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.

Reversal of nerve damage in streptozotocin-diabetic rats by acute application of insulin in vitro

1988 ◽  
Vol 75 (6) ◽  
pp. 629-635 ◽  
Author(s):  
Geoffrey Burnstock ◽  
Rhona Mirsky ◽  
Abebech Belai
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Calcitonin Gene Related Peptide ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Rat Ileum ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Enteric Nerves ◽  
Intestinal Polypeptide

1. Immunohistochemical, immunoblotting and release experiments were performed on ileum from control rats, from 8-week streptozotocin-diabetic rats and from diabetic rats after acute application of insulin in vitro. 2. There was an increase in vasoactive-intestinal-polypeptide-like and a decrease in calcitonin-gene-related-peptide-like immunoreactivity in the myenteric plexus of the diabetic rat ileum, although electrically evoked release of both peptides from enteric nerves was defective. Acute application of insulin in vitro reversed the defective release and changes in immunoreactivity of vasoactive intestinal polypeptide and calcitonin-gene-related peptide seen in the enteric nerves of streptozotocin-diabetic rat ileum. 3. In addition, using a monoclonal neurofilament antibody RT 97 that recognizes a phosphorylated neurofilament epitope present in normal enteric nerves, it was shown that this phosphorylated neurofilament epitope was absent in diabetic nerves, even though a polyclonal neurofilament antibody revealed that neurofilaments were present in both axons and cell bodies of the myenteric plexus of diabetic rat ileum. After only 2 h of insulin incubation in vitro, the phosphorylated neurofilament epitope was again present in the nerves. 4. It is suggested that the abnormal distribution of phosphorylated neurofilaments and defective storage and release of vasoactive intestinal polypeptide and calcitonin-gene-related peptide in the present study may be a more general feature of diabetes. The restoration of these abnormalities by continuous acute insulin application in vitro shown here suggests that the availability of a steady level of insulin might prevent some of the changes which occur in early stages of diabetes. If so, this could influence the use of insulin in the treatment of diabetes, particularly in view of the recent report that short-term continuous subcutaneous insulin infusion restores the function of the autonomic and peripheral nerves in type I diabetic patients [Krönert, K., Hülsen, J., Luft, D., Stetter, T. & Eggstein, M. (1987) Journal of Clinical Endocrinology and Metabolism, 64, 1219–1223].

NE-induced contraction, alpha 1-adrenergic receptors, and Ins(1,4,5)P3 responses in cerebral arteries

1996 ◽  
Vol 270 (3) ◽  
pp. H915-H923 ◽  
Author(s):  
L. D. Longo ◽  
N. Ueno ◽  
Y. Zhao ◽  
L. Zhang ◽  
W. J. Pearce
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Contractile Response ◽  
Cerebral Arteries ◽  
Cerebral Microvessels ◽  
Middle Cerebral Arteries ◽  
Lower Maximum ◽  
Pharmacomechanical Coupling ◽  
Dissociation Constant Kd

Adrenergic-mediated responses in cerebral vessels in vitro differ with vessel segment. We performed this study to test the hypothesis that these vessel-specific cerebral artery norepinephrine (NE)-induced contractility changes are mediated in part by differences in alpha 1-adrenergic receptor (alpha 1-R) density (Bmax) or antagonist dissociation constant (KD), and/or inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] synthesis. In common carotid (Com), circle of Willis (Wil), and middle cerebral arteries (MCA) from adult sheep we measured NE-induced contractions. We also quantified alpha 1-R in these, and in anterior, middle, and posterior (AMP) cerebral arteries and cerebral microvessels (Micro). In addition, we quantified NE-induced Ins(1,4,5)P3 synthesis. pD2 values of Com and MCA were 5.2 +/- 0.1 and 6.3 +/- 0.1, respectively. In contrast, the MCA maximum response to NE compared with K+ was much lower than that of the Com. In the Com, Wil, AMP, and Micro, alpha 1-R Bmax was 54 +/- 3, < 5 +/- 2, 23 +/- 3, and 35 +/- 3 fmol/mg protein, respectively. KD averaged 0.20 +/- 0.05 nM in the several vessel groups. In Com and in AMP cerebral arteries, NE produced a rapid increase in Ins(1,4,5)P3 with a peak at 45 s, and 50% effective concentration of 5.5 +/- 0.2 microM. NE stimulated a 240% increase of Ins(1,4,5)P3 in both Com and AMP, whereas Wil showed essentially no response. The ovine MCA was more sensitive to NE than was the Com. In contrast, MCA showed a much lower maximum contractile response to NE compared with K+. Cerebral arteries (AMP) had only about half the alpha 1-R density of the Com. In AMP cerebral arteries, both the basal and NE-stimulated Ins(1,4,5)P3 values were much less than those of the Com. In MCA, the ratio of Ins(1,4,5)P3 response to alpha 1-R Bmax was much greater than in Com. These findings suggest important artery-to-artery differences in components of the cerebrovascular alpha 1-R-mediated contractile pathway. They also suggest considerable potential for modulation of pharmacomechanical coupling and homeostatic regulation of cerebrovascular tone.

