Amplifying Effect of Serotonin in the Control of Vascular Tone

Janssens, W. J.; Nueten, J. M. Van

doi:10.1007/978-94-009-1912-9_10

Cited by 4 publications

(4 citation statements)

References 24 publications

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“…response of 5HT (17,31). These experiments show that an interaction between the different agonists is required to strengthen these effects (28). The fact that sumatriptan does not modify ergofamine vasoconstriction (32,33) could be due to a common action of these drugs on 5HT receptors.…”

Section: Discussionmentioning

confidence: 78%

“…This agrees with results in human saphenous vein; venoconstriction induced by high concentrations of sumatriptan was abolished by ketanserin (26). 5HT, even in subconstrictive concentrations, amplifies the vasoconstrictive response to NA, an effect which involves 5HT 2 receptors because it is blocked by ketanserin (27,28). Noradrenaline-induced venoconstriction in the hand vein is equally increased by 5HT after constrictive and non-constrictive doses (17).…”

Section: Discussionmentioning

confidence: 99%

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Amplifying Effect of Sumatriptan on Noradrenaline Venoconstriction in Migraine Patients

et al. 1993

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The venoconstrictive activity of sumatriptan and its interaction with noradrenaline (NA)- and 5-hydroxytryptamine (5HT) venoconstriction was studied in vivo in the hand vein of migraineurs. Sumatriptan, injected at increasing doses into the vein, caused local venoconstriction after a 500 microgram dose, comparable to that induced by 0.5-1 micrograms of 5HT. This venoconstriction was completely inhibited by low doses of ketanserin (5 micrograms). Subcutaneous sumatriptan (6 mg) provoked a minor increase in vein tone, lasting less than 30 min. Non-venoconstrictive doses of sumatriptan (10-100 micrograms), injected in the hand vein, produced an amplification of NA-venoconstriction but not of 5HT-induced venoconstriction. A similar increased effect was displayed by subcutaneous sumatriptan (6 mg) for at least 1 h. Sumatriptan appears to cause peripheral venoconstriction only at high doses locally applied (in the hand vein), by acting on 5HT2 receptors. Clinical subcutaneous doses (6 mg) do not show significant venoconstrictive effects. The amplifying effect on NA venoconstriction, also caused by 5HT, ergotamine and dihydroergotamine in human cranial arteries, may be important in explaining the therapeutic action of sumatriptan in migraine attacks.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Amplifying Effect of Sumatriptan on Noradrenaline Venoconstriction in Migraine Patients

et al. 1993

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“…Bar = 50 pm. sodilation or vasoconstriction (for references, see Janssens and Van Neuten, 1990) and that it is involved in the regulation of blood flow through the ovarian and uterine arteries (Schmidt et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Localization of 5‐hydroxytryptamine‐like immunoreactive cells and nerve fibers in the rat female reproductive system

Amenta

Rícci

et al. 1992

Anat. Rec.

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The presence of 5-hydroxytryptamine (5-HT)-like immunoreactivity (IR) was studied in the rat female reproductive system using polyclonal antibodies directed against 5-HT. Moreover, 5-HT levels in the ovary, oviduct, uterus, and cervix were measured by high-pressure liquid chromatography with electrochemical detection. The highest 5-HT concentrations were found in the oviduct, followed in descending order by the cervix, the ovary, and the uterus. Most 5-HT-like IR was observed in the cytoplasm of mast cells. These cells were found in the connective tissue around the fimbria, in the oviduct, in the uterus, and in the ovary. Mast cells are clustered in the proximity of the parenchymal blood vessels. Moreover, a few 5-HT-like nerve fibers were found distributed mainly perivascularily in the uterine cervix and in the uterine horns as well as in the oviduct. IR nerve fibers were rarely seen within the ovary. The present data provide direct evidence that 5-HT in the female reproductive system not only is associated with mast cells but is located in nerve fibre-like structures as well. The functional significance of this probable 5-HT-ergic innervation of the female reproductive tract discovered in the present study should be clarified in future investigations.

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“…It should be kept in mind, however, that threshold or subthreshold concentrations of serotonin, either exogenously applied or released from platelets, amplify the vasoconstriction caused by low concentrations of neurohumoral mediators like epinephrine, norepinephrine, angiotensin II, histimines, prostaglandin F2~ and fibrin(ogen)-degradation products, in large and small arteries [13]. This amplifying effect of serotonin is larger than would be expected on the basis of merely additive effects.…”

mentioning

confidence: 98%

Serotonin and acute cardiovascular disorders

Reneman

Starre

1990

Cardiovasc Drug Ther

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In this survey the possible role of serotonin in such acute disorders as systemic and pulmonary hypertension following cardiac surgery is discussed. Although platelets are activated during cardiopulmonary bypass, the increase in serotonin plasma levels is limited because the serotonin released is taken up by normal platelets and endothelial cells. This does not imply that serotonin is not involved in the origin of systemic hypertension during and after cardiac surgery, because subthreshold or threshold doses of this amine amplify the vasoconstrictive effect of, for example, epinephrine and norepinephrine, the levels of which are significantly elevated under these circumstances. That serotonin plays a role through its amplifying effect is supported by the finding that ketanserin, a specific S2-serotonergic receptor antagonist with alpha 1-adrenergic receptor blocking properties, effectively lowers arterial blood pressure in patients with systemic postoperative hypertension by combined blockade of these receptors. The compound is also effective in the treatment of pulmonary hypertension after valve replacement, indicating that serotonin plays a role in the origin of this disorder. This idea is supported by the experimental finding that serotonin induces pulmonary hypertension. It is an interesting observation that, unlike such compounds as nitroprusside, ketanserin does not affect intrapulmonary shunting in patients with systemic hypertension and even reduces the intrapulmonary shunt fraction in patients with pulmonary hypertension. These findings indicate that this compound dilates the resistance vessels in well-ventilated, but not in poorly ventilated areas, and may dilate constricted bronchi.(ABSTRACT TRUNCATED AT 250 WORDS)

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Amplifying Effect of Serotonin in the Control of Vascular Tone

Cited by 4 publications

References 24 publications

Amplifying Effect of Sumatriptan on Noradrenaline Venoconstriction in Migraine Patients

Amplifying Effect of Sumatriptan on Noradrenaline Venoconstriction in Migraine Patients

Localization of 5‐hydroxytryptamine‐like immunoreactive cells and nerve fibers in the rat female reproductive system

Serotonin and acute cardiovascular disorders

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