5-HT causes splanchnic venodilation

Bridget M. Seitz, Hakan S. Orer, Teresa Krieger-Burke, Emma S. Darios, Janice M. Thompson, Gregory D. Fink, Stephanie W. Watts

Research output: Contribution to journalArticle

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Abstract

Serotonin [5-hydroxytryptamine (5-HT)] causes relaxation of the isolated superior mesenteric vein, a splanchnic blood vessel, through activation of the 5-HT7 receptor. As part of studies designed to identify the mechanism(s) through which chronic (≥24 h) infusion of 5-HT lowers blood pressure, we tested the hypothesis that 5-HT causes in vitro and in vivo splanchnic venodilation that is 5-HT7 receptor dependent. In tissue baths for measurement of isometric contraction, the portal vein and abdominal inferior vena cava relaxed to 5-HT and the 5-HT1/7 receptor agonist 5-carboxamidotryptamine; relaxation was abolished by the 5-HT7 receptor antagonist SB-269970. Western blot analyses showed that the abdominal inferior vena cava and portal vein express 5-HT7 receptor protein. In contrast, the thoracic vena cava, outside the splanchnic circulation, did not relax to serotonergic agonists and exhibited minimal expression of the 5-HT7 receptor. Male Sprague- Dawley rats with chronically implanted radiotelemetry transmitters underwent repeated ultrasound imaging of abdominal vessels. After baseline imaging, minipumps containing vehicle (saline) or 5-HT (25 ≥g·kg-1·min-1) were implanted. Twenty-four hours later, venous diameters were increased in rats with 5-HT-infusion (percent increase from baseline: superior mesenteric vein, 17.5 ± 1.9; portal vein, 17.7 ± 1.8; and abdominal inferior vena cava, 46.9 ± 8.0) while arterial pressure was decreased (~13 mmHg). Measures returned to baseline after infusion termination. In a separate group of animals, treatment with SB-269970 (3 mg/kg iv) prevented the splanchnic venodilation and fall in blood pressure during 24 h of 5-HT infusion. Thus, 5-HT causes 5-HT7 receptor-dependent splanchnic venous dilation associated with a fall in blood pressure. NEW & NOTEWORTHY This research is noteworthy because it combines and links, through the 5-HT7 receptor, an in vitro observation (venorelaxation) with in vivo events (venodilation and fall in blood pressure). This supports the idea that splanchnic venodilation plays a role in blood pressure regulation.

LanguageEnglish (US)
PagesH676-H686
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume313
Issue number3
DOIs
StatePublished - Sep 12 2017

Profile

Viscera
Serotonin
Blood Pressure
Inferior Vena Cava
Portal Vein
Mesenteric Veins
Splanchnic Circulation
Serotonin Receptor Agonists
Venae Cavae
Isometric Contraction
Baths

Keywords

  • Blood pressure
  • Imaging
  • Pharmacology
  • SB-269970
  • Serotonin
  • Veins

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

5-HT causes splanchnic venodilation. / Seitz, Bridget M.; Orer, Hakan S.; Krieger-Burke, Teresa; Darios, Emma S.; Thompson, Janice M.; Fink, Gregory D.; Watts, Stephanie W.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 313, No. 3, 12.09.2017, p. H676-H686.

Research output: Contribution to journalArticle

Seitz BM, Orer HS, Krieger-Burke T, Darios ES, Thompson JM, Fink GD et al. 5-HT causes splanchnic venodilation. American Journal of Physiology - Heart and Circulatory Physiology. 2017 Sep 12;313(3):H676-H686. Available from, DOI: 10.1152/ajpheart.00165.2017
Seitz, Bridget M. ; Orer, Hakan S. ; Krieger-Burke, Teresa ; Darios, Emma S. ; Thompson, Janice M. ; Fink, Gregory D. ; Watts, Stephanie W./ 5-HT causes splanchnic venodilation. In: American Journal of Physiology - Heart and Circulatory Physiology. 2017 ; Vol. 313, No. 3. pp. H676-H686
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