Answer
The extrinsic GFR control mechanisms are located outside the kibneys. They include neural and hormonal systems. The neural component is the sympathetic nervous system; the hormonal component comprises the renin-angiotensin- aldosterone system, and antidiuretic hormone (ADH) from the posterior pituitary.
The function of sympathetic control of kidney blood vessel diameters is to maintain a blood hydrostatic pressure (BP) that can keep GFR from falling too low. If blood pressure (hydrostatic pressure), falls below 20% of normal rate, glomerular filtration may stop altogether wilh consequent health threatening anuria.
Work Step by Step
1. Sympathetic Nervous system control:
If If the volume of the extracellular fluid is normal the sympathetic system is at rest--blood vessels are dilated and intrinsic regulation of GFR is adequate. However, if extracellular fluid (blood) volume falls-- as my happen in cases of severe hemorrhage--the body shunts blood to vital organs (brain heart). When this happens kidney blood flow may get so low that kidney damage may occur. In such cases the fall of BP causes the release of catecholamine neurotransmitters from sympathetic nerve endings and from the adrenal medulla. Nor-epinephrine and epinephrine will cause vascular smooth muscles to contract and constrict blood vessels. As a consequence peripheral vascular resistance is increased. which increases friction and elevates BP, and GFR towards normal levels.
2. The second important extrinsic mechanism in the regulation of GFR is the renin-angiotensin-aldosterone system:
When blood pressure becomes abnormally low this stimulates the glandular cells of the juxtaglomerular apparatus to release renin. Also, if constriction of afferent blood vessels cause blood flow to the kidneys to fall, this will decrease GFR and the flow rate of filtrate will decrease . When the macula densa cells detect a low concentration of Na+ in the filtrate , they will cause the granular cells to release renin
Renin converts angiotensinogen of the liver to antiogensin I. The angiotensin converting enzyme (ACE) from the lungs then converts angiotensin I to angiotensin II. Angeotensin II has many actions: in the first place it acts on the adrenal cortex to cause the release of aldosterone. it also acts on distal convoluted tubules (DCTs) to increase the resorption of sodium and water, and induces thirst by its influence on the hypothalamus.; finally, it stimulates the posterior pituitary to release the antidiuretic hormone (ADH), ADH raises blood pressure by increases kidney fluid resorption and increasing arterial vascular resistance. Elevation in blood pressure increases GFR.
