Autoregulation of GFR & RBF in animals
RBF and GFR remains almost relatively constant when the systemic arterial pressure changes from 75 mm Hg to 160 mm Hg. This ability of the RBF and GFR to resist severe changes in the arterial pressure is called as ‘autoregulation of RBF and GFR’. It is an intrinsic mechanism which is independent of the nerve supply. Two theories have been proposed to explain autoregulation- Myogenic Theory and JG Theory in animals.
Myogenic theory
According to this theory, the increase in BP would expand an artery and it would respond by contracting. In this way, RBF would be decreased and glomerular HP reduced. The reduced glomerular HP reduces GFR.
A reduction in BP causes less tension and blood vessel would dilate to increase RBF and glomerular HP with subsequent increase in GFR. That is, when arterial pressure rises, arterioles are stretched, once stretched, arterioles contract forcefully. This decreases RBF to normal level. A decrease in arterial pressure dilates the blood vessels which increases RBF and GFR.
JG theory
Juxta glomerular apparatus (JGA) contains renin (a proteolytic enzyme). Renin is released when- Reduced GFR, Reduced glomerular pressure and Increased sympathetic stimulation of kidneys.
The last two occur during low BP and always cause reduced GFR. Reduced GFR causes reduced sodium concentration in the tubular fluid as it flows past the macula densa and this low sodium causes release of renin from JGA. Once renin is released from JG cells it diffuses into the blood of afferent arteriole and circulates through out the body.
In the blood it splits a renin substrate, an alpha 2 globulin to angiotensin I, a decapeptide. Angiotensin I is rapidly converted to angiotensin II by converting enzyme which is present in high concentration in the lungs. Angiotensin II is a powerful vasoconstrictor and causes vasoconstriction through out the body thereby increasing the BP. Some amount of Angiotensin II is formed in the glomerulus, i.e. in the JG cells.
Angiotensin II causes marked constriction of efferent arteriole which increase glomerular pressure and also GFR but decreases RBF. Increase in pressure increases GFR but decrease in blood flow decreases GFR and in effect there is a less change in GFR.
Decreased blood flow to peritubular capillaries decreases peritubular pressure, which causes increased tubular reabsorption, so excretion is reduced. When efferent arterioles are constricted, GFR is normal, excretion of waste products such as urea, creatinine is normal. At the same time there is an increase in tubular reabsorption of salt and water. Therefore, effect of angiotensin is to conserve water and salt while allowing normal excretion of waste products.
Angiotensin II constricts the efferent arterioles to a greater extent than that of afferent arteriole. Reabsorption of water and salt by renin-angiotensin system helps to control arterial BP.
Tubulo-glomerular feedback
The mechanism of tubulo glomerular feedback (TGF) is also associated with the JG theory of autoregulation. TGF refers to alteration in GFR with changes in the tubular flow rate.
It is mediated by the macula densa cells of the JG apparatus. These cells sense changes in the sodium and chloride to their region. If GFR is increased because of increased glomerular HP there will be increase in macula densa flow and sodium and chloride delivery intiates a response that returns GFR and macula densa flow towards the normal by afferent arteriole constriction (which lowers glomerular HP).
When renal blood flow falls too low it decreases the GFR thereby, decreases in sodium and chloride delivery to the distal tubule which initiate a signal from macula densa and dilates the afferent arterioles and it increases glomerular blood flow and glomerular pressure. This causes the GFR to increase to normal.