test 10 part 3 Flashcards
(23 cards)
Sympathetic Control of renal function
Kidneys receive extensive sympathetic innervation
When blood volume is low, decreased pressures in pulmonary blood vessels cause reflex activation of the sympathetic nervous system
Increased renal sympathetic nerve activity
Constriction of renal arterioles, decreased GFR
Increased tubular reabsorption of salt and water
Stimulation of renin release and increased angiotensin II and aldosterone formation i.e. Increased tubular reabsorption
- RESULT: Decreased sodium and water excretion
Angiotensin II effect on renal function
- One of the most powerful controllers of sodium excretion
When sodium intake is elevated above normal
- renin secretion is decreased
Decreased angiotensin II formation
Decreased tubular reabsorption of sodium and water
Increased excretion of sodium and water
When sodium intake is decreased below normal
- renin secretion is increased
Increased angiotensin II formation
Increased tubular reabsorption of sodium and water
Decreased excretion of sodium and water
Angiotensin II and Pressure Natriuresis
- Angiotensin II makes pressure natriuresis mechanism more effective
Functional [angiotensin II] and arterial pressure
Minor changes in blood pressure will produce big increase in sodium excretion when sodium intake is raised
As sodium intake increased angiotensin II production is greatly decreased
High [angiotensin II] and arterial pressure
Takes bigger change in BP to produce needed change in sodium excretion
Can occur with hypertensive patients who cannot decrease angiotensin II production when sodium intake is increased
Patient becomes salt intolerant
Blocking Angiotensin II and arterial pressure
Improves kidney’s ability to excrete salt and water i.e. can excrete same amount of salt at much lower pressure (excretion curve moves to the left)
Lower slope not a problem since there is enhance excretion at lower pressures
Basis of function for angiotensin converting
enzyme (ACE) inhibitors
Excessive Angiotensin II Under normal physiologic conditions
Increases or decreases in concentration do not cause large increases or decreases in ECF volume
Increased arterial pressure increases sodium and water output which counterbalances the angiotensin mediated sodium retention
Excessive Angiotensin II If heart function is compromised
Cardiac pumping ability may not be great enough to increase arterial pressure high enough to overcome the sodium retaining effects of high angiotensin II
Sodium and water retention can progress to congestive heart failure
ACE inhibitors can relieve the sodium and water retention
Aldosterone
Increases sodium reabsorption, especially in the cortical collecting tubules
Associated with water retention
Associated with potassium secretion
Increased angiotensin II levels associated with low sodium intake stimulate aldosterone secretion, which contributes to the reduction of urinary sodium excretion
Chronic Oversecretion of Aldosterone
- The increased sodium reabsorption and decreased excretion is transient
After 1-3 days of sodium and water retention, ECF volume increases by 10-15%
Simultaneous increase in blood pressure
Kidneys “escape” from the sodium and water retention and excrete amounts equal to intake, despite high levels of aldosterone
Primary reason for this escape is pressure natriuresis and diuresis
Antidiuretic Hormone (ADH)
ADH plays a role in allowing the kidneys to form a small volume of concentrated urine while excreting normal amounts of salt
Especially important during water deprivation
Excess Secretion of ADH
Usually causes SMALL INCREASES in ECF volume but LARGE DECREASES in sodium concentration
Infusion of large amounts initially causes 10-15% increase in ECF volume
Arterial pressure rises in response to this volume increase
Pressure diuresis mechanism excretes this excess volume
Pressure natriuresis reduces sodium in ECF
Atrial Natriuretic Peptide
Released by cardiac atrial muscle fibers
Stimulus for release is increased stretch of the atria
Increased volume / preload
Helps reduce changes in blood volume
Excessive production or lack of ANP does not cause major changes in blood volume
Effects overcome by the changes in blood pressure
Atrial Natriuretic Peptide enters circulation and acts on
the kidneys
Small increase in GFR
Decrease in sodium reabsorption by collecting ducts
Increased excretion of salt and water
As intake in Na increases, output initially
- lags slightly behind
ECF volume increases and triggers various mechanisms to increase excretion
Activation of low-pressure receptor reflexes to inhibit sympathetic nerve activity to the kidneys -> decreased tubular sodium reabsorption
Suppression of angiotensin II formation -> decreased tubular sodium reabsorption and decreased aldosterone secretion
Stimulation of natriuretic systems (ANP) -> increased sodium excretion
Small increases in arterial pressure cause pressure natriuresis -> increased sodium excretion
Heart Diseases Causing Large Increases in ECF and Blood Volume
Congestive heart failure
Reduced cardiac output decreases arterial blood pressure
Multiple sodium-retaining systems activated
Kidneys retain volume in an attempt to return BP and CO to normal
Valvular disease
Congenital abnormalities
Conditions of Increased Capacity of Circulation Causing Large Increases in ECF and Blood Volume
Pregnancy
Blood volume increased 15-25%
Varicose veins
Large ones may hold up to 1 liter of blood!
Conditions Causing Large Increases in ECF Volume with NORMAL Blood Volume
- Nephrotic Syndrome
- Liver Cirrhosis
Nephrotic Syndrome
Important clinical cause of edema
Glomerular capillaries leak large amounts of protein into the filtrate and the urine
30-50g of protein lost each day
Protein concentration drops to less than 1/3 normal
Plasma colloid osmotic pressure falls
Kidneys continue to retain sodium and water until plasma volume is restored
Plasma protein concentration becomes further diluted
More plasma leaks into tissues
Massive fluid retention
Liver Cirrhosis
Reduction in plasma protein concentration due to destruction of liver cells
Similar sequence of events as nephrotic syndrome
Fibrous tissue causes increased capillary pressure in portal bed and leakage into peritoneal cavity (ascites)
Renal Response
Retain salt / water to restore CBV
Much of the fluid leaks into interstitial fluid – more edema
