Long term control of blood pressure Flashcards
Long Term Control of Blood Pressure
Keeps mean arterial blood pressure (MAP) constant over long period of time (ideally our life time)
Tied into control of body fluid volume (i.e. extracellular fluid (ECF) volume & circulating blood volume (CBV)
Increased circulating blood volume assuming no change in vascular compliance
Increased volume in arteries & veins Pressure in both arteries and veins will increase (Assuming no change in vascular compliance)
IncreasedvenousreturnIncreasedpreload Increased stroke volume Increased cardiac output Increased blood pressure
increased circulating blood volume(Assuming no change in systemic vascular resistance)
Increased cardiac output Increased flow through tissues Stimulation of autoregulation response Increased constriction of metarterioles / precapillary sphincters of all autoregulated tissues Increases SVR Increased blood pressure
Small change in cardiac output can cause a large change
in blood pressure
5 to 10% increase in CO can raise MAP from 100 mmHg to 150 mmHg
Relationship Between CBV and MAP
Increasing CBV will produce an Increase in MAP Decreasing CBV will produce a Decrease in MAP
Control of CBV in terms of fluid and salt intake
Fluid Intake = Fluid Output = Constant CBV Fluid Intake > Fluid Output = Increased CBV Fluid Intake < Fluid Output = Decreased CBV
Salt Intake = Salt Output = Constant CBV Salt Intake > Salt Output = Increased CBV Salt Intake < Salt Output = Decreased CBV
Under normal circumstances fluid and salt output is controlled by the kidneys
Fluid intake per day
2300 mls
Fluid intake Synthesized by oxidation of carbohydrates
200 mls
fluid intake ingested fluids per day
2100 mls
Fluid output per day
[2300 mls/day] Insensible loss via respiratory tract and skin (not sweat)
(700 mls/day) Sweat (100 mls/day) Feces (100 mls/day) Urine (1400 mls/day)
Renal Output of Water & Salt
OUTPUT = FILTRATION – REABSORPTION Increased filtration / No change reabsorption
Increased output of water & salt Decreased CBV No change filtration / Increased reabsorption
Decreased output of water & salt Increased CBV
Factors affecting renal filtration
MAP / Renal blood flow / Pressure in glomerular capillaries / Oncotic pressure in glomerular capillaries
factors affecting renal absorption
Concentration of angiotensin II, aldosterone, antidiuretic hormone (all increase rate of reabsorption)
Renal-Body Fluid System
Slow acting, but very powerful – able to bring blood pressure back to baseline
Links changes in MAP to changes in renal filtration / reabsorption (i.e. renal output) which produces changes in CBV
MAP effect on renal body fluid system
IncreasedMAPIncreasedfiltration(pressurediuresis and pressure natriuresis) / Decreased reabsorption (decreased [angiotensin II, aldosterone]) Water / salt output > intake Decreased CBV Decreased MAP
Decreased MAP Decreased filtration / Increased reabsorption (increased [angiotensin II, aldosterone]) Water / salt output < intake Increased CBV Increased MAP
pressure diuresis Renal function curve (acute changes)
50 mmHg – 0 urine output
90 mmHg – Normal urine output
150 mmHg – urine output over 4 times normal
Cannot change long term MAP without
changing either the renal output curve or the intake curve.
What happens if there is a long term change in SVR???
