Foley-Physiology of Blood Pressure

blood vessel arrangement one after the other (aorta-->artery-->arteriole-->capillary-->venule-->vein)
Total resistance is additive

multiple ducts flowing in same direction (i.e. multiple capillaries for every artierole)
This decreases total resistance (reciprocals of each resistance mechanism are added)

flow=volume/unit time
velocity=distance/unit time
velocity=flow/cross sectional area

fastest in arteries, drops down in arterioles, slowest in capillaries, speeds up in venous system (relates to cross sectional area)

allows for greater exchange and diffusion into and out of the tissues

Venous system
veins can be distended more than arteries, allowing them to carry a larger volume of blood.
Veins can constrict, which will put more blood into the systemic circulation when needed (exercise)

laminar flow-smooth flow, low resistance
turbulent flow-narrowing of blood vessel, increased velocity, mixing of layers, creation of vibrations/sounds
turbulence doesn't always indicate pathology (exercise), but does if it occurs during rest

Arterioles
Arterioles can constrict, regulating amount of blood flow into different organs. Everything downstream of arterial constriction will be reduced pressure (functions like a dam)

Added pressure of cardiac output from ventricle contraction and reflex pressure of arteries downstream

Arteriole constriction-decreases capillary pressure, allows for greater exchange/diffusion into tissues
Arteriole dilation-increases capillary pressure, decreases capillary exchange/diffusion

AKA Systemic Vascular Resistance (SVR)
This is a major determinant of mean arterial blood pressure.
The largest percentage of TPR is in the systemic arterioles.

compliance=change in volume/change in pressure
compliance=elasticity
Arterial vessels have very small compliance
Venous vessels have large compliance; this allows them to hold large volumes of blood (serve as blood reservoirs)

MAP=CO * TPR (CO *SVR)
MAP=Diastolic pressure + 1/3 pulse pressure (pulse pressure=systolic - diastolic pressure)
works best at resting heart rate

Age-atherosclerosis will decrease compliance

Stroke volume-directly related
Compliance-inversely related
With age, stroke volume will decrease, but compliance will also decrease, usually resulting in overall increased pulse pressure

Electromechanical coupling-occurs because the smooth muscle surface membrane contains voltage-operated channels for calcium. Membrane depolarization increases the open-state probability of these channels and thus leads to smooth muscle cell contraction and vessel constriction.
Pharmacomechanical coupling-chemical agents (eg, released neurotransmitters) can induce smooth muscle contraction without the need for a change in membrane potential.

Vasodilator factors (CO2, K, ATP, H, adenosine) enter the interstitial space from the tissue cells at a rate proportional to tissue metabolism. These vasodilator factors are removed from the tissue at a rate proportional to blood flow. Whenever tissue metabolism is proceeding at a rate for which the blood flow is inadequate, the interstitial vasodilator factor concentrations automatically build up and cause the arterioles to dilate. This, of course, causes blood flow to increase. The process continues until blood flow has risen sufficiently to appropriately match the tissue metabolic rate and prevent further accumulation of vasodilator factors.

release substances:
vasodilators-nitric oxide, prostacyclin, "endothelial-derived hyperpolarizing factor"
vasoconstrictors-endothelin

Sympathetic noradrenergic vasoconstrictor nerves

Vasocontriction-circulating epinephine and norepinephrine, aginine vasopressin, and angiotensin II

Sympathetic noradrenergic nerves

baroreceptors send afferents to synapse in the medulla, which upon processing will have three different responses:
1. enhance parasympathetics (decrease cardiac output)
2. enhance sympathetics (increase CO, vasoconstriction)
3. inhibit sympathetics (decrease CO, vasodilation)

short term (within seconds/minutes) response
baroreceptor discharge is directly related to mean arterial pressure (MAP)
Decrease in MAP-->decrease in baroreceptor discharge-->increased sympathetic activity; decreased parasympathetic activity-->increased MAP
(initial increased MAP will have opposite effect)

Sense the pressure (or volume) in the atria and central venous pool. Increased central venous pressure and volume cause receptor activation by stretch, which elicits a reflex decrease in sympathetic activity. Decreased central venous pressure produces the opposite response

Low PO2 and/or high PCO2 levels in the arterial blood cause reflex increases in respiratory rate and mean arterial pressure due to arterial chemoreceptors, located in the carotid arteries and the arch of the aorta, and central chemoreceptors, located somewhere within the CNS

An extremely strong reaction triggered by inadequate brain blood flow (ischemia) and can produce a more intense sympathetic vasoconstriction and cardiac stimulation than is elicited by any other influence on the cardiovascular control centers (last ditch effort to increase arterial pressure in order to perfuse the brain)

fluid balance-works through mechanisms of the kidney and urinary output rate

Decreased arterial pressure-->decreased glomerular capillary pressure-->decreased glomerular filtration rate-->decreased urine output
decreased glomerular filtration rate-->increased release of renin, then angiotensin II, then aldosterone-->increased renal sodium resorption-->increased renal fluid resorption-->decreased urinary output
(increased arterial pressure will have opposite effects)

highly regulated-small changes in arterial pressure have big affects on urine output (very steep curve on graph)

In hypertension, this mechanism is not as highly regulated. Changes in arterial pressure will have the same affects on urine output, but the affects are minimized (curve is not as steep)
Diuretics will help to get the regulation closer to normal (increase the slope of the graph)