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Biomedical subjects

L Edvinsson

Publications and source records attributed to L Edvinsson.

At least 469 records · Page 26Linked to original sources
PubMed1977

Histochemical, ultrastructural and functional evidence for a neurogenic control of cerebrospinal fluid production from the choroid plexus.

Histochemical studies have shown that the rabbit choroid plexus receives a well-developed adrenergic and cholinergic nerve supply. The adrenergic innervation, which orginates almost entirely from the superior cervical sympathetic ganglia, begins to develop around birth and is fully established 3 weeks later. Electron microscopy has shown that the nerve terminals innervate both the plexus arterioles and its secretory epithelium. The sympathetic fibres have been shown to influence the plexus epithelium, as reflected by their effect on its carbonic anhydrase activity. They appear to have an inhibitory effect on the bulk CSF production, as revealed by electrical nerve stimulation and denervation experiments. The control seems to be excerted primarily on the plexus epithelium, though some of the effect may also be associated with alteration in choroid plexus blood flow.

Adrenergic Fibers↗
PubMed1977

Possibilities for a cholinergic action on smooth musculature and on sympathetic axons in brain vessels mediated by muscarinic and nicotinic receptors.

A pharmacological identification and characterization of cholinergic receptors was carried out in pial arteries of cats. In one series of experiments, the middle cerebral artery was suspended in an organ bath for recording fo circular motor activity. Parasympathomimetic compounds produced either a relaxation or a contraction. The relaxation occurred at low doses (up to 10(-6) M), and the response was inhibited in a competitive manner by atropine. The mean KB value (determined with acetylcholine as agonist) was 3.85 X 10(-11) M, and the corresponding pA2 value 10.43. At higher doses, the parasympathomimetics produced a contraction. This effect, too, was inhibited in a competitive manner with atropine. The calculated mean KB value with acetylcholine as agonist was 1.12 X 10(-11) M, and pA2 was 10.07. The motor responses did not require an intact perivascular sympathetic innervation, which shows that the effects were mediated by muscarinic type of cholinergic receptors present in the smooth musculature. In another series of experiments, pial arteries were preincubated in the presence of 3H-norepinephrine, and the amount of tritium efflux was measured in a superfusion system before or during electrical field stimulation (12 V, 1 msec pulse duration, 10 Hz). The efflux was minimized by sympathetic denervation, and the effect of transmural stimulation abolished by bretylium and guanethidine, which shows that the bulk of tritium overflow during stimulation originated from the perivascular sympathetic nerves. The marked elevation of tritium efflux during stimulation was enhanced by hexamethonium, and it was inhibited by nicotine and acetylcholine, whose effects were counteracted by hexamethonium (but not by atropine). This finding indicates the presence of nicotinic type of cholinergic receptors on the perivascular adrenergic nerves, allowing inhibition of norepinephrine by acetylcholine that may be liberated from the adjacent cholinergic terminals in the autonomic nerve plexus.

Acetylcholine↗
PubMed1977

Increased sensitivity of the basilar artery to norepinephrine and 5-hydroxytryptamine following experimental subarachnoid hemorrhage.

The reactivity of rabbit basilar artery to norepinephrine and 5-hydroxytryptamine was tested in vitro three days following cisternal injection of 1.0 ml autologous blood to simulate subarachnoid hemorrhage. Following this treatment the artery became three to five times more sensitive to norepinephrine compared with vessels from untreated animals. This was reflected in a parallel shift of the log dose-response curve towards lower concentrations of norepinephrine in a way resembling that seen after cocaine treatment of sympathectomy and interpreted as a prejunctional supersensitivity of the vascular alpha-receptors. The injection of blood also increased the amount of vasoconstriction with 5-hydroxytryptamine to a level which was three times higher than that obtained in untreated vessels. The results suggest one type of mechanism whereby monoamines might be involved in cerebral vasospasm following subarachnoid hemorrhage.

Animals↗
PubMed1976

Autonomic nerves, mast cells, and amine receptors in human brain vessels. A histochemical and pharmacological study.

The studies were performed on operation material from 17- to 63-year-old patients and on fetuses at 19-23 weeks gestational age. Formaldehyde histofluorescence showed the presence of numerous perivascular adrenergic nerves around pial and intracerebral vessels, the carotid system being better supplied than the vertebral system. Cholinergic nerves, visualized by the cholinesterase technique, followed the adrenergic fibers in the plexus formations of the pial arterial system. Histamine-containing mast cells, often with a perivascular distribution, were located with the o-phthaldiadehyde method. Transmural electrical stimulation of the perivascular nerves contracted isolated pieces of pial arteries in a frequency-dependent manner, and the response was inhibited by the adrenergic nerve blocking agent, guanethidine. On the basis of the relative potency of various amines and related compounds in producing a motor response of isolated pial arteries, and the mode of inhibition caused by specific antagonists, various amine receptors could be demonstrated: adrenergic alpha-receptors (mediating contraction) and beta-receptors (dilation), cholinergic muscarinic receptors (dilation) and histamine H2-receptors (mediating dilation). Thus, the amine mechanisms demonstrated in human brain vessels appear to be principally the same of those shown in more extensive studies on laboratory animals.

Acetylcholinesterase↗
PubMed1976

Fluorescence histochemistry and autoradiography of adrenergic nerves in the renal juxtaglomerular complex of mammals and man, with special regard to the efferent arteriole.

The adrenergic innervation of the juxtaglomerular complex was studied in kidneys from mice, rats, guinea-pigs, rabbits, cats, dogs, pigs, monkeys, and humans using fluorescence histochemistry of neuronal noradrenaline and autoradiography of 3H-noradrenaline. The localization of the nerves was established by phase contrast optics or by perfusing the vascular system with India ink. Adrenergic nerve terminals, exhibiting a formaldehyde-induced fluorescence and having the ability to take up and accumulate 3H-noradrenaline, were easily identified when they enclosed the glomerular afferent arteriole. They continued in between and close to the macula densa and lacis cells to supply the glomerular efferent arteriole. The nerves could be seen to accompany this arteriole for a considerable distance until they branched off to the vasa recta in the juxtamedullary region and to adjacent cortical veins. This innervation pattern was found to be a constant feature except in kidneys from guinea-pigs and cats, in which post-glomerular units. The fluorescence in all adrenergic fibres supplying the juxtaglomerular complex disappeared after removal of the aortico-renal ganglion, showing that they belong to a common system of renal sympathetic nerves.

Adult↗
PubMed1976

Influence of pH and pCO2 on alpha-receptor mediated contraction in brain vessels.

The response of isolated brain vessels to various pH levels or carbon dioxide tensions was analyzed. Reduction of the pH induced a slight relaxation of the vessel, whereas an increase in the pH produced a slight contraction. These effects were markedly exaggerated when the alpha-adrenergic receptors in the vascular wall were activated by noradrenaline. During these conditions the contractile response to noradrenaline was reduced by about 40% at a pH of 7.01, while, on the other hand, the response was enhanced 3-fold at a pH of 7.80. Variations in carbon dioxide tension of the buffer solution between 16 mmHg and 64 mmHg produced no consistent change, provided the pH remained constant. The results indicate that an interaction between the perivascular pH and the adrenergic alpha-receptor mediated contraction in brain vessels may occur.

Animals↗