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: Research - peer-reviewArticle

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
In Vitro Techniques
SB 269970
Splanchnic Circulation
Serotonin Receptor Agonists
Venae Cavae
Isometric Contraction
Baths
Blood Vessels
Sprague Dawley Rats
Dilatation
Ultrasonography
Arterial Pressure
Thorax
Western Blotting

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: Research - peer-reviewArticle

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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