Critical Care Medicine-Endocrine Disorders>>>>>Renin-Angiotensin-Aldosterone System
Question 3#

An 18-year-old male with multiple stab wounds to his abdomen is brought by ambulance to the trauma bay. He is bleeding profusely, with HR 128 beats/min, BP 72/41 mm Hg, SpO2 92% on 15 L oxygen via nonrebreathing face mask. Of the following statements regarding this patient’s renin-angiotensin-aldosterone system (RAAS), which is FALSE? 

A. Decreased oxygenation in the macula densa activates the RAAS
B. Increased conversion of angiotensin I to II via renin results in angiotensin (AT1)-receptor–mediated vasoconstriction of arteriolar smooth muscle
C. Angiotensin II has a greater effect on efferent glomerular arterioles than afferent, preserving glomerular pressure
D. Aldosterone release promotes sodium and water retention in the kidneys leading to greater volume retention

Correct Answer is A

Comment:

Correct Answer: A

There are many compensatory biological and neuroendocrine mechanisms in response to acute hypovolemic shock. In the juxtaglomerular apparatus, renin is released in response to three stimuli:

  1. Low arterial blood pressure, which activates the baroreceptors in the afferent arterioles.
  2. Decreases in chloride ion concentration in the distal tubules, secondary to decreased renal perfusion and glomerular filtration rate.
  3. β1-adrenergic receptor activation via catecholamines and sympathetic nervous system activity. 

Renin hydrolyzes angiotensinogen into angiotensin I, which is further cleaved in the lungs by endothelial-bound ACE into angiotensin II, a potent vasoconstrictor which acts directly on the AT1-receptor on arteriolar smooth muscles to maintain systemic perfusion. Angiotensin II also acts on glomerular arterioles, with greater vasoconstrictive effect on efferent arterioles than afferent. This preserves glomerular pressure and the glomerular filtration rate in shock states.

Angiotensin II also stimulates the adrenal glands to release aldosterone, which triggers the epithelial cells in the distal tubule and collecting ducts of the kidney to increase reabsorption of sodium and water and excretion of potassium and hydrogen ions.

References:

  1. Bock HA, Hermle M, Brunner FP, et al. Pressure dependent modulation of renin release in isolated perfused glomeruli. Kidney Int. 1992;41:275.
  2. Lorenz JN, Weihprecht H, Schnermann J, et al. Renin release from isolated juxtaglomerular apparatus depends on macula densa chloride transport. Am J Physiol. 1991;260:F486.
  3. Heyeraas KJ, Aukland K. Interlobular arterial resistance: influence of renal arterial pressure and angiotensin II. Kidney Int. 1987;31:1291.