Renal Control Of Blood Pressure And CO Flashcards
Where are baroreceptors found?
Aortic arch
Carotid sinuses
What is used for short term control of BP? How does it work?
Baroreceptor reflex
Nerve endings are sensitive to stretch caused by increased arterial pressure
Send signal along afferent pathway to medulla
Signals down efferent pathway adjust sympathetic input which adjusts TPR
Adjusts sympathetic and parasympathetic inputs to heart to alter cardiac output
How is the sympathetic NS used in long term renal control of BP?
High levels of sympathetic stimulation reduce renal blood flow by vasoconstriction (α1 receptor)
Decrease in GFR -> decrease in Na+ excretion
Activates apical Na-H exchanger and NaKATPase in PCT
Stimulates renin release
What are the ways for long-term control of BP?
Sympathetic nervous system
Natriuretic peptides
RAAS
ADH
What does atrial natriuretic peptide (ANP) do?
Promotes Na+ excretion
Causes vasodilatation of afferent arteriole, increasing GFR
Inhibits Na reabsorption along the nephron
Where is ANP synthesised and stored?
Atrial myocytes
What causes release and inhibition of release of ANP?
Stimulates release - Stretch
Inhibits release - low pressure volume sensors in atria detect reduced effective circulating volume (reduced filling of the heart)
Where is renin released from?
Granular cells of juxtaglomerular apparatus
What causes release of renin?
Reduced perfusion pressure in the kidney which is detected by baroreceptors in the afferent arteriole
Decreased NaCl concentration at the macula densa (due to low GFR) causes sympathetic stimulation to the JGA, increasing renin release.
Action of renin?
Increases BP
Converts angiotensin to angiotensin I
What receptors does angiotensin II act on?
AT1 (mostly) (GPCR)
AT2
Actions of angiotensin II?
Arterioles - vasoconstriction by working on smooth muscle cells, increasing TPR and BP. Also constricts afferent arteriole in kidney
Kidneys - enhanced Na+ reabsorption in PCT by stimulating NaH exchanger
Sympathetic NS - increases release of NA
Adrenal cortex - release of aldosterone
Hypothalamus - increased thirst sensation by stimulating ADH release
Action of aldosterone?
Acts on intracellular receptors
Increases expression of apical Na+ channel (ENaC) and NaKATPase in principal cells of collecting duct
What works against aldosterone?
Spironolactone
What stimulates release of ADH
Increases in plasma osmolarity
Severe hypovolaemia
What is the main role of anti-diuretic hormone?
Formation of concentrated urine by retaining water
Stimulates Na reabsorption
Acts on thick ascending limb to stimulate Na-K-Cl co-transporter (therefore less water can leave thin ascending limb due to less of a gradient)
How is ADH released?
Baroreceptors detect a 5-10% drop in BP
Signals to brain stem via vagus nerve
Modulates sympathetic nerve outflow
Secretion of ADH (and reduction of ANP)
Overall action of ANP?
Decrease BP
What do prostaglandins do?
Vasodilation
Locally - enhance glomerular filtration and reduce Na reabsorption
Act as a buffer to excessive vasoconstriction by sympathetic NS and RAAS
Important when angiotensin II is high
Overall action of prostaglandins?
Reduce blood pressure
What is pathway involved in the formation of prostaglandins? What can interfere with it?
Cyclo-oxygenase (COX) pathway
NSAIDS
When can administration of NSAIDs be dangerous? Why?
When renal perfusion is compromised
They can further decrease GFR
Cause acute renal failure
Due to inhibition of prostaglandins
In heart failure/hypertensive patients, can worsen condition by increasing NaCl and water retention
What is hypertension?
Sustained increase in blood pressure
What is essential hypertension and what proportion of cases does this make up?
Where there is no definable cause
95% of cases
