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Effects of Myoendothelial Interactions on Arteriolar Myogenic and Agonist‐mediated Vascular Control
Author(s) -
Pradhan Ranjan,
Lu Xiao,
Kassab Ghassan,
Beard Daniel,
Carlson Brian
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.787.10
Subject(s) - vasoconstriction , vasodilation , vascular smooth muscle , agonist , myogenic contraction , electrical impedance myography , phenylephrine , chemistry , biophysics , myograph , contraction (grammar) , medicine , anatomy , biology , smooth muscle , blood pressure , receptor
Local regulation of blood flow to tissue is governed by contraction and relaxation of circumferential vascular smooth muscle in resistance vessels. Interaction between endothelial cells (EC) and smooth muscle cells (SMC) play a critical role in regulating vascular tone. Although ion flux, IP 3 and nitric oxide (NO) transport between cells are known to be involved in regulation of SMC activity, little is known about their relative contributions to myogenic and agonist‐mediated vascular tone. To quantify their contributions we have assembled an isolated vessel model of a resistance artery by integrating models of vessel wall mechanics, smooth muscle force generation, and SMC and EC Ca 2+ dynamics and electrophysiology. Steady‐state pressure‐diameter and agonist response data from pressure and isovolumic myography studies are analyzed to determine contributions of ionic, IP 3 and NO transport between ECs and SMCs on isolated vessel tone. The model predicts levels of SMC and EC Ca 2+ at a given vascular tone and can also show how the presence/absence of endothelial layers influences pressure/agonist‐induced contraction response, under isobaric and isovolumic conditions. In order to replicate experimentally observed vasoconstriction response to the smooth muscle agonist phenylephrine, the model analysis shows there is a limit to ionic and IP 3 coupling allowed between cells. Below these limits, the NO‐cGMP pathway has a minimal effect on vasoconstriction response to pressure but yet still has a significant effect on endothelial agonist‐induced vasodilatory response. Supported by NIH U01 HL118738, NSF CBET 1133260 and NIH P50‐GM094503.