Study Set Content:
Plays in myointimal proliferation that occurs after
vascular injury such as that caused by
angioplasty.
12( R )-HETE
Its stereoisomer, is not a chemoattractant, but is a potent
inhibitor of the (blank) in the cornea
Na + /K + -ATPase
reduce myocardial contractility and
coronary blood flow, leading to cardiac depression.
LTC 4 and LTD 4
exert coronary vasoconstrictor
effects in vitro. Epoxyeicosatrienoic acid EETs
Lipoxin A and lipoxin
In addition to their vasodilatory action,
Epoxyeicosatrienoic acid EETs may reduce (blank) as well as systemic and pulmonary vascular
smooth muscle
cardiac hypertrophy, proliferation and migration.
Gastrointestinal Human colonic epithelial cells
synthesize
LTB 4
The colonic
mucosa of patients with inflammatory bowel disease
contains substantially increased amounts of
LTB4
a chemoattractant for neutrophils.
LTB4
are potent bronchoconstrictors and
cause increased microvascular permeability, plasma
exudation, and mucus secretion in the airways.
LCT 4 & LTD 4
There is a substantial evidence for a role of the
(blank) products in regulating renal function
although their exact role in the human kidney remains
unclear.
epoxygenase
Both (blank) are
generated in renal tissue.
20-HETE & Epoxyeicosatrienoic acid EETS
potently
blocks the smooth muscle cell Ca 2+ - activated K +
channel and leads to vasoconstriction of the renal arteries,
has been implicated in the pathogenesis of hypertension.
In contrast, studies support an (blank) of
the EETS because of their vasodilating and natriuretic
actions
20- Hydroxyeicosatetraenoic acid HETE, antihypertensive effect
increase renal blood flow and may protect against
inflammatory renal damage by limiting glomerular
macrophage infiltration.
EETs
Block all the known pathways of eicosanoid synthesis,
CORTICOSTEROIDS
Block all the known pathways of eicosanoid synthesis, partly by
stimulating the synthesis of several inhibitory proteins collectively
called
annexins or lipocortins.
CORTICOSTEROIDS They inhibit (blank) activity, probably by interfering with
phospholipid binding, thus preventing the release of arachidonic
acid.
phospholipase A 2
Block both prostaglandin and thromboxane formation by
reversibly inhibiting COX activity.
NSAIDS
are not selective for COX-1 or COX-2.
traditional NSAIDs
which were developed more recently,
vary-as do the older drugs-in their degree of selectivity.
Selective COX-2 inhibitors,
usually do not inhibit lipoxygenase activity at
concentrations that inhibit COX activity
NSAIDs
