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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The serotonin (5-hydroxytryptamine, 5-HT) antagonist, ketanserin, has a high affinity for 5-HT2-receptors but it also binds to alpha 1-adrenoceptors. The compound (10 mg i.v.) lowered mean arterial pressure by 22% +/- 2% (mean +/- SEM, p less than 0.001) in 30 patients with essential hypertension. Measurements of heart rate, cardiac output, cardiac filling pressures, forearm blood flow, renal blood flow, and glomerular filtration rate revealed a hemodynamic pattern compatible with vasodilation of both resistance and capacitance vessels. This was accompanied by moderate reflex cardiostimulation. Ketanserin did not alter the pressor effect of bolus injections of (-)-phenylephrine hydrochloride (25, 50, 100, and 200 micrograms i.v.). Ketanserin also had a distinct hypotensive effect in four normotensive patients with autonomic insufficiency due to an efferent sympathetic lesion, who were unresponsive to phentolamine (20 mg i.v.). Thus, ketanserin in the dose we have used appears to lower blood pressure independently of alpha 1-adrenoceptor blockade. On the other hand, in patients with essential hypertension the antihypertensive effect of ketanserin was blunted by pretreatment with prazosin (12 mg/day). Therefore, a certain degree of alpha 1-adrenergic tone seems to be required for the compound to exert its full antihypertensive action. The findings are indirect evidence for a role of 5-HT in the maintenance of increased vascular resistance in essential hypertension. This may be related, at least in part, to the alleged amplifying effect of 5-HT on alpha 1-adrenoceptor-mediated vasoconstriction.
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PMID:5-HT, alpha-adrenoceptors, and blood pressure. Effects of ketanserin in essential hypertension and autonomic insufficiency. 631 78

The serotonin (5-hydroxytryptamine, 5-HT) content of tissue compartments in the medicinal leech, Hirudo medicinalis, was measured by means of high-pressure liquid chromatography coupled with electrochemical detection (HPLC-EC). Each segmental ganglion contains 21.3 +/- 2.9 (9) pmol 5-HT [X +/- SEM (N)]. The pharynx contains 7.1 +/- 1.1 (9) pmol 5-HT/mg wet weight; the salivary glands 3.2 +/- 0.9 (10), ventral body wall 2.0 +/- 0.2 (11), and vasofibrous tissue 1.2 +/- 0.2 (11). The blood of hungry leeches contains 8.7 +/- 1.9 (7) nM 5-HT while that of well-fed leeches is 2.2 +/- 0.4 (6) nM. Leeches were injected with the cytotoxic analog of serotonin, 5,7-dihydroxytryptamine (5,7-DHT) producing selective lesions of the peripherally projecting serotonin-containing neurons, and which in turn abolished their feeding behavior. The serotonin content of the pharynx and ganglia of these toxin-treated leeches were lowered significantly. The serotonin levels within the body wall and salivary glands were not altered significantly by the toxin treatment, but the levels within the vasofibrous tissue and blood were elevated substantially.
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PMID:Quantitative effects of a neurotoxin upon serotonin levels within tissue compartments of the medicinal leech. 650 56

The effect of live Escherichia coli on the pulmonary extraction of the biogenic amines 14C 5-hydroxytryptamine, (5-HT) and 3H-epinephrine was investigated. The labeled isotopes were injected into a central venous catheter and collected from an aortic catheter. One hundred per cent of the labeled epinephrine was recovered in the control and septic state. Only 32.8 +/- 3.6% SEM of the 5-hydroxytryptamine was recovered before sepsis and 42.5 +/- 4.9% SEM after sepsis. During sepsis, mean arterial pressure fell to 58 mm Hg from 121 mm Hg. Pulmonary shunt increased from .7 +/- .05 SEM to .33 +/- .09 SEM.
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PMID:Pulmonary extraction of biogenic amines during septic shock. 675 77

