Enhanced constrictor responses of skeletal muscle arterioles during chronic myocardial infarction

Sean P. Didion, Pamela K. Carmines, Hideki Ikenaga, William G. Mayhan

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


The goal of this study was to test the hypothesis that chronic myocardial infarction potentiates agonist-induced constrictor responses of rat skeletal muscle arterioles in vivo. Eight weeks after we performed coronary artery ligation or sham (control) surgery, the spinotrapezius muscle was prepared for direct visualization of the microcirculation. Diameter of third-order arterioles (40.7 ± 0.5 μm) to topical suffusion of angiotensin II (ANG II; 0.1-10 nM), arginine vasopressin (AVP; 0.1-10 nM), endothelin-1 (ET-1; 1.0-100 pM), and the thromboxane analog U-46619 (1.0-100 nM) was measured in both groups. Myocardial-infarcted rats exhibited enhanced arteriolar constrictor responses to ANG II and AVP compared with the responses in controls. In contrast, ET-1- and U-46619-induced constrictor responses were similar in control and myocardial-infarcted rats. Additional experiments explored the impact of N(G)-monomethyl-L-arginine (L-NMMA; 0.1 mM) on arteriolar reactivity. In control animals, L-NMMA potentiated ANG II- and AVP-induced vasoconstriction, achieving values similar to those observed in myocardial-infarcted rats. L-NMMA did not alter vasoconstrictor responses in rats with chronic myocardial infarction. These observations suggest that enhanced agonist-induced vasoconstriction during heart failure may reflect a loss of nitric oxide-mediated modulation of arteriolar tone.

Original languageEnglish (US)
Pages (from-to)H1502-H1508
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number3 42-3
StatePublished - 1997


  • Angiotensin II
  • Arginine vasopressin
  • Endothelin-1
  • N(G)-monomethyl-L- arginine
  • Rats
  • U-46619

ASJC Scopus subject areas

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


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