In: Anatomy and Physiology
Like all viral pathogens, severe acute respiratory syndrome coronavirus 2, or SARS-CoV 2 (I know, how topical), requires a cell surface receptor in order to invade a given host cell. For SARS-CoV 2, this receptor is actually the enzyme Angiotensin Converting Enzyme 2, or ACE2. ACE2 is responsible for downregulation of the Renin-Angiotensin-Aldosterone System by deactivation of Angiotensin II. Explain the RAAS in detail, including the roles played by kidneys and the lungs, and then explain what effects using recombinant human ACE2, or rhACE2, to treat acute respiratory distress syndrome could have on blood pressure.
Renin–angiotensin–aldosterone system(RAAS), is a hormone system that regulates blood pressure and fluid and electrolytebalance, as well as systemic vascular resistance.
When renal blood flow is reduced , juxtaglomerular cells in the kidneys convert the precursor prorenin into renin and secrete it to circulation.
Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I.
Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs.
Angiotensin II is a potent vasoconstrictivepeptide that causes blood vessels to narrow, resulting in increased blood pressure.
Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex.
Aldosterone causes the renal tubulesto increase the reabsorption of sodium and causes the reabsorption of water into the blood, while at the same time causing the excretion of potassium.
This increases the volume of extracellular fluid in the body, which also increases blood pressure.
In the kidneys, angiotensin II constrict glomerular arterioles, having a greater effect on efferent arterioles than afferent. As with most other capillary beds in the body, the constriction of afferent arterioles increases the arteriolar resistance, raising systemic arterial blood pressure and decreasing the blood flow.
While using the recombinant human ACE 2 to treat ARDS, Within the RAS, angiotensin converting enzyme (ACE) converts angiotensin I into the vasoconstrictor Ang II, which mediates its effects via the angiotensin type 1 receptor (AT1R). Ang II has actions to raise blood pressure through vasoconstriction and salt and water retention.