Membrane potential changes induced by 5-hydroxytryptamine (5-HT), gamma-aminobutyric acid (GABA) and 1,1-dimethyl-4-phenyl piperazinium (DMPP) were recorded from nodose ganglia (NG) by the sucrose-gap method. An amount of 0.002-0.5 mumol of the depolarizing agent was injected into the superfusion stream to the ganglion. Responses to 5-HT were also evoked from superior cervical (SCG) and dorsal root ganglia (DRG). 5-Hydroxytryptamine elicited depolarizations of graded amplitude. Maximal responses were 4.5 +/- 0.4 mV in nodose ganglia compared to 2.2 +/- 0.2 mV in superior cervical and 0.6 +/- 0.1 mV in dorsal root ganglia (means +/- SEM). In nodose ganglia, GABA induced smaller maximal depolarizations than did 5-HT, similar to those evoked by DMPP; dopamine was a weak depolarizing agent while substance P was apparently inactive. The dose-response curve for 5-HT in nodose ganglia was parallel to that for 5-HT in superior cervical ganglia and significantly to the left (ED50 values 0.029 and 0.098 mumol). Curves for 5-HT and GABA in nodose ganglia were superimposable. The high sensitivity of nodose ganglia cells to 5-HT is briefly discussed. Analogues of 5-HT lacking a hydroxyl group at position 5 on the nucleus were relatively inactive as depolarizing agents. Picrotoxin (10(-6)-10(-5) M) reduced or suppressed responses in nodose ganglia to GABA, whereas responses to 5-HT and DMPP were not much affected or, in the case of 5-HT, sometimes somewhat reduced. Quipazine (10(-6) M) was a selective antagonist of 5-HT responses in nodose ganglia; those to GABA and DMPP were not significantly altered. Neither trazodone nor LSD displayed antagonist properties at 5-HT receptors in nodose ganglia.
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PMID:Depolarizing responses recorded from nodose ganglion cells of the rabbit evoked by 5-hydroxytryptamine and other substances. 706 7

Eosinophils are supposed to play a critical role in the pathology of several allergic diseases because after activation they can release toxic and proinflammatory agents. In this study we have investigated whether IgE-mediated rat pleurisy could be affected by an ongoing pleural eosinophilic inflammatory response. IgE-passively sensitized rats were challenged with an intrapleural (i.pl.) injection of allergen (dinitrophenylated bovine serum albumin, 1 microgram/cavity) and exudation assessed by measuring the amount of protein extravasated into the pleural cavity within 4 h. We have confirmed that lipopolysaccharide (LPS) stimulation (250 ng/cavity i.pl.) was followed by a marked pleural neutrophilia, apparent at 3 h, which was followed by an eosinophil accumulation noted within 48-72 h postchallenge. We have also confirmed that a boiled sample of LPS pleural washing (LPS-PW, 200 microliters i.pl.) caused selective eosinophilia in recipient rats. Pleural exudation remained unaltered when the allergenic challenge was performed 3 h after LPS in a condition of intense pleural fluid neutrophilia. In contrast, this was significantly reduced (P < .001) when the challenge occurred 72 h after LPS or 24 h after LPS-PW in selective pleural fluid eosinophilia. In another series of experiments repeated daily i.pl. injections of platelet-activating factor (PAF; 1 microgram/cavity) resulted in a progressive increase in eosinophil number recovered from the pleural cavity. The values were 1.2 +/- 0.2, 3.0 +/- 0.2, and 5.8 +/- 0.5 x 10(6) eosinophils/cavity (mean +/- SEM) after 0, 1, and 4 injections, respectively. Allergen challenge performed after 0, 1, or 4 PAF stimulations led to pleural protein levels of 88.6 +/- 5.7, 33.7 +/- 0.7, and 19.4 +/- 2.3 mg/cavity, respectively, indicating that the allergic pleurisy is inhibited in a manner dependent on the magnitude of eosinophil accumulation. Furthermore, the impairment of PAF-induced eosinophil accumulation by cetirizine (30 mg/kg i.p.) restored the exudatory response. Exudation triggered by compound 48/80 (25 micrograms/cavity), histamine (200 micrograms/cavity), or 5-hydroxytryptamine (100 micrograms/cavity) was not affected by four previous PAF daily injections. The findings indicate that allergen-induced exudation is selectively down-regulated in the eosinophil-enriched pleural space of rats, a suppression that increased with increasing eosinophil number and disappeared after chemical impairment of the eosinophilia.
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PMID:Pleural fluid eosinophils suppress local IgE-mediated protein exudation in rats. 756 15

