Biomedical Engineering Reference
In-Depth Information
Mechanotransduction and the Myogenic
Response in Diabetes
Sewon Lee, Srijita Dhar, Kwangseok Hong, Yan Yang
and Michael A. Hill
Abstract Tissues of the body possess intrinsic control mechanisms for regulating
hemodynamics at the local level. These mechanisms largely occur independently of
innervation and circulating factors and allow blood flow to be matched to local
metabolic requirements. In the case of the myogenic response, or pressure-induced
vasoconstriction, this mechanism is dependent on the cells of the vessel wall
detecting and responding to a mechanical stimulus. This mechanical event then must
be conveyed across the smooth muscle cell membrane to the contractile proteins to
affect an appropriate contractile response. Diabetes and related metabolic disorders
that lead to hyperglycemia may interfere with this process by either alterations to the
vessel wall (for example, remodeling events, increased stiffness, decreased disten-
sibility) or impairment of signal transduction mechanisms (including ion channel
function, Ca
2+
handling and contractile protein interactions). This chapter reviews
the cellular mechanisms underlying myogenic contraction and how these may be
altered in hyperglycemic states.
Abbreviations
AGE
Advanced glycation endproducts
AT
1
R
Angiotensin II type 1 receptor
DAG
Diacylglycerol
ECM
Extracellular matrix
EM
Membrane potential
GK
Goto-Kakizaki
GPCRs
G-protein coupled receptors
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