7: Regulation of Sodium and Water Excretion Flashcards
What are the 2 short-term ways the body can keep circulating blood volume constant?
- splanchnic vascular beds vary their blood volumes
- fluid movement between the vascular and interstitial spaces
Explain the relationship of sodium content and extracellular fluid volume
the body will keep osmolality as tightly controlled as possible, therefore water will be retained additionally to account for the amount of sodium
i.e., sodium always needs water to not increase the overall osmolality
ECF osmolality = ECF osmolar content /ECF volume
osmolar content ~ Na x2
ECF volume = Na x 2/ECF osmolality
Where does the brain detect and respond to changes in extracellular sodium concentrations?
- glial cells in the region of the brain called circumventricular organ –> express sensory channels Nax –> sense extracellular Na cc –> glial cells then modulate the activity of nearby neurons involved in the Na control
- neurons in the hypothalamus –> Na channels detecting Na cc in the cerebrospinal fluid
What are the ways of (1) short-term, (2) intermediate-term, and (3) long-term control of the regulation of vascular volume and pressure
- short-term (seconds to minutes): baroreceptor reflex –> regulates cardiac performance and vascular resistance
- intermediate-term (minutes to hours): responses of renal sensors of blood pressure –> production of renin and angiotensin II –> alter vascular resistance and BP
- long-term (hours to days): renal regulation of water and salt output
Describe the 3 different baroreceptors and how they control blood pressure
1) Arterial baroreceptors
* nerve cells located in the carotid arteries and arch of the aorta
* sense arterial BP on a beat-by-beat basis
2) Cardiopulmonary baroreceptors
* nerve ending located in the cardiac atria and part of the pulmonary vasculature
* de facto measure blood volume –> atrial and pulmonary pressures increase with increased circulatory volume
–> information from both goes to the vasomotor center = collection of nuclei in the medulla oblongata (lower region of the brainstem)
* controls vascular tone throughout the body via the sympathetic nervous system and activation of RAAS
* sympathetic tone maintains total peripheral resistance by arteriole constricton and maintain venous pressure by controlling compliance of large veins
* can shift vascular volume between splanchnic organs and central circulation via venous constriction
* baroreceptors exert tonic INHIBITION of the vasomotor center –> reduce sympathetic drive
* increased BP –> detected by baroreceptors –> increased firing –> suppression of the sympathetic drive (opposite for low BP)
3) renal pressure sensors
* not really baroreceptors because no neuronal component but often called intrarenal baroreceptors
What are the two names for the cells producing renin?
Juxtaglomerular cells
Granular cells
What are the 3 ways by which the renin secretion of the JGA is controlled?
- sympathetic innvervation - Beta-1 receptors
- “renal baroreceptors” - JGA senses renal afferent arteriole stretch - if low stretch –> renin released
- macula densa sense NaCl and flow through end of ascending loop of Henle, low NaCl or flow –> renin release
In detail, how does the macula densa control renin release?
high Na flow macula densa –> ATP binds to purinergic receptors on Granular cells –> increases intracellular Ca++ –> reduces renin release
Low tubular Na –> prostaglandis rlease –> stimulates/prolongs life-time of cAMP –> relase of renin
Name 4 actions of Angiotensin II
- vasoconstriction
- Na resorption
- CNS effects - thirst and salt appetite, sympathetic drive
- Aldosterone secretion
List in what part of the nephron angiontensin II affects which Na channel/transporter.
- proximal tubules: NaHe and NaKATPase
- NaCl early distal tubule
- ENaC connecting tubule and late distal tubule
How and where in the nephron does Aldosterone excert its effects?
steroid hormone –> crosses cell membrane easily –> mineralocorticoid receptors in cytosol –> combine –> nucleus –> gene expression
- increased activity of ENaC and NaKATPase
- increaed NaCl symporter activity (but only in the presence of AII)
What does aldosterone require present for its activity on Na-Cl symporters?
AII
What percentage of the filtered sodium load is controlled by aldosterone?
2%
Other than in the kidneys where does aldosterone affect sodium reabsorption?
gut
salivary glands
What is the plasma half-life of renin, angiotesnin II, and aldosterone?
15 min, < 1 min, 15 min
Other than angiotensin II, what affects aldosterone secretion?
hyperkalemia –> increases secretion
hypokalemia –> inhibits secretion
atrial natriuretic peptide –> inhibits
List the effects of norepinephrine from sympathetic innvervation on the kidneys (3)
- renin release (beta 1)
- arteriolar vasoconstriction (alpha 1)
- stimulates NaHE3 and NAKATPase
How does ADH affect Na reabsorption?
NaK2Cl ascending limb of henle
ENaC (decreases their removal)
How does dopamine reduce Na resorption?
- reduces AII expression
- causes vesicle internalization of NHE antiporters and NaKATPase
What are the two main natriuretic peptides? Where are they produced and what is the trigger for their production?
atrial natriuretic peptide (ANP)
brain antriuretic peptide (BNP)
produced in the heart
atrial stretch
What is the effect of natriuretic peptides?
- inhibits renin, ATII, aldosterone secretion
- relax afferent arterioles
How does high plasma K cc affect Na reabsorption?
increases aldosterone secretion
inhibits NaCl symporter activity
When the RAAS system is activated the angiotensin II causes vasoconstriction. How can the kidneys upkeep their GFR despite arteriolar vasoconstriction?
prostaglandin release –> arteriolar vasodilation –> maintains GFR
How does the macula densa sense Na content?
high Na –> NaK2Cl channels –> uptake of ions –> cells swell –> ATP/adenosine –> binds to purinergic receptors of afferent arteriolar smooth muscles –> increased IC Ca++ –> contraction –> reduces GFR
How does the macula densa sense flow?
cilia –> bending of cilia –> NO release –> vasodilation
negative feedback mechanism to prevent TG feedback to reduce GFR too mcuh
Name the equation for urine water excretion
urine water excretion = urine solute excretion/urine osmolality
What is different about the circumventricular organs compared to the rest of the brain and how does this help affect ADH levels?
extensive capillary network, sensing systemic vascular contents –> rest of brain, tight BBB
What is the half-life of ADH?
few minutes
Where are the baroreceptors that affect ADH secretion located?
carotid bodies, aortic arch
What are the effects of extremely high ADH levels? (e.g., after hemorrhage)
can excert vasoconstriction of afferent arterioles –> sacrificing GFR for maintaining ECV
How does glomerular disease cause hypertension?
can lead to inappropriate renin release and RAAS activation
