Principal Cells:
Have receptors for both Antidiuretic Hormone (ADH) and Aldosterone reabsorb Na+ & Cl- secrete K+
Intercalated Cells:
Play a role in the homeostasis of blood pH reabsorb K+ and HCO3- secrete H+ & urea
In contrast to earlier segments of the nephron, Na+ passes through the apical membrane of the principal cells via Na+ leakage channels rather than by means of symporters or antiporters. The concentration of Na+ in the cytosol remains low, as usual because the Na+/K+ pumps actively transport Na+ across basolateral membranes. Then Na+ passively diffuses into the peritubular capillaries from the interstitial spaces around the tubule cells. Normally reabsorption in the PCT and the loop of Henle return most of the filtered K+ to the bloodstream. To adjust for varying dietary intake of K+, and to maintain stable levels of K+ in body fluids, principal cells secrete a variable amount of K+ through K+ leakage channels .
Hormonal Regulation of Tubular Reabsorption and Tubular Secretion
5 hormones affect the extent of Na+, Cl-, Ca++ and water reabsorption as well as K+ secretion by the renal tubules. They are: Angiotensin II, Aldosterone, Antidiuretic Hormone (ADH) (Vasopressin), Atrial Natriuretic Peptide (ANP), Parathyroid Hormone (PTH).
(1&2) Renin-Angiotensin-Aldosterone System
When blood volume and blood pressure decrease, the walls of the afferent arterioles are stretched LESS, and the juxtaglomerular cells secrete the enzyme Renin into the blood. This is also accomplished by sympathetic stimulation of the juxtaglomerular cells. Through a series of reactions using renin, Angiotensin Converting Enzyme (ACE) converts Angiotensin I to Angiotensin II which is the active form of the hormone.
Angiotensin II affects renal physiology in 3 main ways :
1. It decreases glomerular filtration rate by causing vasoconstriction of the afferent arterioles.
2. It enhances reabsorption of Na+, Cl-, and water in the PCT by stimulating the activity of the Na+/H+ Antiporters.
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