Regulation of Kidney Function

An excessive loss of fluid from the body can activate osmoreceptors which stimulate the hypothalamus to release ADH. Hence, switch on osmoreceptors. ADH causes an increase in blood pressure. An increase in blood pressure can increase the glomerular blood flow and thereby the GFR.

(a), (b) and (c) are correct. ADH (vasopressin) is released by the hypothalamus through the neurohypophysis, not the adenohypophysis, and it causes vasoconstriction, not vasodilation.

The adrenal cortex secretes mineralocorticoids like aldosterone, which increase the reabsorption of $Na^+$ and water from the renal tubules. This prevents diuresis. (ANF causes vasodilation, decreased renin reduces reabsorption, and undersecretion of ADH causes more water loss.)

Renin from the juxtaglomerular apparatus converts angiotensinogen to angiotensin I, which is converted to angiotensin II.
This increases reabsorption of $Na^+$ and water, raising blood pressure and producing concentrated urine — not dilute urine.

Aldosterone acts on the distal parts of the tubule and increases the reabsorption of $Na^+$ and water.

The kidney regulates its own filtration rate through the juxtaglomerular apparatus (JGA).
A fall in GFR (or in glomerular blood flow or pressure) directly activates the juxtaglomerular (JG) cells to release renin.
Renin converts angiotensinogen in the blood into angiotensin I, which is further converted into angiotensin II.
Angiotensin II is a powerful vasoconstrictor that raises glomerular blood pressure and thereby GFR; it also stimulates the adrenal cortex to release aldosterone.
So aldosterone release is a later, indirect step, and vasopressin release is triggered by osmoreceptors responding to changes in body fluid volume and concentration.
Hence a fall in GFR activates the juxtaglomerular cells to release renin.

Osmoreceptors in the body respond to changes in blood volume, body fluid volume and ionic concentration.
When a person drinks a lot of water, the body fluid volume increases and its osmolarity falls; this switches off the osmoreceptors and suppresses ADH release. Less water is reabsorbed and dilute urine is passed. This statement is correct.
In summer, heavy loss of water by evaporation activates the osmoreceptors and stimulates (not suppresses) ADH release, so that water is conserved.
Exposure to cold reduces sweating and decreases ADH release, which is why more urine is passed in cold weather.
Angiotensin II is formed when the JG cells release renin in response to a fall (not an increase) in glomerular blood flow or pressure.
Hence the correct statement is that ADH release is suppressed when someone drinks a lot of water.

Angiotensinogen is a plasma protein produced and secreted into the blood by the liver cells.
When the glomerular blood flow or blood pressure falls, the juxtaglomerular (JG) cells of the kidney release the enzyme renin.
Renin converts angiotensinogen in the blood into angiotensin I.
Angiotensin I is converted into angiotensin II by the angiotensin converting enzyme, mainly in the lungs.
Angiotensin II is a powerful vasoconstrictor; it raises the glomerular blood pressure and stimulates the adrenal cortex to release aldosterone.
So the JG cells secrete renin, not angiotensinogen, and the macula densa cells only sense the composition of the filtrate.
Angiotensinogen is produced and secreted by the liver cells.