scholarly journals Substance P: immunohistochemical localization and effect upon cat pial arteries in vitro and in situ.

1981 ◽  
Vol 318 (1) ◽  
pp. 251-258 ◽  
Author(s):  
L Edvinsson ◽  
J McCulloch ◽  
R Uddman
1991 ◽  
Vol 11 (4) ◽  
pp. 567-575 ◽  
Author(s):  
I. Jansen ◽  
C. Alafaci ◽  
J. McCulloch ◽  
R. Uddman ◽  
L. Edvinsson

The vasomotor responses of tachykinins have been studied in the cerebral vasculature of human, pig, cat, and guinea pig. Substance P (SP), neurokinin A (NKA), neurokinin B (NKB), and neuropeptide K (NPK) induced concentration-dependent relaxations of precontracted cerebral arteries in all species when examined by a sensitive in vitro technique. In addition, the relaxant responses to SP, NKA, and NKB were studied in cat pial arterioles by peptide microapplication in situ. In human pial vessels, the order of relaxant potency was SP > NKB > NKA > NPK; in the pig middle cerebral artery, there was no difference in potency between the tachykinins; in the cat middle cerebral artery, SP = NKB > NKA = NPK; and in the guinea pig basilar artery, SP » NPK = NKA > NKB. Responses induced by SP, NKA, and NKB in the cat were comparable in vitro and in situ. Removal of the endothelium abolished relaxation induced by all four tachykinins. The relaxant responses of guinea pig basilar arteries to SP, NKA, and NPK were competitively antagonized by the SP antagonist Spantide. However, Spantide lowered the Imax of the NKB concentration–response curve without any rightward shift, suggesting action at a different site than the other tachykinins. In the guinea pig basilar artery, the relaxation seems to be exerted via a NK-1 receptor subtype while the receptor subtype is more unclear in cerebral arteries from human, cat, and pig. It is concluded that relaxations induced by SP, NKA, NKB, and NPK are dependent on the endothelium, and are antagonized either competitively or non-competitively by the SP antagonist Spantide. The origin of tachykinins acting through the endothelium is discussed.


1983 ◽  
Vol 3 (2) ◽  
pp. 231-237 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner

The effect of bradykinin on cerebrovascular resistance vessels was investigated by the use of in vitro and in situ preparations. Bradykinin, in the range of 10−10 to 10−5 M, elicited a concentration-dependent vasodilatation on both feline and human pial arteries in vitro; the half-maximal response was found to be approximately at 2.8 × 10−7 M and 1.3 × 10−8 M (EC50), respectively. This dilatatory effect of bradykinin in vitro was found only in arteries preconstricted with prostaglandin F2α or 5-hydroxytryptamine. In order to determine the effects of bradykinin on the diameter of cat pial arteries in situ, perivascular microapplication was employed. The dose-response curves obtained showed vasodilatation; the EC50 and the maximal response (EAm) were 4.4 × 10−7 M and 45.5% at 10−5 M, respectively. Statistically significant (p < 0.01) reactions were observed at 10−7 M and higher concentrations of bradykinin. The observed effects were independent of initial vessel size (80–260 μm). These in situ findings are very similar to those found in vitro. The isolated guinea pig ileum was used to check the stability of the bradykinin solutions. In this instance, a concentration-dependent contraction was found when “freshly prepared” or “5 hours stored” bradykinin was applied, indicating no measurable degradation of bradykinin. We conclude that bradykinin is a powerful vasodilator of both human and feline pial arteries.


Cephalalgia ◽  
1985 ◽  
Vol 5 (3_suppl) ◽  
pp. 482-483 ◽  
Author(s):  
Inger Jansen ◽  
Kai Jensen ◽  
Pia Stjernholm ◽  
Jes Olesen ◽  
Rolf Uddman ◽  
...  
Keyword(s):  

1983 ◽  
Vol 3 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner

Bradykinin is known to effect a vasodilatation of feline cerebral arteries in situ and of both human and feline pial arteries in vitro. In order to demonstrate whether kininase II (localized within the vessel wall or in the surrounding tissue or fluid) influences the response to bradykinin, two different inhibitors of this bradykinin degradation enzyme were tested. Perivascular microapplication of potentiator C (10−10–10−4 M) or captopril (10−10–10−3 M) did not, by itself, change the diameter of feline pial arteries (87–305 μm) in situ. In a similar investigation, the dilating action of bradykinin (10−8–10−5 M) was not modified by the simultaneous application of potentiator C or captopril (10−5 M). Furthermore, the relaxing effect of bradykinin (10−10–10−4 M) on isolated feline middle cerebral arteries (preconstricted with 5-hydroxytryptamine or prostaglandin F2α) was not influenced by the presence of captopril (10−7 M). In contrast, when studied on isolated extracranial vessel segments (feline sublingual artery), bradykinin caused a concentration-dependent constriction of the artery. This constriction was completely reversed to dilatation in the presence of captopril (10−7 M). Moreover, the characteristic effect of kininase II inhibition was demonstrated in the isolated guinea pig ileum preparation. In this instance, bradykinin induced a concentration-dependent contraction that was enhanced by potentiator C or captopril. We conclude, therefore, that bradykinin exerts variable responses on vascular smooth muscle, depending on the species used, the muscle location and experimental conditions. Finally, the in situ and in vitro findings for pial and middle cerebral arteries demonstrate that kininase II does not modify the dilating effect of bradykinin under our experimental conditions.


