Biomedical Engineering Reference
In-Depth Information
MLCK
Myosin light chain kinase
MYPT1
Myosin targeting subunit of myosin phosphatase
NSCCs
Non-selective cation channels
OZR
Obese zucker rat
PKC
Protein kinase C
RAGE
Receptor for advanced glycation endproducts
ROS
Reactive oxygen species
S-1-P
Sphingosine-1-phosphate
SACs
Stretch-activated channels
SD
Sprague dawley
SK
Src kinase
SR
Sarcoplasmic reticulum
STZ
Streptozotocin
TK
Tyrosine kinase
Trp
Transient receptor potential
Voltage-gated Ca 2+
VGCCs
channels
VSM
Vascular smooth muscle
VSMC
Vascular smooth muscle cells
1 Introduction
Tissues of the body possess intrinsic control mechanisms for regulating hemody-
namics at the local level. These mechanisms largely occur independently of inner-
vation and circulating factors and allow blood flow to be matched to local metabolic
requirements. Principal amongst these local hemodynamic regulatory mechanisms
are myogenic, metabolic, flow-dependent and conducted responses [ 1 - 3 ]. These
mechanisms do not, however, exist in isolation, for example, neurohumoral factors
modulate and interact with these local regulatory mechanisms [ 4 , 5 ]. Thus arteriolar
myogenic or pressure-dependent vasoconstriction (the focus of this chapter) while
itself being a basic smooth muscle cell phenomenon, is modulated by neural input as
well as endothelium-derived and locally produced parenchymal factors.
Type 1 diabetes (also known as insulin-dependent diabetes) is an autoimmune
condition in which the insulin producing pancreatic b-cells are destroyed, whereas
type 2 diabetes (non insulin-dependent diabetes) occurs when the metabolic system
is no longer able to utilize insulin efficiently and/or becomes resistant to insulin's
action. Both types of diabetes increase the risk for development of vascular com-
plications, which can negatively impact both quality and length of life. From a
clinical perspective, the complications of diabetes typically include retinopathy,
nephropathy and neuropathy, while also increasing the risk for coronary and
cerebrovascular disease. While the exact mechanisms leading to vascular dys-
function are uncertain, it is clear that their severity is generally related to the quality
of metabolic control and the duration of diabetes [ 6 , 7 ].
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