Question

1. Explain the relationship between blood volume and blood pressure.

2. List the functions of the hormones/enzyme listed below: • Aldosterone • Renin • Antidiuretic Hormone (ADH)

3. Heart failure is when the heart cannot eject enough blood to meet the body’s oxygen and blood demand. Describe what would be the expected response from the RAAS (renin-angiotensin-aldosterone system) system in a patient with heart failure.

4. How is RAAS upregulation detrimental to heart failure patients over time?

5. How does the sodium ion influence blood volume and blood pressure?

6. Give three examples of pathologies in which there is an upregulation of RAAS. Next to each one explain your reasoning.

7. How would high levels of angiotensin II (Ang II) affect someone with hypertension?

Answer 1

1. Cardiac output = Heart rate X stroke volume

Also Blood pressure = Cardiac output x systemic vascular resistance .

Cardiac output decides Systolic blood pressure and systemic vacular resistance Diastolic blood pressure .

2.Changes in blood volume affect arterial pressure by changing cardiac output.

3.An increase in blood volume increases central venous pressure. This increases right atrial pressure, right ventricular end-diastolic pressure and volume.

4This increase in ventricular preload increases ventricular stroke volume by the Frank-Starling mechanism

.5.Frank starling law states to that force of contraction of muscle is directly proportional to the stretching of Muscles fibres by enddiastolic volume .

6.An increase in right ventricular stroke volume increases pulmonary venous blood flow to the left ventricular, thereby increasing left ventricular preload and stroke volume.

7.An increase in stroke volume then increases cardiac output and arterial blood pressure.Increase cardiac output cause increase in Systolic Blood pressure .

Functions of hormones

1.ALDOSTERONE is secreted by the Zona glomerulosa layer of adrenal cortex and is stimulated by rise in Angiotensin 2 and potassium in blood .
Main functions of aldosterone
1. Sodium ( Na +) reabsorption and increase in total body sodium .
2.Potassium (K+) secretion and decrease in level of Potassium in plasma .
3.Hydrogen ( H+) secretion and promotes metabolic alkalosis
4.Bicarbonate production (Hco3) and promotes metabolic alkalosis
5 .Water reabsorption and cause volume expansion .

2.Renin - When there is low Blood pressure or decrease in MAP mean arterial pressure then Renin is released .

Renin convert Angiotensinogen To Angiotensin 1 and further to Angiotensin 2 through ACE angiotensin converyting enzyme .Angiotensin 2 act on AT receptor 1 and 2 and cause vasoconstriction . Also it increase the release of Aldosterone .Aldosterone actions already explained .

ADH -

ADH act on Principal cells of cortical collecting duct and and act on V2 receptor and through aquaporins cause facultative water absorption and increasing intravascular volume increasing sytolic blood pressure and through V1 receptors cause vasocontriction of blood vessels and increase in diastolic Blood pressure..

.​​​​​3a).When there is heart failure then there is Decreased in Cardiac output ,so effective blood volume is Decreased so the Glomerular filtration rate ,which results in Decreased delivery of Sodium in Macula densa cells and there is Activation of RAAS .Renin Angiotensinogen Aldosterone Axis .

b)Renin convert Angiotensinogen To Angiotensin 1 and further to Angiotensin 2 through ACE angiotensin converyting enzyme .Angiotensin 2 act on AT receptor 1 and 2 and cause vasoconstriction . Also it increase the release of Aldosterone .

c)Aldosterone cause sodium and water retention and potassium excretion.AT 2 cause vasoconstriction so decreased GFR and further activation of RAAS and more and more sodium and water rebasorptiom occur and increase in blood volume and increase in blood pressure .

4.Persistent and excessive RAAS activation causes adverse cardiac remodeling and contributes to fluid retention with signs and symptoms of congestion.

Cardiac remodelling is because of increased aldosterone levels and also there is increase in sympathetic activity present .

For this reason, PRA and plasma aldosterone levels are of potential interest not only as markers of disease severity but as mediators of heart failure progression.