S4) Blood Pressure and The Kidney Flashcards
What is the formula for calculating blood pressure?
mean arterial BP = CO x TPR
What is the formula for calculating cardiac output?
CO = SV x HR
Explain the 2 actions which allow for the short term regulation of blood pressure
Baro-receptor reflex:
- Adjust sympathetic and parasympathetic inputs to the heart to alter CO
- Adjust sympathetic input to blood vessels to alter TPR
Describe the long term regulation of blood pressure
Neurohormonal response to affect salt and water balance
Identify 4 processes which act on the kidney to regulate blood pressure
- Renin-angiotensin-aldosterone system
- Sympathetic nervous system
- Prostaglandins
- ADH
Describe the events which occur in RAAS

Identify 3 factors which stimulate renin release from the JGA cells in the kidney

- Reduced NaCl delivery to macula densa in distal tubule
- Reduced perfusion pressure in the kidney (detected by baroreceptors in afferent arteriole)
- Sympathetic stimulation to JGA increases release of renin
What are the direct effects of Angiotensin II on the kidney?
- Vasoconstriction of efferent arteriole (AA > EA)
- Enhances Na+ reabsorption at the PCT (stimulates Na-H exchanger in apical membrane)
Angiotensin II stimulates aldosterone release from the adrenal cortex.
Identify 2 of its actions on the kidney
Acts on principal cells of collecting duct:
- Stimulate Na+ and water reabsorption by increasing expression of the apical Na+ channel (ENaC)
- Increases basolateral Na+ extrusion via Na/K/ATPase
How does the sympathetic nervous system act on the kidney?
- Reduce renal blood flow (vasoconstriction of renal artery)
- Stimulates Na+ reabsorption (NHE3 & Na/K ATPase) in PCT
- Stimulates renin release from JGA
In normal situations, prostaglandins have little effect.
Regardless, how does it act in RAAS?
- Vasodilates the afferent arteriole
- Enhances renin release
What stimulates the release of prostaglandins?
Release stimulated by vasoconstrictors:
- Angiotensin II
- Noradrenaline
- ADH
Prostaglandins and RAAS interact to stimulate each other.
What is the net effect of both of these substances?
- Systemic vasoconstriction
- Vasoconstriction of the efferent arteriole
- Vasodilation of afferent arteriole
- Preservation of GFR

What is the main role of ADH?
- Increases water reabsorption in distal nephron (AQP2) in order to control plasma osmolarity through water retention
- Concentrated urine formed
What stimulates the release of ADH?
- Plasma osmolarity
- Severe hypovolaemia
ADH is also called arginine vasopressin.
Why is this?
ADH also causes vasoconstriction
Atrial Natriuretic Peptide acts in the opposite direction of other neurohormonal regulators.
What are its 2 main actions?
- Causes vasodilation of afferent arteriole, increasing GFR
- Inhibits Na+ reabsorption especially in collecting duct, causing natriuresis

What stimulates the release of ANP and what inhibits its release?
- Low circulating blood volume = inhibits ANP release
- High circulating blood volume = stimulates ANP release
In terms of evolution, why is hypertension an anticipated problem?
- Mechanisms which increase/maintain BP are stronger than the mechanisms which reduce BP when it is too high
- Hence, volume depletion (dehydration or blood loss or sepsis) is more of a risk than hypertension
What is hypertension?
Hypertension is a persistent increase in blood pressure
Identify 2 pathological processes involving RAAS
- Secondary hypertension
- Secondary hyperaldosteronism (oedema)
Identify 4 clinical conditions resulting in secondary hypertension
- Renovascular hypertension
- Coarctation of the aorta
- Primary hyperaldosteronism (Conn’s syndrome)
- Cushing’s syndrome
Describe the pathophysiology of renovascular disease
- Renal artery stenosis
- 1/both kidneys affected
- Due to atheroma (75%) or fibromuscular dysplasia (25%)
Identify 5 endocrine causes of hypertension
- Primary hyperaldosteronism (Conn’s syndrome)
- Cushing’s syndrome
- Liquorice
- Phaeochromocytoma
- Hyperthyroidism / Hypothyroidism