The effect of 5-hydroxytryptamine on the spontaneous activity of neurons of the subthalamic nucleus was examined by recording the extracellular unitary activity in an in vitro slice preparation. The most frequent response to 5-hydroxytryptamine (84% of 57 neurons tested) was an increase (twofold of basal at 10 microM) of the discharge frequency. The EC50 for the 5-hydroxytryptamine-induced effect was 1.8 +/- 0.5 microM (mean +/- SEM). The response was dose-dependently blocked by the serotoninergic antagonist mianserin and was not prevented by removal of calcium ions from the perfusing buffer. These results indicate that the serotoninergic input to the rat subthalamic nucleus exerts a postsynaptic excitatory action on most neurons of the nucleus.
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PMID:5-Hydroxytryptamine increases spontaneous activity of subthalamic neurons in the rat. 767

A clonal cell line derived from rat renal mesangial cells was shown to express endogenous 5-hydroxytryptamine (serotonin, 5-HT) receptors that mediate inhibition of cyclic AMP accumulation. These receptors were characterized as being of the 5-HT1B receptor subtype. 5-HT1 receptor agonists inhibited forskolin-stimulated cyclic AMP accumulation in rat renal mesangial cells (60-70% maximal inhibition) with the following rank order of potency (mean pEC50 values +/- SEM, n > or = 3): ergotamine (9.58 +/- 0.51) > RU 24969 (8.67 +/- 0.23) > or = 5-CT (8.42 +/- 0.06) > or = CP 93129 (8.15 +/- 0.27) > 5-HT (7.75 +/- 0.11) > sumatriptan (6.29 +/- 0.30) > 8-OH-DPAT (4.32 +/- 0.15). 5-HT2 and 5-HT4 receptor agonists were without effect. 5-HT-induced inhibition of cyclic AMP accumulation was abolished by a pre-treatment of the cells with pertussis toxin. (-)Propranolol was a partial agonist (27% maximal inhibition, pEC50 7.19 +/- 0.24, n = 3); when used as an antagonist at 1 microM, it shifted the concentration-response curve of 5-HT to the right (pKB 7.22 +/- 0.35, n = 3). Methiothepin was a competitive antagonist of 5-HT (pA2 8.04 +/- 0.10, Schild slope 0.87 +/- 0.21, n = 3). Rauwolscine (10 microM) had no antagonist activity. There was a significant correlation (r = 0.98, P = 0.0001) between the cyclic AMP data obtained in rat mesangial cells and 5-HT1B binding data reported in rat brain cortex. The same pattern of responses was observed in early passages of primary cultures of rat mesangial cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:5-Hydroxytryptamine 5-HT1B receptors inhibiting cyclic AMP accumulation in rat renal mesangial cells. 771 39

