Disposition of Serotonin in the Rat Blood Vessels and Heart

Berkowitz, Barry A.; Lee, C.‐H.; Spector, Sydney

doi:10.1111/j.1440-1681.1974.tb00561.x

Cited by 22 publications

(7 citation statements)

References 9 publications

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“…This amount did not change when rats were perfused with 75 ml of iced saline by intracardiac injection or after rats were made severely thrombocytopenic (Table 1). These results suggest that serotonin is present within the walls of cerebral microvessels-a finding previously reported in larger blood vessels of the peripheral circulation (20).…”

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confidence: 70%

Serotonin Neurons Project to Small Blood Vessels in the Brain

Reinhard

Liebmann

Schlosberg

et al. 1979

Science

196

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Electrolytic lesions of the nucleus raphe dorsalis and medianus reduce the concentration of serotonin (5-hydroxytryptamine) within rat brain intraparenchymal blood vessels. The concentration of serotonin within these vessels increases or decreases after the administration of drugs that modify the biosynthesis and degradation of serotonin or destroy nerve terminals by an uptake-dependent mechanism. These studies provide evidence for the existence of a serotonin-containing pathway seemingly analogous to the neuronal projection that terminates on small parenchymal blood vessels from noradrenergic neurons of the locus coeruleus.

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confidence: 70%

Serotonin Neurons Project to Small Blood Vessels in the Brain

Reinhard

Liebmann

Schlosberg

et al. 1979

Science

196

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“…An excess of serotonin, such as found in the carcinoid syndrome, is well known to be cardiotoxic [19]. Serotonin has been identified in the heart of several mammalian species including humans and rats [2,20]. It is metabolized in the heart [16] and has specific receptors in the ventricle [14].…”

Section: Discussionmentioning

confidence: 98%

Influence of experimental hyperthyroidism on blood and myocardial serotonin in rats

et al. 1988

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Recent reports suggest a role for serotonin in the pathogenesis of primary hypertension and left ventricular (LV) hypertrophy. In this study, we have induced LV hypertrophy by oral feeding of thyroxine at increasing dosages (150-450 micrograms/kg b.wt.) over a 5-week period. The effects of hyperthyroidism on cardiovascular parameters, blood and myocardial serotonin concentrations were assessed. Water-fed rats and formerly hyperthyroid recovered animals served as controls. Thyroxine caused a significant LV hypertrophy: hyperthyroid rats 2.19 +/- 0.16*; controls 1.65 +/- 0.13 g/kg b.wt. (mean +/- SD; *P less than 0.05). An almost complete regression of LV hypertrophy occurred in the recovery group (1.66 +/- 0.20 g/kg b.wt.) 3 weeks after cessation of thyroid hormone application. Thyroxine-treated animals showed a significant increase of serotonin blood levels (thyroxine rats: 2108 +/- 781*, recovery: 1132 +/- 726, controls: 705 +/- 480 ng/ml; *P less than 0.05). The concentrations of serotonin in left ventricular myocardium were increased after thyroid hormone application, whereas the highest levels were found in the recovery group (thyroxine rats: 139.1 +/- 30.4, recovery: 167.2 +/- 43.1, controls: 68.9 +/- 27.9 mg/ml homogenate). Serotonin-containing cells in the left ventricular myocardium were stained immunohistochemically. They were localized perivascularly and were assumed to represent tissue mast cells. In experimental hyperthyroidism the serotonin levels in blood and heart are increased possibly indicating an interaction of both hormones in thyroxine-induced cardiomyopathy.

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“…Although the specificity of the antisera was not assessed, previous reports of antisera from the same source described its relative affinity for morphine, morphine metabolites, and other opiate alkaloids (5). The detection limit of this assay was 1 ng/ml, and the pooled coefficient of variation was 8.3% for a series of two to three identical samples containing known concentrations of morphine ranging from 1.0 to 45 ng/ml.…”

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confidence: 99%