Altered reactivity of coronary arteries located distal to a chronic coronary occlusion

Julie A. Rapps, Michael Sturek, Allan W. Jones, Janet L. Parker

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The coronary vasculature located distal to a chronic occlusion (collateral-dependent) has been shown to exhibit altered reactivity to vasoactive agonists. Thus we evaluated effects of chronic coronary artery occlusion on vasomotor responsiveness of collateral-dependent arteries isolated from a canine model of Ameroid occlusion of the left circumflex (LCX) coronary artery. We compared in vitro responses of large (-1.3- to 1.4-mm-ID) and small (∼0.6-mm-ID) LCX arteries located distal to an occlusion with responses of similar-sized segments of the unoccluded left anterior descending (LAD) coronary artery. α-Adrenergic receptor-mediated contractile responses to norepinephrine (10-9-10-4 M) and phenylephrine (10~9-10~4 M) in the presence of propranolol were markedly enhanced in large LCX arteries compared with LAD arteries (P <0.001). Prazosin (1 μM.), an a1-adrenergic receptor antagonist, abolished contractile responses of LCX and LAD arteries to norepinephrine. Inhibition of nitric oxide synthesis with N-nitro-L-arginine methyl ester (100 μM) enhanced norepinephrine-induced contractions of LAD arteries to a greater extent than contractions of LCX arteries. We simultaneously measured myoplasmic free Ca2+ (fura 2 fluorescence ratio) and contractile responses in LCX and LAD arteries denuded of endothelium; norepinephrine-induced increases in myoplasmic free Ca2+ and contractile tension were significantly enhanced in LCX arteries compared with LAD arteries. In addition, large and small LCX arteries exhibited impaired relaxation in response to adenosine (10-8-10-3 M) compared with LAD arteries (P <0.05). In contrast, relaxation in response to the β-adrenergic agonist isoproterenol (10-9-10-4 M) and sodium nitroprusside (10-10-10-4 M) was not significantly different in LCX and LAD arteries. Thus collateral-dependent coronary arteries exhibit enhanced aadrenergic vasoconstriction and impaired vasorelaxation in response to adenosine. The enhanced a-adrenergic contractile responsiveness involves at least two mechanisms: 1) enhanced aradrenergic reactivity of smooth muscle and 2) decreased a-adrenergic-induced synthesis of nitric oxide by the endothelium. coronary artery occlusion; norepinephrine; phenylephrine;.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Physiology
Volume273
Issue number4 PART 2
StatePublished - 1997
Externally publishedYes

Fingerprint

Coronary Occlusion
Coronary Vessels
Arteries
Norepinephrine
Phenylephrine
Adrenergic Agents
Adenosine
Endothelium
Nitric Oxide
Adrenergic Agonists
Adrenergic Antagonists
Fura-2
Prazosin
Nitroprusside
Vasoconstrictor Agents
Vasoconstriction
Isoproterenol
Vasodilation
Propranolol
Adrenergic Receptors

Keywords

  • Adenosine
  • Myoplasmic free calcium

ASJC Scopus subject areas

  • Physiology (medical)
  • Physiology

Cite this

Altered reactivity of coronary arteries located distal to a chronic coronary occlusion. / Rapps, Julie A.; Sturek, Michael; Jones, Allan W.; Parker, Janet L.

In: American Journal of Physiology - Renal Physiology, Vol. 273, No. 4 PART 2, 1997.

