Volume of regulation: Blood pressure and the kidneys

Question 1

explain the relationship between salt intake and blood pressure

Answer 1

-higher Na+ intake excretion–> higher blood pressure

Question 2

Why are Na+ levels linked to blood pressure

Answer 2

-Na+ is the major electrolyte of the extracellular fluid volume (ECFV), interstitial fluid, plasma fluid, cerebrospinal fluid.
-intracellular volume has little Na+ due to Na/K+ ATPase.
-BP= CO x TPR. SV is a major deteminant of CO
-increased blood volume leads to ventricular filling and increased SV
-regulate Na levels- blood volume- long term control of blood pressure
-in contrast to baroreceptors- short term control

Question 3

How does the CVS control Na+ levels

Answer 3

-we control Na+ output by conserving Na+
-Na conservation happens through the RAAS pathway
-major factors that stimulate renin release
-reduced BP and BV; reduced renal blood flow (afferent arteriole mechanoreceptors
-reduced Na levels at macula densa
-sympathetic nerve activation of B1-adrenoceptors
-due to changes in baroreceptors activity, and cardiac volume receptors

-Na conserve; aldosterone (steroid hormone synthesised in Zona glomerulosa of adrenal gland; released by action of Ang II)

Question 4

Explain Na+ excretion; cardiac natriuretic peptides (oppose RAAS)

Answer 4

-atrial natriuretic peptide (ANP) and brain natriretic peptide (BNP) found in specialised cardiac myocytes; released by increased cardiac filling pressures (ECFV)

Question 5

Give a summary of effects of ANP

Answer 5

Renal effects:
-natriuresis (increased Na excretion)
-diuresis (increased H20 excretion)

Vasculature effects:
-vasodilation by stimulaton of PKG in VSMCs- increased systemic BP

Hormonal:
-decreased renin and aldosterone secretion
-Na excretion; pressure natriuresis

Question 6

explain Na+ excretion (pressure natriuresis)

Answer 6

-increase renal Na+ excretion due to a rise in renal arterial pressure
-GFR changes not involved as renal arterial pressure does not increase GFR due to powerful renal arterial auto-regulation
-rise in medullary capillary pressure
-increases fluid filtration and interstitial pressure
-prevent tubular reabsorption

Question 7

explain the control of blood pressure by the kidney as clinical importance

Answer 7

-Hypertension present when; systolic > 140mmGg and diastolic >90mmHg
-Classified as:
* secondary (identifiable cause in 5-10% of the cases)
* essential (unknown cause in over 90% of cases)

secondary causes of hypertension involve:
-excess renal Na+ reabsorption and abnormaliies in hormone secretion
-Liddle’s syndrome
-Conn’s syndrome
-Renal artery stenosis
-essentail hypertension may involve abnormal handing of Na+ balance

Question 8

explain Liddle’s syndrome

Answer 8

-a rare genetic form of high blood pressure associated in epithelial Na+ channel (ENaC).
-increase ENaC activity
-increase renal Na+ retention
-suppresses renin/aldosterone
-increased ECFV + increased BP with low renin/aldosterone levels

Question 9

explain Conn’s syndrome aka primary aldosteronism

Answer 9

-overproduction of aldosterone by adrenal gland tumour (adenoma)
-high blood pressure- low renin levels- high aldosterone

In comparison; Addison’s disease, insufficient release of aldosterone, chronic Na+ loss, large ECFV, severe hypertension, leading to collapse and death
-Renal artery stenosis- abnormal narrowing of vessels

-essential hypertension
-agents that decrease RAAS are frontline anti-hypertensive treatments. Ang II receptor blockers.
-high Na+ intake linked to high blood pressure