RAAS and blood pressure

Question 1

What is a normal blood pressure?

Answer 1

80-180mmHg systolic

120 is the reference

Question 2

How is BP maintained by myogenic feedback?

Answer 2

High BP leads to increased renal blood flow which stretches the VSM in the Afferent arteriole

Low BP leads to a reduced renal blood flow which relaxes the VSM in the afferent arteriole

Question 3

What is the mechanism for stretch influencing vasomotor tone?

Answer 3

Stretch stimulates calcium entry into VSMC and release from internal stores – vasomotor tone influenced

Question 4

How is BP maintained by tuboglomerular feedback?

Answer 4

Flow through the distal tubule feeds back to the same nephron to increase GFR

Question 5

How does the macula densa cause afferent vasodilation?

Answer 5

If NaCl low the cells at macula densa generate less adenosine which stimulates decrease of intracellular Ca in VSMC in afferent and leads to afferent vasodilatation. The reverse is also true

Question 6

If there is a hemorrhage what mechanisms kick in to maintain BP?

Answer 6

Sympathetic Nervous System (vasoconstrict)
Angiotensin II, as described (vasoconstrict)
Endothelin to some extent (vasoconstrict)
Prostaglandins (vasodilate afferent)
Nitric Oxide (vasodilate afferent)

Question 7

What is the effect of efferent arteriole constriction on reabsorption?

Answer 7

In addition, efferent arteriole constriction reduces peritubular capillary pressure (downstream from efferent arteriole). This independently stimulates increased tubular reabsorption of Na and thus water to help fluid retention and boost pressure.

Question 8

What changes does angiotensin II make to the cells of the tubules?

Answer 8

Insertion of Na+ channels in renal tubules via AT1
In the Proximal tubule apical Na+/H+ exchanger and basolateral Na+(HCO3-)3 and Na+K+ATPase
In the Thick ascending limb apical Na+/H+ exchanger and Na+K+2Cl-
In the Collecting duct: Epithelial Na+ channel (ENaC)

Question 9

In cardiac disease what does angiotensin do?

Answer 9

Contraction of vascular smooth muscle, producing vasoconstriction.
Increased sodium reabsorption in proximal tubule
Stimulation of hypertrophy of the myocardium and vascular smooth muscle.
Enhanced sympathetic adrenergic tone and increased release of noradrenaline from sympathetic nerve terminals.

Question 10

What are the actions of ang II in renal disease?

Answer 10

Increased glomerular capillary pressure (primarily via efferent renal arteriolar vasoconstriction).
Increased glomerular protein loss (via increased permeability and vasoconstriction of efferent artery).
Activation of inflammatory cells (via proinflammatory mediators).

Question 11

Angiotensin II may be involved in the development of systemic hypertension associated with some renal disease, why is this a problem?

Answer 11

Hypertension can contribute to progressive renal damage due to the loss of intrinsic autoregulation of intraglomerular pressure that occurs with chronic renal disease.

Question 12

So by using ACE inhibitors sytemically to inhibit angiotensin II production results in…

Answer 12

Lack of vasoconstriction.
Reduced aldosterone production leads to decreased renal salt and water retention which will prevent or reduce oedema
Inhibit hypertrophy of myocardium and vascular smooth muscle
Decreased water intake.
Decreased sympathetic activation.
Decreased vasopressin release.

Question 13

ACE inhibitors are considered balanced vasodilators, what does this mean?

Answer 13

They are both arteriolar and venous dilators

Question 14

ACE inhibitors can prevent hypertrophy and fibrosis of what tissue?

Answer 14

heart and blood vessels,

Reduce glomerular capillary hypertension in kidney = reduce proteinuria = protect nephron loss and prevent replacement with collagen