PMID- 16960982
OWN - NLM
STAT- MEDLINE
DCOM- 20061204
LR  - 20220317
IS  - 0163-7258 (Print)
IS  - 0163-7258 (Linking)
VI  - 111
IP  - 3
DP  - 2006 Sep
TI  - 5-hydroxytryptamine receptors in the human cardiovascular system.
PG  - 674-706
AB  - The human cardiovascular system is exposed to plasma 5-hydroxytryptamine (5-HT, 
      serotonin), usually released from platelets. 5-HT can produce harmful acute and 
      chronic effects. The acute cardiac effects of 5-HT consist of tachycardia 
      (preceded on occasion by a brief reflex bradycardia), increased atrial 
      contractility and production of atrial arrhythmias. Acute inotropic, lusitropic 
      and arrhythmic effects of 5-HT on human ventricle become conspicuous after 
      inhibition of phosphodiesterase (PDE) activity. Human cardiostimulation is 
      mediated through 5-HT4 receptors. Atrial and ventricular PDE3 activity exerts a 
      protective role against potentially harmful cardiostimulation. Chronic exposure 
      to high levels of 5-HT (from metastatic carcinoid tumours), the anorectic drug 
      fenfluramine and its metabolites, as well as the ecstasy drug 
      3,4-methylenedioxymethamphetamine (MDMA) and its metabolite 
      3,4-methylenedioxyamphetamine (MDA) are associated with proliferative disease and 
      thickening of cardiac valves, mediated through 5-HT2B receptors. 5-HT2B receptors 
      have an obligatory physiological role in murine cardiac embryology but whether 
      this happens in humans requires research. Congenital heart block (CHB) is, on 
      occasion, associated with autoantibodies against 5-HT4 receptors. Acute vascular 
      constriction by 5-HT is usually shared by 5-HT1B and 5-HT2A receptors, except in 
      intracranial arteries which constrict only through 5-HT1B receptors. Both 5-HT1B 
      and 5-HT2A receptors can mediate coronary artery spasm but only 5-HT1B receptors 
      appear involved in coronary spasm of patients treated with triptans or with 
      Prinzmetal angina. 5-HT2A receptors constrict the portal venous system including 
      oesophageal collaterals in cirrhosis. Chronic exposure to 5-HT can contribute to 
      pulmonary hypertension through activation of constrictor 5-HT1B receptors and 
      proliferative 5-HT2B receptors, and possibly through direct intracellular 
      effects.
FAU - Kaumann, Alberto J
AU  - Kaumann AJ
AD  - Department of Physiology, University of Cambridge, UK.
FAU - Levy, Finn Olav
AU  - Levy FO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - England
TA  - Pharmacol Ther
JT  - Pharmacology & therapeutics
JID - 7905840
RN  - 0 (Receptors, Serotonin)
RN  - 333DO1RDJY (Serotonin)
SB  - IM
MH  - Animals
MH  - Blood Vessels/*physiology
MH  - Cardiovascular Diseases/*etiology
MH  - *Heart Rate
MH  - Humans
MH  - Mutation
MH  - *Myocardial Contraction
MH  - Polymorphism, Genetic
MH  - Receptors, Serotonin/genetics/*physiology
MH  - Serotonin/physiology
RF  - 385
EDAT- 2006/09/09 09:00
MHDA- 2006/12/09 09:00
CRDT- 2006/09/09 09:00
PHST- 2006/09/09 09:00 [pubmed]
PHST- 2006/12/09 09:00 [medline]
PHST- 2006/09/09 09:00 [entrez]
AID - 10.1016/j.pharmthera.2005.12.004 [doi]
PST - ppublish
SO  - Pharmacol Ther. 2006 Sep;111(3):674-706. doi: 10.1016/j.pharmthera.2005.12.004.