Blood Pressure And Kidneys Flashcards
What is the relationship between salt intake (Na) and blood pressure?
The higher the Na intake , the higher the blood pressure.
Why are Na levels linked to blood pressure? PART 1
- Na is the major electrolyte of the extracellular fluid volume (ECFV).
- Increased blood volume leads to ventricular filling and increased stroke volume.
- Stroke volume is a major determinant of cardiac output.
Why are Na levels linked to blood pressure? PART 2
Regulating Na levels affects blood volume, which makes it a long-term control of blood pressure.
How does the CVS control Na levels? PART 1
- change in Na+ intake so change in ECFV
- activates afferent pathways (such as cardiac volume receptors, baroreceptors, renal arterial pressure)
How does the CVS control Na levels? PART 2
- activates efferent pathways (neuronal, such as the sympathetic nervous system, hormonal, such as RAAS or ANP, or haemodynamic: changing GFR, pressure natriuresis)
- changes renal Na+ output
How does the RAAS affect Na levels in the blood?
- Aldosterone causes water retention in the kidney by reabsorbing more Na+ back into circulation.
- Increased RAAS activity, increased Na reabsorption.
List some factors that stimulate renin release.
- decreased BP and decreased renal blood volume
- decreased Na levels in the macula densa
- sympathetic nerve activation of β1 adrenoreceptors
Describe the role of aldosterone in the kidney.
- Acts at steroid receptors inside cells
- Increases the expression of ENaC and the Na/K pump.
- Increases Na reabsorption at distal tubular sites so increased renal K excretion.
What is the result of excess aldosterone and why?
Hypokalaemia.
→ K+ into the cell via Na+/K+ pump
→ K+ passively diffuses out of the cell into the lumen of tubule
Summarise the renal effects of ANP.
- natriuresis (increased Na excretion)
- diuresis (increased water excretion)
Summarise the vascular effects of ANP.
Vasodilation by the stimulation of PKG in vascular smooth muscle cells, decreasing systemic BP
Summarise the hormonal effects of ANP
decreases renin and aldosterone secretion
What system does ANP oppose?
RAAS
Describe pressure natriuresis.
- Rise in medullary capillary pressure
- Increases fluid filtration and interstitial pressure
- Prevents tubular reabsorption.
- Increase in renal Na+ excretion due to a rise in renal arterial pressure
Why does GFR not increase during natriuresis?
Renal arterial pressure doesn’t increase GFR
- Due to autoregulation
What is the clinical importance of the control of blood pressure by the kidney?
If uncontrolled, can cause hypertension
When is hypertension present?
- Systolic pressure > 140 mmHg
- Diastolic pressure is > 90 mmHg.
What are the two types of hypertension?
- Primary/ essential (unknown cause, > 90% of the cases)
- Secondary (identifiable cause, 5-10% of cases),
What are some secondary causes of hypertension?
- excess renal Na re-absorption
- Liddle’s Syndrome
- Conn’s Syndrome
- renal artery stenosis
What may essential hypertension involve?
Abnormal handling of Na+ balance
What is Liddle’s Syndrome?
Genetic form of high blood pressure associated with the epithelial Na+ sodium channel (ENaC)
How does Liddle’s Syndrome lead to hypertension?
- increases ENaC activity
- increases renal Na retention
- suppresses renin/aldosterone
What is Conn’s Syndrome?
Overproduction of aldosterone by an adrenal gland tumour (adenoma)
How does Conn’s Syndrome lead to hypertension?
- increased renal Na reabsorption, due to increased ENaC
- increased ENaC increases Na/K ATPase, which increases K excretion
- ECFV expansion, which decreases renin secretion
