Neuropeptide Y: Immunocytochemical localization to and effect upon feline pial arteries and veins in vitro and in situ

1984 ◽  
Vol 122 (2) ◽  
pp. 155-163 ◽  
Author(s):  
LARS EDVINSSON ◽  
PIERS EMSON ◽  
JAMES McCULLOCH ◽  
KAZUHIKO TATEMOTO ◽  
ROLF UDDMAN
Keyword(s):  
Neuropeptide Y ◽  
Immunocytochemical Localization ◽  
Pial Arteries ◽  
Arteries And Veins

Small vessel membrane potential, sympathetic input, and electrogenic pump rate in SHR

1986 ◽  
Vol 250 (4) ◽  
pp. C547-C556 ◽  
Author(s):  
W. J. Stekiel ◽  
S. J. Contney ◽  
J. H. Lombard
Keyword(s):  
Jejunal Loop ◽  
Physiological Salt Solution ◽  
Mesenteric Vessel ◽  
Small Arteries ◽  
Wistar Kyoto ◽  
6 Hydroxydopamine ◽  
Arteries And Veins ◽  
Made In

Comparative measurements of transmembrane potential (Em) were made in situ in vascular smooth muscle cells (VSM) of mesenteric small principal arteries and veins with innervation and circulation intact. Vessels were in an externalized, topically suffused jejunal loop in 4- to 5-wk-old (initial hypertension) and 12- to 15-wk-old (established hypertension) anesthetized, spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive control rats. Comparable in vitro measurements of Em were also made in VSM of isolated intact small mesenteric vessel segments (from the 12- to 15-wk-old animals) maintained at their in situ lengths and suffused with physiological salt solution (PSS). During suffusion in situ with control PSS, VSM of both small veins and arteries in older (but not younger)SHR were less polarized than in WKY. Local chemical sympathetic denervation in situ (with 6-hydroxydopamine) hyperpolarized VSM of both vessel types in older (but not younger) SHR to the same Em levels measured in situ in respective WKY vessels. After local denervation, VSM of small arteries (but not veins) of both SHR and WKY remained less polarized in situ than in vitro, suggesting the presence of one or more circulating factors with a specific depolarizing action on the arterial side in both animal types. In vitro, VSM of both small arteries and veins from WKY but not SHR were depolarized immediately by 10(-3) M ouabain. In contrast, reduction of the PSS suffusate temperature to 16 degrees C caused a significantly greater depolarization in VSM of SHR vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effects of Bradykinin on Pial Arteries and Arterioles in vitro and in situ

1983 ◽  
Vol 3 (2) ◽  
pp. 231-237 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner
Keyword(s):  
Maximal Response ◽  
Guinea Pig Ileum ◽  
Response Curves ◽  
Pial Arteries ◽  
Cerebrovascular Resistance ◽  
Resistance Vessels ◽  
Prostaglandin F ◽  
The Stability

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.

scholarly journals Effects of Kininase II Inhibitors on the Vasomotor Response to Bradykinin of Feline Intracranial and Extracranial Arteries in vitro and in situ

1983 ◽  
Vol 3 (3) ◽  
pp. 339-345 ◽  
Author(s):  
Michael Wahl ◽  
Alan R. Young ◽  
Lars Edvinsson ◽  
Franz Wagner
Keyword(s):  
Cerebral Arteries ◽  
Surrounding Tissue ◽  
Experimental Conditions ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Kininase Ii ◽  
Middle Cerebral Arteries ◽  
Prostaglandin F

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.

scholarly journals Vasomotor Effects of Neurotransmitters and Modulators on Isolated Human Pial Veins

1987 ◽  
Vol 7 (5) ◽  
pp. 612-618 ◽  
Author(s):  
Jan Erik Hardebo ◽  
Jan Kåhrström ◽  
Christer Owman ◽  
Leif G. Salford
Keyword(s):  
Substance P ◽  
Vasoactive Intestinal Polypeptide ◽  
Adrenergic Receptors ◽  
Calcium Influx ◽  
Free Solution ◽  
Pial Arteries ◽  
Calcitonin Gene ◽  
Lower Maximum ◽  
Arteries And Veins

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.

Interaction of histamine with noradrenergic constrictory mechanisms in cat cerebral arteries and veins

1983 ◽  
Vol 61 (7) ◽  
pp. 756-763 ◽  
Author(s):  
Paul M. Gross ◽  
A. Murray Harper ◽  
Graham M. Teasdale
Keyword(s):  
Cerebral Arteries ◽  
Sympathetic Nerves ◽  
Histamine Receptor ◽  
Inhibitory Influence ◽  
Sympathetic Nerve Stimulation ◽  
Pial Arteries ◽  
Simultaneous Application ◽  
Arteries And Veins ◽  
Stimulation Of

We examined responses of pial arteries and veins in situ to noradrenergic stimuli in the presence of histamine. Electrical stimulation of sympathetic nerves and perivascular microapplication of norepinephrine in mock cerebrospinal fluid produced constriction of arteries and veins in anesthetized cats. During simultaneous perivascular injection of histamine, these noradrenergic responses were attenuated or reversed. In both arteries and veins, constriction from sympathetic nerve stimulation was prevented by simultaneous application of the histamine receptor agonists, pyridylethylamine (H1) or impromidine (H2), results that suggest interference involving both types of histamine receptors. In arteries, impromidine, but not pyridylethylamine, inhibited constriction resulting from exogenous norepinephrine. Our findings indicate that histamine may have an inhibitory influence, exerted through both receptor types, on noradrenergic mechanisms in cerebral vessels.

Correlated Studies of Cellular Interactions Using TEM, Freeze Etching, and SEM

1974 ◽  
Vol 32 ◽  
pp. 320-321
Author(s):  
J. P. Revel
Keyword(s):  
Developmental Stages ◽  
Three Dimensional ◽  
Cell Movement ◽  
Cellular Interactions ◽  
Serial Sections ◽  
Cell Sheets ◽  
Freeze Etching ◽  
Early Developmental

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.

In vitro and in vivo polysaccharides assembly: ultrastructural and cytochemical study of growing plant cell wall components.

1978 ◽  
Vol 36 (2) ◽  
pp. 434-435
Author(s):  
D. Reis ◽  
B. Vian ◽  
J. C. Roland
Keyword(s):  
Cell Wall ◽  
Self Assembly ◽  
Plant Cell Wall ◽  
Higher Plants ◽  
Three Dimensional ◽  
Cytochemical Study ◽  
Wall Components

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.

In Situ Localization of PPAR Gamma and Uncoupling Protein in Mouse Embryo Sections Using Digoxigenin-Labeled Riboprobes

1996 ◽  
Vol 54 ◽  
pp. 32-33
Author(s):  
C. Jennermann ◽  
S. A. Kliewer ◽  
D. C. Morris
Keyword(s):  
Alkaline Phosphatase ◽  
Room Temperature ◽  
Uncoupling Protein ◽  
Ppar Gamma ◽  
Nuclear Hormone Receptor ◽  
Full Length ◽  
Northern Analysis ◽  
Peroxisome Proliferator

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.

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