Lecture 21: Renal System 3 Flashcards
Describe where/when renin is secreted from the kidneys. What 3 factors mediate release?
Renin secreted from granular cells in the afferent arteriole. Secreted in response to 3 factors: sympathetic innervation (NE & beta-adrenergic receptors), macula densa sense low NaCl in the tubular fluid, baroreceptors in the afferent arteriole sense decreased stretch (less renal blood flow)
Explain how ANGII is produced
Renin is an enzyme that converts circulating angiotensinogen to angiotensin I. Angiotensin I goes through the blood to the pulmonary circulation where it encounters angiotensin converting enzyme that turns ANGI to ANG II.
Describe the 4 effects of ANG II
ANG II is a potent vasoconstrictor of vascular smooth muscle (global effect) via the AT1 receptor and Gq pathway.
Increases Na+ reabsorption in the distal tubule and collecting duct via aldosterone release from the adrenal cortex.
Increases Na+ reabsorption in the proximal tubule via increased expression of NHE via the Gi pathway.
Cause increased thirst and salt appetite in the midbrain.
How does aldosterone work? What are its effects?
Aldosterone will either secrete K+ or absorb Na+
Aldosterone increases abundance of NCC channels in early DT, increases expression/activity of ENaC in the late DT as well as activity of Na/K ATPases
Secretion of K+: aldo inhibits NCC usually in the early DT. This means more gets deflected to the DT/CD. at this point, aldo activates ENaC. This pulls Na in, Na/K pushes it out and brings K in to provide gradient for K secretion.
Na reabsorption: presence of ANGII reduces inhibition of NCC, get Na reabsorption in early DT. DT/CD have same function, but just clean up the rest of the Na. Paracellular reabsorption of Cl.
How is ADH released? how does it function?
released by posterior pituitary based on ECF osmolarity, ECF volume, and ANG II
inserts more AQP2 receptors by ADH binding to V2 receptors, leads to Gs pathway