Cyclooxygenase Inhibitors Modify the Relaxant Effect of Vasoactive Intestinal Polypeptide and Substance P in Isolated Porcine Ophthalmic Artery

Cephalalgia ◽  
1992 ◽  
Vol 12 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Maurice B Vincent
Keyword(s):  
Substance P ◽  
Ophthalmic Artery ◽  
Calcitonin Gene Related Peptide ◽  
Cyclooxygenase Inhibitors ◽  
Plasma Extravasation ◽  
Relaxant Effect ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Ophthalmic Arteries

The absolute indomethacin effect in some unilateral headaches may, at least partially, be cyclooxygenase inhibition-independent. Aspirin and indomethacin, for example, may inhibit the neurogenically induced plasma extravasation in rat dura mater. Given the putative involvement of trigeminal neuropeptides in the pathophysiology of these conditions, the influence of cyclooxygenase inhibitors (indomethacin, acetylsalicylic acid (ASA) and naproxen) has been studied upon substance P, calcitonin gene-related peptide and vasoactive intestinal peptide (VIP)-induced vasodilatation in PGF2a precontracted porcine ophthalmic arteries in vitro. None of the cyclooxygenase inhibitors significantly altered the effects of calcitonin gene-related peptide. The 10-10 mol/1 VIP-induced relaxation was inhibited significantly by all three cyclooxygenase inhibitors. Substance P-induced relaxation (from 10-10 to 10-8 mol/l) was enhanced by ASA and inhibited both by naproxen and, to a lesser extent, by indomethacin. The results suggest mainly that VIP-induced relaxations, particularly at lower concentrations, may be inhibited by all three cyclooxygenase inhibitors, and that naproxen, to a greater extent than aspirin or indomethacin, showed a tendency to inhibit vasodilatation induced by all peptides.

Nostril Capsaicin Application as a Model of Trigeminal Primary Sensory Neuronal Activation

Cephalalgia ◽  
1994 ◽  
Vol 14 (2) ◽  
pp. 134-138 ◽  
Author(s):  
M Nicolodi
Keyword(s):  
Substance P ◽  
Cluster Headache ◽  
Vasoactive Intestinal Polypeptide ◽  
Separate Study ◽  
Sensory Neurones ◽  
Related Peptide ◽  
Capsaicin Application ◽  
Episodic Cluster Headache ◽  
Calcitonin Gene ◽  
Neurochemical Changes

Capsaicin was applied unilaterally to the nostril mucosa of 18 episodic cluster headache sufferers in remission. Plasma and saliva levels of substance P (SP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay. Increase of salivary SP-LI and CGRP-LI as well as of plasma CGRP-LI occurred after capsaicin stimulation. Capsaicin-induced neurochemical changes in saliva and in plasma were compared to the changes observed during cluster headache attacks measured in a separate study. The comparative changes in SP, CGRP and VIP characterizing these two conditions suggest that trigeminal capsaicin-sensitive sensory neurones are unlikely to play any fundamental role in the mechanics of cluster headache.

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