Escolar Documentos
Profissional Documentos
Cultura Documentos
Andrew Couch
Andrew Couch
The above relationship also indicates that there is a linear and proportionate
relationship between flow and perfusion pressure. This linear relationship,
however, is not followed when pathological conditions lead to turbulent flow,
because turbulence decreases the flow at any given perfusion pressure.
Furthermore, the pulsatile nature of flow in large arteries also alters this
relationship so that greater pressures are required for a given flow. In other
words, pulsatility, like turbulence, increases resistance to flow.
As depicted above, the vascular tree is divided into segments, and flow is equal
in each segment. The resistance in each segment determines the pressure drop.
Thus if we increase arteriolar resistance, we should note an increase in arterial
pressure, and a decrease in capillary pressure.
Thus resistance in the arterioles is very important. It determines:
-
Sympathetic
o Systemic resistance
o HR/ contractility
o Venous return
o Renin secretion (via B1 receptors on JG cells in kidney)
Parasympathetic
Andrew Couch
Andrew Couch
Andrew Couch
RENAL CONTROL:
Renin
Renin release is stimulated by 2 mechanisms:
1. Sympathetic beta-1 adrenergic receptor stimulation in JG apparatus
2. Decreased renal arteriole pressure
Angiotensin II
Works by three mechanisms:
1. Vascular smooth muscle vasoconstriction
2. Increased aldosterone secretions
3. Increases sympathetic nerve ending noradrenaline
Aldosterone Na+ and H20 retention
Summary:
Red = increased
Purple = decreased
HYPERTENSION:
Essential (primary) Hypertension (80-95%)
Secondary Hypertension (5-20%)
Andrew Couch
Pathogenesis of HTN
Resetting of baroreceptor and renin response to maintain a higher blood pressure
When we initially commence patients on anti-hypertensive therapy, there is
generally a counteraction by compensatory receptors by baroreceptors and the
renin system:
Compensatory Reaction:
-
VSM contraction
the following
-
Andrew Couch
generally works by
mechanism:
Stimulation of
L-type voltage
gated Ca2+
channels results in
increased IC
Ca2+ ions
This is further
contributed to by
release of Ca2+ ions from SR
Ca++ then binds calmodulin which interacts with myosin light chain
kinase (MLCK)
o Calmodulin is a calcium-binding messenger protein expressed in all
eukaryotic cells
With consumption of an ATP molecule, this phosphorylates Myosin
light chain
This results in actin-myosin interaction and subsequent contraction of VSM.
When Potassium
channels open,
hyperpolarization of
the cell occurs. This
results in decreased
Ca2+ flow through
the L-type calcium
channels. Again this
Andrew Couch
Andrew Couch
Beta 2 (adrenaline)
A2 (adenosine)
IP (PGI2) - IP = prostacyclin receptor
Andrew Couch
Andrew Couch
Note that the endothelium plays an important role in vascular smooth muscle
tone. Relaxation associated with endothelium derived factors is often associated
with K+ channel related hyperpolarization.
-
Nitric Oxide
Prostacyclin (PGI2)
Andrew Couch
ANTI-HYPERTENSIVE DRUGS
CLASSIFICATION:
SYMPATHOPLEGIA
-
ANGIOTENSIN ANTAGONISM
Ace inhibitors
Angiotensin receptor blockers
Andrew Couch
VASODILATORS:
-
DIURETICS
Initially diuretics lead to a decrease in ECF and blood volume. This obviously will
result in an initial direct effect of decreased blood pressure:
-