Nongenomic vasodilator action of progesterone on primate coronary arteries

Richard D. Minshall, Dusan Pavcnik, David L. Browne, Kent Hermsmeyer

Research output: Contribution to journalArticle

59 Scopus citations

Abstract

In the present investigation, we test the hypothesis that progesterone can rapidly relax, via a nongenomic mechanism, persistent flow occluding, agonist-activated coronary artery (CA) vasospasm, and hyperreactive vascular muscle cell (VMC) Ca2+ responses in ovariectomized rhesus monkeys. CA vasospasm, induced by injection of 100 μM serotonin and 1 μM U-46619 (5-HT+U; 1 ml/30 s), resulted in a decrease in CA diameter (φ) from 1.8 ± 0.2 to 0.3 ± 0.1 mm at the site of focal constriction. Injection of 100 ng progesterone into the CA significantly relieved the severe vasoconstriction (1.3 ± 0.2 mm) and reestablished distal flow in 3 min; the preconstriction φ was completely restored in 8.2 ± 2.6 min (n = 6). Similarly, cell impermeant albumin-conjugated progesterone, but not albumin-conjugated 17β-estradiol, decreased 5-HT+U stimulated VMC Ca2+ responses (250 ± 34% of basal 30 min after stimulation) back to the prestimulation level (113 ± 17% of basal) in 25 min (half time = 7 min). The presence of a rapid vasodilator action of progesterone in the primate CA and isolated VMC suggests its benefits in hormone replacement therapy may also include nongenomic vascular relaxant actions.

Original languageEnglish (US)
Pages (from-to)701-708
Number of pages8
JournalJournal of Applied Physiology
Volume92
Issue number2
DOIs
StatePublished - Jan 1 2002

Keywords

  • Angiography
  • Low-dose progesterone
  • Nongenomic effects
  • Ovarian steroids
  • Vascular muscle cell
  • Vasospasm

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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