Myogenic constriction of human coronary arterioles.

Published

Journal Article

Myogenic constriction is an important mechanism of blood flow regulation; however, it has never been demonstrated in the human coronary circulation. We examined responses of human coronary resistance vessels in vitro to changes in intraluminal pressure and evaluated the role of protein kinase C (PKC). Microvessels (passive diameter 44-227 microns) were dissected from atrial appendages obtained during cardiac surgery and studied under conditions of zero flow. In response to stepped increases in pressure, there was a graded response such that at 100 mmHg, vessels constricted to 55 +/- 4% of their passive diameter. There was an inverse relationship between vessel diameter and myogenic responsiveness. Basal tone was attenuated by inhibition of voltage-dependent calcium channels (VDCC) with diltiazem and by inhibition of PKC with calphostin C. Activation of PKC with phorbol 12-myristate 13-acetate (PMA) enhanced basal tone. Active myogenic constriction was also impaired by calphostin C and augmented by PMA. Arterioles from patients with hypertension demonstrated enhanced myogenic constriction compared with vessels from normotensive patients (0.55 +/- 0.04 vs. 0.74 +/- 0.03; P < 0.01). These results demonstrate myogenic constriction in the human coronary microcirculation. Regulation of extracellular calcium by VDCC and intracellular calcium by PKC are important in mediating the magnitude of basal tone and myogenic responsiveness of these vessels.

Full Text

Duke Authors

Cited Authors

  • Miller, FJ; Dellsperger, KC; Gutterman, DD

Published Date

  • July 1997

Published In

Volume / Issue

  • 273 / 1 Pt 2

Start / End Page

  • H257 - H264

PubMed ID

  • 9249498

Pubmed Central ID

  • 9249498

International Standard Serial Number (ISSN)

  • 0002-9513

Digital Object Identifier (DOI)

  • 10.1152/ajpheart.1997.273.1.H257

Language

  • eng

Conference Location

  • United States