This study focuses on the histomorphologic damage produced by an acute elongation process, as well as on quantifying the alterations in arterial contractility following the application of this technique. Light microscopy and scanning electron microscopy studies were prepared from expanded and non-expanded pig superficial femoral arteries (SFA) harvested immediately following expansion, and again at 24- and 72-hr intervals. Histologically, the expanded vessels showed minor, patchy, endothelial slough, but not fragmentation of the internal or external elastic lamina. At 24 hr, the endothelium showed reactive changes, but no evidence of smooth-muscle necrosis of the tunica media was observed. At 72 hr, healing of the endothelium was evident by SEM. Similar specimens, also from the SFA, were harvested and placed in organ chambers immediately following expansion and 24 hr later, to measure contractility when exposed to alpha-adrenergic agonists. The vessels were exposed to the contractile agonists, phenylephrine and 5-hydroxytryptamine, which evoked similar concentration-dependent increases in tension in both the expanded group and the controls. From these observations, the authors conclude that acute intraoperative elongation of arteries results in only minor endothelial damage, without affecting the inherent contractility of the vessel wall.
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PMID:Acute intraoperative arterial elongation: histologic, morphologic, and vascular reactivity studies. 788 32

To investigate the role of endogenous catecholamines and 5-hydroxytryptamine in the control of growth hormone (GH) secretion, secretory profiles of GH and prolactin were measured in conscious, male rats following intravenous administration of either 1) alpha 2 antagonist idazoxan 2 mg/kg, a dose that blocked alpha 2 agonist induced GH rise, 2) alpha 1 antagonist prazosin 1 mg/kg, 3) non-specific beta-blocker propranolol 1.5 mg/kg, a dose that prevented beta 2 agonist (salbutamol) induced inhibition, 4) serotonin antagonist cyproheptadine 0.5 mg/kg, a dose that inhibited serotonin agonist quipazine induced GH rise, or 5) control. No drug altered mean GH or prolactin levels and pulsatile GH release persisted. Unilateral injections of prazosin, propranolol and idazoxan were made into the medial basal hypothalamus and preoptic-anterior hypothalamic area and of cyproheptadine into the medial basal hypothalamus, all with no effect on short-term GH release. GH and prolactin secretory profiles were measured after giving rats 6 units/kg intravenous insulin. Blood glucose levels fell to less than 50% basal. Hypoglycaemia caused a non-significant 30% fall in mean 2 h GH. Intravenous idazoxan, prazosin, propranolol and cyproheptadine (doses as in first study) did not modify the blood glucose fall, but idazoxan produced a significant reduction of mean GH compared to insulin alone (4 +/- 1.1 ng/ml SEM, idazoxan/insulin versus 16 +/- 5.6 ng/ml, saline/insulin). The lack of an effect of alpha- and beta-blockers on normal, pulsatile GH release is against a role for endogenous catecholamines in controlling this release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endogenous catecholamines modulate growth hormone release in the conscious rat during hypoglycaemia but not in the basal state. 809 43

1. The involvement of plasma 5-hydroxytryptamine in normal subjects during sympathetic stimulation and in patients with Raynaud's phenomenon was studied. 2. Arterial and venous plasma levels of 5-hydroxytryptamine were measured in normal subjects in a warm room, during reflex sympathetic stimulation by body cooling and during intra-arterial infusions of tyramine. Normal subjects (n = 19) had significantly higher levels of 5-hydroxytryptamine in venous plasma [mean 1.42 (SEM 0.23) ng/ml] than in arterial plasma [0.67 (0.12) ng/ml; P < 0.01]. Body cooling (n = 10) or tyramine infusion (n = 8) did not increase venous levels of 5-hydroxytryptamine despite significant decreases in blood flow and increases in vascular resistance. 3. Venous plasma levels of 5-hydroxytryptamine were also determined in patients with primary Raynaud's phenomenon (n = 12) or secondary Raynaud's phenomenon due to scleroderma (n = 11). Patients with primary or secondary Raynaud's phenomenon did not have significantly higher venous plasma levels of 5-hydroxytryptamine than normal subjects, even during vasospastic attacks (n = 3). 4. It is concluded that either 5-hydroxytryptamine is not involved in sympathetic nerve vasoconstriction or in Raynaud's phenomenon, or 5-hydroxytryptamine released in the microcirculation is largely taken up or metabolized by endothelial cells or platelets.
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PMID:Plasma levels of 5-hydroxytryptamine during sympathetic stimulation and in Raynaud's phenomenon. 815 37


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