 Dear students, in this topic we shall discuss the renal regulatory mechanisms. The osmoregulatory function of mammalian kidney is regulated by a combination of nervous and hormonal controls. First we shall discuss the nervous controls in detail. The kidney is innervated with efferent sympathetic nerve fibers. These efferent sympathetic nerve fibers are supplied to the renal vasculature, renal tibials, juxta glomerular cells and renal pelvic wall. Their stimulation causes reduced renal blood flow, reduced urinary sodium excretion and increased renin secretion. These are also supplied with renal sensory nerves. They mainly innervate the renal pelvic wall. Their activation or stimulation elicits an inhibitory reflex causing a decrease in the efferent renal sympathetic nerve activity, which leads to natural uruses that is excretion of sodium in the urine. Dear students, now we shall discuss the hormonal controls of kidney functions. Hormones which affect kidney functions include anti-diuretic hormone, renin angiotensin aldosterone system, ROS, and arterial natriuretic peptide. The anti-diuretic hormone is released from posterior pituitary in response to an increase in the osmolarity above the set point which is about 300 milliosmole per liter. When anti-diuretic hormone reaches the kidney, its main targets are the loop of Henle, distal tubule and collecting ducts. Anti-diuretic hormone makes the epithelium more permeable to water. Its action results in increased water reabsorption, concentration of urine, reduced urine volume, and lowering back the blood osmolarity to the set point. The renin angiotensin aldosterone system, that is ROS, is present in specialized tissue which is called juxtaglomerular apparatus or JGA located near the efferent arterial, efferent arterial which is supplied to the nephron through the supply of blood. When blood pressure or blood volume drops in the efferent arterial, the JGA releases the enzyme renin. Renin results in yielding a peptide which is called angiotensin II. Angiotensin II raises blood pressure by constricting the arterioles as a result decreasing blood flow to the nephron. Angiotensin II also stimulates the adrenal glands to release aldosterone. Aldosterone acts on distal tubules making them reabsorb more sodium and water. As a result the blood volume and pressure increase. The arterial natriuretic peptide is released from the walls of the atria of the heart in response to an increased blood volume and pressure. The RAS is released in decreased blood volume and decreased pressure so these are the opposite of the RAS. It inhibits the release of renin. It inhibits sodium chloride or sodium ion and chloride ion reabsorption. It reduces aldosterone release as a result the blood volume and pressures are lowered.