1984 ◽  
Vol 122 (2) ◽  
pp. 155-163 ◽  
Author(s):  
LARS EDVINSSON ◽  
PIERS EMSON ◽  
JAMES McCULLOCH ◽  
KAZUHIKO TATEMOTO ◽  
ROLF UDDMAN

1987 ◽  
Vol 7 (5) ◽  
pp. 612-618 ◽  
Author(s):  
Jan Erik Hardebo ◽  
Jan Kåhrström ◽  
Christer Owman ◽  
Leif G. Salford

Vasomotor reactivity of human pial veins, obtained in conjunction with neurosurgical operations, was studied in vitro. The effect of transmitters in nerves previously recognized in these vessels, as well as that of neuromodulators, was characterized. A comparison of these effects with their effects in the nearby pial arteries of the same patients was made. It was found that the veins were equipped with more sensitive α-adrenergic receptors (lower EC50 values) than the arteries. The reverse was found for 5-hydroxytryptamine. Acetylcholine, which causes an endothelium-dependent dilation of pial arteries, contracted the veins despite an apparently intact endothelium. Considering the lower maximum values in veins, responses to histamine, the neuropeptides calcitonin gene-related peptide, bradykinin, and neuropeptide Y; and prostaglandins (PGE1 and PGF2α) were principally the same in the arteries and veins. The dilatory responses to vasoactive intestinal polypeptide and substance P were less pronounced in veins than in arteries. The veins only transiently contracted to a depolarizing potassium solution; calcium influx promotors and inhibitors, as well as calcium-free solution, did not affect the contractile ability of the vein, contrasting to the reactivity of the artery. This clearly indicates that the veins are not substantially dependent upon calcium influx for their acute contractile ability.


Author(s):  
J. P. Revel

Movement of individual cells or of cell sheets and complex patterns of folding play a prominent role in the early developmental stages of the embryo. Our understanding of these processes is based on three- dimensional reconstructions laboriously prepared from serial sections, and from autoradiographic and other studies. Many concepts have also evolved from extrapolation of investigations of cell movement carried out in vitro. The scanning electron microscope now allows us to examine some of these events in situ. It is possible to prepare dissections of embryos and even of tissues of adult animals which reveal existing relationships between various structures more readily than used to be possible vithout an SEM.


Author(s):  
D. Reis ◽  
B. Vian ◽  
J. C. Roland

Wall morphogenesis in higher plants is a problem still open to controversy. Until now the possibility of a transmembrane control and the involvement of microtubules were mostly envisaged. Self-assembly processes have been observed in the case of walls of Chlamydomonas and bacteria. Spontaneous gelling interactions between xanthan and galactomannan from Ceratonia have been analyzed very recently. The present work provides indications that some processes of spontaneous aggregation could occur in higher plants during the formation and expansion of cell wall.Observations were performed on hypocotyl of mung bean (Phaseolus aureus) for which growth characteristics and wall composition have been previously defined.In situ, the walls of actively growing cells (primary walls) show an ordered three-dimensional organization (fig. 1). The wall is typically polylamellate with multifibrillar layers alternately transverse and longitudinal. Between these layers intermediate strata exist in which the orientation of microfibrils progressively rotates. Thus a progressive change in the morphogenetic activity occurs.


Author(s):  
C. Jennermann ◽  
S. A. Kliewer ◽  
D. C. Morris

Peroxisome proliferator-activated receptor gamma (PPARg) is a member of the nuclear hormone receptor superfamily and has been shown in vitro to regulate genes involved in lipid metabolism and adipocyte differentiation. By Northern analysis, we and other researchers have shown that expression of this receptor predominates in adipose tissue in adult mice, and appears first in whole-embryo mRNA at 13.5 days postconception. In situ hybridization was used to find out in which developing tissues PPARg is specifically expressed.Digoxigenin-labeled riboprobes were generated using the Genius™ 4 RNA Labeling Kit from Boehringer Mannheim. Full length PPAR gamma, obtained by PCR from mouse liver cDNA, was inserted into pBluescript SK and used as template for the transcription reaction. Probes of average size 200 base pairs were made by partial alkaline hydrolysis of the full length transcripts. The in situ hybridization assays were performed as described previously with some modifications. Frozen sections (10 μm thick) of day 18 mouse embryos were cut, fixed with 4% paraformaldehyde and acetylated with 0.25% acetic anhydride in 1.0M triethanolamine buffer. The sections were incubated for 2 hours at room temperature in pre-hybridization buffer, and were then hybridized with a probe concentration of 200μg per ml at 70° C, overnight in a humidified chamber. Following stringent washes in SSC buffers, the immunological detection steps were performed at room temperature. The alkaline phosphatase labeled, anti-digoxigenin antibody and detection buffers were purchased from Boehringer Mannheim. The sections were treated with a blocking buffer for one hour and incubated with antibody solution at a 1:5000 dilution for 2 hours, both at room temperature. Colored precipitate was formed by exposure to the alkaline phosphatase substrate nitrobluetetrazoliumchloride/ bromo-chloroindlylphosphate.


1989 ◽  
Vol 120 (3_Suppl) ◽  
pp. S202-S203
Author(s):  
G. WESTHOF ◽  
J. BENSCH ◽  
W. L. BRAENDLE

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