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Flashcards in Blood Pressure and the Kidneys Deck (14)
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Simply put, what is the relationship between salt intake (Na) and blood pressure?

The higher the Na intake excretion, the higher the blood pressure.


Why are Na levels linked to blood pressure?

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.

Therefore, regulating Na levels affects blood volume, which makes it a long-term control of blood pressure. This is in contrast to short-term control, baroreceptors, which control it minute to minute.


How does the CVS control Na levels?

- there is a change in Na+ intake
- leading to a change in ECFV
- this activates afferent pathways (such as cardiac volume receptors, baroreceptors, renal arterial pressure)
- this then activates efferent pathways (neuronal, such as the sympathetic nervous system, hormonal, such as RAAS or ANP, or haemodynamic: changing GFR, pressure natriuresis)
- this then 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 the circulation.

This means with increased activity of the RAAS system, we can increase Na reabsorption.
Renin secretion is central to the control of Na.


List some factors that stimulate renin release.

- decreased BP and decreased BV, this leads to decreased renal blood flow, sensed by afferent arteriole mechanoreceptors
- decreased Na levels in the macula densa
- sympathetic nerve activation of β1 adrenoreceptors


Describe the role of aldosterone in the kidney.

It acts at steroid receptors inside cells and increases the expression of ENaC and the Na/K pump.
This increases Na reabsorption at distal tubular sites, which results in increased renal K excretion. This means that excess aldosterone can lead to hypokalaemia.


Summarise the effects of ANP.

- natriuresis (increased Na excretion)
- diuresis (increased water excretion)

- vasodilation by the stimulation of PKG in VSMCs, decreasing systemic BP

- decreases renin secretion
- decreases aldosterone secretion

The ANP system opposes the RAAS.


Describe pressure natriuresis.

There is an increase in renal Na+ excretion due to a rise in renal arterial pressure. GFR changes are not involved as renal arterial pressure doesn't increase GFR due to powerful renal arterial auto-regulation.
It is a rise in medullary capillary pressure, which increases fluid filtration and interstitial pressure and prevents tubular reabsorption.


What is the clinical importance of the control of blood pressure by the kidney?

If uncontrolled, it can cause hypertension.

Hypertension is present when the systolic pressure is > 140 mmHg and/or the diastolic pressure is > 90 mmHg.
It can be classified as primary/ essential (unknown cause, > 90% of the cases) or secondary (identifiable cause, 5-10% of cases),

Some secondary causes of hypertension involve:
- excess renal Na re-absorption and abnormalities in hormone secretion
- Liddle's Syndrome
- Conn's Syndrome
- renal artery stenosis

Primary/ essential hypertension may involve the abnormal handling of Na+ balance.


What is Liddle's Syndrome, and how does it produce high blood pressure?

It is a rare genetic form of high blood pressure associated with the epithelial Na+ sodium channel (ENaC).

- it increases ENaC activity
- it increases renal Na retention
- it suppresses renin/aldosterone


What is Conn's Syndrome, and how does it produce high blood pressure?

It is the overproduction of aldosterone by an adrenal gland tumour (adenoma).

With the raised aldosterone:
- there is increased renal Na reabsorption, due to (?) increased ENaC
- the increased ENaC increases Na/K ATPase, which increases K excretion
- this causes an ECFV expansion, which decreases renin secretion


In comparison, how does Addison's Disease affect blood pressure?

With Addison's Disease, we have the insufficient release of aldosterone, leading to chronic Na loss. This causes a large decrease in ECFV, severe hypotension, leading to collapse and death.


Describe renal artery stenosis and how it produces high blood pressure.

Renal artery stenosis is the abnormal narrowing of the vessel.

There is a decrease in renal artery pressure due to the pressure drop caused by the stenosis; this decreases blood flow.
This stimulates renin secretion, which stimulates Angiotensin II production. Angiotensin II increases aldosterone and vasoconstriction, which lead to Na retention and high blood pressure.


Describe essential hypertension.

Its causes are unknown.

Genetic predisposition and environmental factors (such as lifestyle: exercise, diet: salt intake, alcohol, diabetes) lead to intermediate phenotypes that result in an increased blood pressure.

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