Formation of Serotonin by Rat Kidneys in Vivo

Stier, Charles T.; Itskovitz, Harold D.

doi:10.3181/00379727-180-42216

Cited by 26 publications

(13 citation statements)

References 6 publications

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“…There is evidence from studies in rats that 5-HT can be formed within the kidney and that urinary excretion of 5-HT reflects renal production of 5-HT [2,3,11,12]. The results of the present study are consistent with the hypothesis that 5-HT can be synthesised in the human kidney.…”

Section: Discussionsupporting

confidence: 88%

“…It has been demonstrated in rats that 5-HT is formed from its immediate precursor, 5-hydroxy-L-tryptophan (5-HTP), under the action of renal aromatic L-amino acid decarboxylase (LAAD) and the amine reduces renal blood flow, urine output and sodium excretion [2][3][4]. -y-L-glutamyl-5-hydroxy-L-tryptophan (glu-5-HTP) may be another putative 5-HT prodrug, sequentially converted by y-glutamyl transferase (-yGT) to 5-HTP and then decarboxylated by LAAD to 5-HT.…”

Section: Introductionmentioning

confidence: 99%

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A comparison of the effects of two putative 5‐hydroxytryptamine renal prodrugs in normal man.

Freestone

Samson

et al. 1993

Brit J Clinical Pharma

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1. The effects of 1 h intravenous infusions of equimolar amounts of two putative 5‐hydroxytryptamine (5‐HT) renal prodrugs, 5‐hydroxy‐L‐ tryptophan (5‐HTP, 10 micrograms kg‐1 min‐1) and gamma‐L‐glutamyl‐5‐ hydroxy‐L‐tryptophan (glu‐5‐HTP, 16.6 micrograms kg‐1 min‐1) were examined in five healthy male volunteers in a randomised, placebo‐ controlled, cross‐over study. 2. Both compounds increased urinary excretion of 5‐HT and there was greater extra‐renal formation of 5‐HT following 5‐HTP administration than after glu‐5‐HTP. 3. Glu‐5‐HTP was significantly antinatriuretic. 5‐HTP reduced mean urinary sodium excretion but this effect was not statistically significant. 4. 5‐HTP, but not glu‐5‐HTP, significantly increased plasma aldosterone. There was no increase in plasma renin activity with either compound. 5. There were no significant changes in pulse rate or blood pressure. Two subjects complained of nausea at the end of 5‐HTP infusion but none had any adverse reactions with glu‐5‐HTP. 6. The results of this study suggest that both prodrugs generate 5‐HT in man and that glu‐5‐HTP is antinatriuretic. The glutamyl derivative may have greater renal specificity than 5‐HTP and, as a result, causes less systemic side effects.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

A comparison of the effects of two putative 5‐hydroxytryptamine renal prodrugs in normal man.

Freestone

Samson

et al. 1993

Brit J Clinical Pharma

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“…29 In the kidney, 5-HT functions as a mesangial cell mitogen, increases renal perfusion pressure when given exogenously 30 and promotes sodium retention /phosphate loss.…”

Section: Kidneymentioning

confidence: 99%

5‐hydroxytryptamine in the Cardiovascular System: Focus on the Serotonin Transporter (Sert)

Watts

2006

Clin Exp Pharma Physio

154

102

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SUMMARY1. The function of the serotonin transporter (SERT) is to take up and release serotonin (5-hydroxytyptamine (5-HT)) from cells and this function of SERT in the central nervous system (CNS) is well-documented; SERT is the target of selective serotonin reuptake inhibitors used in the treatment of CNS disorders, such as depression.2. The aim of the present review is to discuss our current knowledge of 5-HT and SERT in the cardiovascular (CV) system, as well as their function in physiological and pathophysiological states.3. The SERT protein has been located in multiple CV tissues, including the heart, blood vessels, brain, platelets, adrenal gland and kidney. Modification of SERT function occurs at both transcriptional and translational levels. The functions of SERT in these tissues is largely unexplored, but includes modulation of cardiac and smooth muscle contractility, platelet aggregation, cellular mitogenesis, modulating neuronal activity and urinary excretion.4. Recent studies have uncovered potential relationships between the expression of SERT gene promoter variants (long (l) or short (s)) with CV diseases. Specifically, the risk of myocardial infarction and pulmonary hypertension is increased with expression of the ll promoter, a variant associated with increased expression and function of SERT. The relationship between promoter variants and other CV diseases has not been investigated.5. Newly available experimental tools, such as pharmacological compounds and genetically altered mice, should prove useful in the investigation of the function of SERT in the CV system. 6. In summary, the function of SERT in the CV system is just beginning to be revealed.

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“…The proximal tubules of the kidney are a site of synthesis for 5-HT (Stier and Itskovitz, 1985;Sole et al, 1986;Stier et al, 1986;Itskovitz et al, 1989;Hafdi et al, 1996). As a positively charged molecule, 5-HT is excreted by SERT and other cation transporters within the nephron, where it may reduce the inhibitory effect of parathyroid hormoneinduced inhibition of sodium-phosphate transport (Hafdi et al, 1996).…”

Section: -Hydroxytryptamine Synthesis and Handlingmentioning

confidence: 99%