Question

A
RETURN TO HOMEOSTASIS
Restoration of normal
blood pressure
INPUT
Decreased arterial
pressure in kidney
Increases glomerular
blood flow and pressure
OUTPUT
Increases blood
volume and blood
Nat level
Stimulates juxtaglomerular
apparatus to send a signal
to afferent arterioles
Stimulates juxtaglomerular
apparatus to secrete renin
into the blood
Vasodilation of
efferent arterioles
Stimulates
juxtaglomerular
apparatus to secrete
renin into the blood
Angiotensin Iis converted
into angiotensin II​

Answer 1

Answer:

Function

An important interplay between RBF and proper kidney functioning is the renin-angiotensin-aldosterone system, also known as RAAS. Renin is secreted by juxtaglomerular cells in response to decreased renal arterial pressure, increased renal sympathetic activation from beta-1 adrenergic receptors, or decreased sodium delivery to macula densa cells.[1] Renin converts angiotensinogen which is made in the liver to angiotensin I. Angiotensin-converting enzyme (ACE) produced by the lungs then converts angiotensin I into angiotensin II. Angiotensin II plays many different roles. It acts on angiotensin II receptors to induce vasoconstriction and increase blood pressure. It also preferentially constricts efferent arterioles to increase the filtration when RBF is low. Angiotensin II also induces the expression of aldosterone in the adrenal cortex which increases sodium channel insertion, increases the activity of sodium/potassium pump, enhances potassium and hydrogen excretion in principal cells. These simultaneous effects act to create a gradient for sodium and water reabsorption. Another important effect of angiotensin II is to increase expression of antidiuretic hormone (ADH) in the posterior pituitary which inserts aquaporin channels on the apical membrane of principal cells for water absorption. Interestingly, it stimulates the hypothalamus to increase thirst, which may be one of the body’s mechanisms of signaling low volume states or dehydration.[2]

Mechanism

RBF originates at the hilum of the kidney through the renal artery. From the segmental artery to the interlobar artery, blood arrives parallel to the corticomedullary junction in the arcuate artery. This gives rise to the interlobular arteries that radiate toward the surface. Afferent arterioles branch off which ultimately leads into the glomerulus of Bowman’s capsule. From here, efferent arterioles begin to form the venous system and subdivide into another set of capillaries known as the peritubular capillaries. Blood then leaves the kidney and enters the venous circulation. However, efferent arterioles that are located above the corticomedullary border travel downward into the medulla. They further divide into vasa recta which surround the Loop of Henle. The purpose of these vessels is to supply capillaries located in the medulla. Differences between blood flow of the renal cortex and medulla play a significant role in the regulation of tubular osmolality. High blood flow and the peritubular capillaries in the cortex maintain a similar interstitial environment of the renal cortical tubules with that of blood plasma. However, in the medulla, the interstitial environment is different than that of blood plasma.[3] This crucial difference plays a significant role in the medullary osmotic gradient and regulation of water excretion.

RBF comprises roughly 20% of the total cardiac output; it is roughly 1 liter per minute. Flow in the kidney follows the same hemodynamic principles seen elsewhere in other organs. RBF is proportional to the difference in pressures between the renal artery and vein, but inversely proportional to the vasculature resistance. Resistance is influenced by whether a vessel is in series or in parallel. Because the kidney has vasculature that is parallel, the total resistance is decreased, thus accounting for the higher blood flow.