Final answer:
A decrease in capsular hydrostatic pressure due to glomerular damage would impede the filtration process, leading to a decrease in the movement of water and solutes into the glomerular filtrate. This condition would not deactivate the RAAS but could potentially activate it to compensate for the reduced filtration.
Step-by-step explanation:
A decrease in capsular hydrostatic pressure due to damage to the glomerulus would decrease the movement of water and solutes into Bowman's capsule, also known as the glomerular filtrate. This happens because hydrostatic pressure is a driving force for the movement of fluid across the semi-permeable membrane of the glomerulus into Bowman's capsule. When the pressure drops due to damage, less filtrate is formed, resulting in a reduced glomerular filtration rate (GFR). Additionally, this drop in pressure could lead to less effective filtration of blood and reduced removal of nitrogenous wastes, such as urea. Contrary to enhancing the movement of water solutes into Bowman's capsule, the filtration process would be impeded.
Furthermore, such a condition does not shut off the renin-angiotensin-aldosterone mechanism (RAAS). Instead, a decrease in GFR could potentially activate the RAAS as it attempts to increase blood pressure and fluid retention to counteract the loss of filtration. This response aims to maintain homeostasis in the body. The RAAS helps to control blood pressure and the balance of fluids and electrolytes in the body by adjusting the volume of water that is reabsorbed in the kidney and thus the volume of urine produced.
Overall, the correct response to the question is that a decrease in capsular hydrostatic pressure as a result of damage to the glomerulus would decrease movement of water and solutes into the glomerular filtrate.