Question

Renin is released by
A. Cortical nephron
B. Collecting duct
C. Juxtaglomerular apparatus
D. Pelvis

Answer 1

A fall in GFR can activate the JG cells to release renin, which converts angiotensinogen to angiotensin-I and further to angiotensin-II. Angiotensin-II is a powerful vasoconstrictor. It increases glomerular blood pressure and hence increases GFR.

Complete answer: Low blood pressure triggers the renin-angiotensin-aldosterone pathway.
Juxtaglomerular apparatus(JGA) operates a multi hormonal renin-angiotensin-aldosterone system(RAAS) which occurs in the following way. A fall in GFR activates the JG cells to release renin, which converts angiotensinogen to angiotensin-I and further to angiotensin-II. Angiotensin-II is a powerful vasoconstrictor. It increases glomerular blood pressure and hence increases GFR. Angiotensin-II increases blood volume by:
a) Increasing reabsorption of sodium ions and water from PCT.
b) Stimulating the release of aldosterone which reabsorbs sodium ions and water from the DCT.
ADH/vasopressin efficiently monitors and regulates the functioning of kidneys. ADH is so-called because diuresis means urine production and this hormone prevents wide swings in water balance, helping to avoid dehydration or water overload. ADH secreted by the hypothalamus is released into the blood from posterior pituitary (Neurohypophysis). Release of ADH causes increased reabsorption of water in the distal part of kidney tubules i.e. DCT and CD prevent diuresis.

Note: ADH results in facultative reabsorption of water. ADH also has a constrictor effect on blood vessels causing an increase in blood pressure and ultimately an increase in GFR. An increase in fluid volume can switch off osmoreceptors and release of ADH.