Increased SVR will produce an acute change in MAP Within few days, MAP returns to normal even
through there is no change in SVR
Works if change in SVR did not affect renal blood flow i.e. equilibrium between intake and output not changed
If intrarenal vascular resistance is increased, this causes a shift of the renal function curve to the right which will result in a change in the baseline MAP
Problem is change in renal vascular resistance NOT the change in overall SVR
prorenin
inactive renin produced in juxtaglomerular cells walls of afferent arterioles) of kidneys,ecrease in pressure results in splitting of the prorenin into renin which is released into the lumen of the afferent arterioles – Circulates to rest of body
Renin remains in the blood for _ and then ___
30- 60 minutes and cts on a plasma protein called renin substrate (angiotensinogen) to release angiotensin I
angiotensin 1
Angiotensin I is mild vasoconstrictor – produces minimal changes in vascular constriction. Angiotensin I is carried to lungs where angiotensin converting enzyme (present in endothelial cells) mediates formation of angiotensin II Other blood vessels contain angiotensin converting enzyme
angiotensin 2
persists for 1 to 2 minutes before being deactivated by variety of blood / tissue enzymes known as angiotensinases. Potent vasoconstrictor of arterioles / minor constriction of veins Interacts with kidneys resulting in increased salt and water
reabsorption*
Causes adrenal gland to secrete aldosterone which increases salt and water reabsorption
Water versus Salt Intake
Easier to excrete water than it is to excrete salt Increased salt concentration in ECF Increased
osmolarity
IncreasedosmolarityIncreasedstimulationofthirst center AND hypothalamus-posterior pituitary gland
IncreasedstimulationofthirstcenterIncreasedwater intake Increased ECF volume
Increased stimulation of hypothalamus-posterior pituitary gland increased release of antidiuretic hormone (vasopressin) Increased reabsorption of salt and water Increased ECF volume Increased salt intake has potential to create bigger changes in CBV than does increased water intake
hypertension
MAP greater than 110 mmHg Produced when diastolic greater than 90 mmHg and systolic
greater than 135 mmHg
Hypertension shortens lifetime by
Excess workload on heart Damage to blood vessels of brain Injury to kidneys
causes of hypertension
Volume loading Renin-Angiotensin imbalance Combination volume loading / vasoconstriction
Types of hypertension
Primary / essential
Renin-Angiotensin Imbalance – Goldblatt Hypertension
Only one kidney and it has a constriction of renal artery
Kidney senses a decrease in pressure and the renin- angiotensin system is stimulated
Increased renin release
Increase in systemic pressure due to increased SVR – Secondary increase in systemic pressure due to increased retention of salt and water
Systemic pressure will continue to increase until renal blood flow is back to normal
Two-Kidney Goldblatt
Hypertension will occur even if one kidney normal, other kidney has obstruction of renal artery
Obstructed kidney will increase reabsorption of water and salt due to lower pressure in tubular capillaries
Obstructed kidney will release renin resulting in overall increase in [angiotensin II] and [aldosterone]
Angiotensin II will increase SVR and MAP Renal pressure returns toward normal for obstructed kidney Renal pressure higher than normal for non-obstructed kidney
Angiotensin II and aldosterone will increase salt and water reabsorption for both kidneys
Essential Hypertension
Accounts for 90 to 95% of all patients with hypertension
Specific cause unknown
Excess weight gain / obesity account for large percentage of risk for developing primary HTN (65 to 75%)
Weight loss / exercise first line of treatment
Characteristics of Essential HTN
ncreased cardiac output Support extra fat tissue / Support increased metabolic
demand of major organs SVR may be increased
Increased sympathetic activity (kidneys)
Hormones released from fat cells may stimulate regions of hypothalamus that provide excitatory stimulation of vasomotor center
Increased levels of angiotensin II and aldosterone 2 to 3 times normal in obese patients Result of increase sympathetic activity???
Impairment of renal function Requires higher pressure to remove normal amounts of salt
and water
In treating, have to give drugs that improve renal function, can’t just decrease MAP
Treatment of Essential HTN
Lifestyle modifications Increased physical activity Decrease weight
Vasodilator drugs – primary target being renal arterioles
Inhibition of sympathetic signals to kidneys Block action of sympathetic neurotransmitter on renal
vasculature and renal tubules Direct relaxation of renal vasculature smooth muscle Block action of renin-angiotensin system
Drugs that reduce reabsorption of salt and water Block active transport of sodium in tubules