Research output: Contribution to journalArticle

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title = "Altered reactivity of coronary arteries located distal to a chronic coronary occlusion",
abstract = "The coronary vasculature located distal to a chronic occlusion (collateral-dependent) has been shown to exhibit altered reactivity to vasoactive agonists. Thus we evaluated effects of chronic coronary artery occlusion on vasomotor responsiveness of collateral-dependent arteries isolated from a canine model of Ameroid occlusion of the left circumflex (LCX) coronary artery. We compared in vitro responses of large (-1.3- to 1.4-mm-ID) and small (∼0.6-mm-ID) LCX arteries located distal to an occlusion with responses of similar-sized segments of the unoccluded left anterior descending (LAD) coronary artery. α-Adrenergic receptor-mediated contractile responses to norepinephrine (10-9-10-4 M) and phenylephrine (10~9-10~4 M) in the presence of propranolol were markedly enhanced in large LCX arteries compared with LAD arteries (P <0.001). Prazosin (1 μM.), an a1-adrenergic receptor antagonist, abolished contractile responses of LCX and LAD arteries to norepinephrine. Inhibition of nitric oxide synthesis with N-nitro-L-arginine methyl ester (100 μM) enhanced norepinephrine-induced contractions of LAD arteries to a greater extent than contractions of LCX arteries. We simultaneously measured myoplasmic free Ca2+ (fura 2 fluorescence ratio) and contractile responses in LCX and LAD arteries denuded of endothelium; norepinephrine-induced increases in myoplasmic free Ca2+ and contractile tension were significantly enhanced in LCX arteries compared with LAD arteries. In addition, large and small LCX arteries exhibited impaired relaxation in response to adenosine (10-8-10-3 M) compared with LAD arteries (P <0.05). In contrast, relaxation in response to the β-adrenergic agonist isoproterenol (10-9-10-4 M) and sodium nitroprusside (10-10-10-4 M) was not significantly different in LCX and LAD arteries. Thus collateral-dependent coronary arteries exhibit enhanced aadrenergic vasoconstriction and impaired vasorelaxation in response to adenosine. The enhanced a-adrenergic contractile responsiveness involves at least two mechanisms: 1) enhanced aradrenergic reactivity of smooth muscle and 2) decreased a-adrenergic-induced synthesis of nitric oxide by the endothelium. coronary artery occlusion; norepinephrine; phenylephrine;.",
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N2 - The coronary vasculature located distal to a chronic occlusion (collateral-dependent) has been shown to exhibit altered reactivity to vasoactive agonists. Thus we evaluated effects of chronic coronary artery occlusion on vasomotor responsiveness of collateral-dependent arteries isolated from a canine model of Ameroid occlusion of the left circumflex (LCX) coronary artery. We compared in vitro responses of large (-1.3- to 1.4-mm-ID) and small (∼0.6-mm-ID) LCX arteries located distal to an occlusion with responses of similar-sized segments of the unoccluded left anterior descending (LAD) coronary artery. α-Adrenergic receptor-mediated contractile responses to norepinephrine (10-9-10-4 M) and phenylephrine (10~9-10~4 M) in the presence of propranolol were markedly enhanced in large LCX arteries compared with LAD arteries (P <0.001). Prazosin (1 μM.), an a1-adrenergic receptor antagonist, abolished contractile responses of LCX and LAD arteries to norepinephrine. Inhibition of nitric oxide synthesis with N-nitro-L-arginine methyl ester (100 μM) enhanced norepinephrine-induced contractions of LAD arteries to a greater extent than contractions of LCX arteries. We simultaneously measured myoplasmic free Ca2+ (fura 2 fluorescence ratio) and contractile responses in LCX and LAD arteries denuded of endothelium; norepinephrine-induced increases in myoplasmic free Ca2+ and contractile tension were significantly enhanced in LCX arteries compared with LAD arteries. In addition, large and small LCX arteries exhibited impaired relaxation in response to adenosine (10-8-10-3 M) compared with LAD arteries (P <0.05). In contrast, relaxation in response to the β-adrenergic agonist isoproterenol (10-9-10-4 M) and sodium nitroprusside (10-10-10-4 M) was not significantly different in LCX and LAD arteries. Thus collateral-dependent coronary arteries exhibit enhanced aadrenergic vasoconstriction and impaired vasorelaxation in response to adenosine. The enhanced a-adrenergic contractile responsiveness involves at least two mechanisms: 1) enhanced aradrenergic reactivity of smooth muscle and 2) decreased a-adrenergic-induced synthesis of nitric oxide by the endothelium. coronary artery occlusion; norepinephrine; phenylephrine;.

AB - The coronary vasculature located distal to a chronic occlusion (collateral-dependent) has been shown to exhibit altered reactivity to vasoactive agonists. Thus we evaluated effects of chronic coronary artery occlusion on vasomotor responsiveness of collateral-dependent arteries isolated from a canine model of Ameroid occlusion of the left circumflex (LCX) coronary artery. We compared in vitro responses of large (-1.3- to 1.4-mm-ID) and small (∼0.6-mm-ID) LCX arteries located distal to an occlusion with responses of similar-sized segments of the unoccluded left anterior descending (LAD) coronary artery. α-Adrenergic receptor-mediated contractile responses to norepinephrine (10-9-10-4 M) and phenylephrine (10~9-10~4 M) in the presence of propranolol were markedly enhanced in large LCX arteries compared with LAD arteries (P <0.001). Prazosin (1 μM.), an a1-adrenergic receptor antagonist, abolished contractile responses of LCX and LAD arteries to norepinephrine. Inhibition of nitric oxide synthesis with N-nitro-L-arginine methyl ester (100 μM) enhanced norepinephrine-induced contractions of LAD arteries to a greater extent than contractions of LCX arteries. We simultaneously measured myoplasmic free Ca2+ (fura 2 fluorescence ratio) and contractile responses in LCX and LAD arteries denuded of endothelium; norepinephrine-induced increases in myoplasmic free Ca2+ and contractile tension were significantly enhanced in LCX arteries compared with LAD arteries. In addition, large and small LCX arteries exhibited impaired relaxation in response to adenosine (10-8-10-3 M) compared with LAD arteries (P <0.05). In contrast, relaxation in response to the β-adrenergic agonist isoproterenol (10-9-10-4 M) and sodium nitroprusside (10-10-10-4 M) was not significantly different in LCX and LAD arteries. Thus collateral-dependent coronary arteries exhibit enhanced aadrenergic vasoconstriction and impaired vasorelaxation in response to adenosine. The enhanced a-adrenergic contractile responsiveness involves at least two mechanisms: 1) enhanced aradrenergic reactivity of smooth muscle and 2) decreased a-adrenergic-induced synthesis of nitric oxide by the endothelium. coronary artery occlusion; norepinephrine; phenylephrine;.

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