the 57,000 mol wt polypeptide which is the major protein of the intermediate-sized filaments predominant in various cells of mesenchymal origin. Cytoskeletal preparations greatly enriched in intermediate-sized filaments show the enrichment of a polypeptide band comigrating with murine vimentin. This shows that the intermediate-sized filaments that are abundant in human endothelial cells are predominantly of the vimentin type and can be demonstrated by their cross-reaction with the vimentin of rodents. These data also strengthen the evidence for several subclasses of intermediate-sized filaments, which can be distinguished by immunological procedures.

scholarly journals A biomimetic orthogonal-bilayer tubular scaffold for the co-culture of endothelial cells and smooth muscle cells

RSC Advances ◽  
2021 ◽  
Vol 11 (50) ◽  
pp. 31783-31790
Author(s):  
Mei-Xi Li ◽  
Lei Li ◽  
Si-Yuan Zhou ◽  
Jian-Hua Cao ◽  
Wei-Hua Liang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Blood Vessels ◽  
Outer Layer ◽  
Muscle Cells ◽  
Tubular Scaffold

To mimic blood vessels, a polycaprolactone tubular scaffold was prepared via electrospinning and winding. Endothelial cells were cultured on the inner layer with axial nanofibers and smooth muscle cells were cultured on the outer layer with circumferential nanofibers.

Endothelial Control of Vascular Function

Physiology ◽  
1989 ◽  
Vol 4 (4) ◽  
pp. 139-142 ◽  
Author(s):  
TO Daniel ◽  
HE Ives
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Blood Vessels ◽  
Vascular Function ◽  
Regional Responses ◽  
Vascular Beds ◽  
Endothelial Control

Endothelial cells are exposed to stimuli within the lumen of blood vessels. Interpreting these signals, endothelial cells regulate production and release of mediators that signal underlying smooth muscle to contract, relax, or proliferate. Specialization of endothelial cells in different vascular beds may determine regional responses.

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