Discuss the role of:

Role of ANF (Atrial Natriuretic Factor) :

Guanylyl cyclase in the kidney is activated by a peptide hormone atrial natriuretic factor (ANF) which is released by the cells in cardiac atrium when the heart is stretched by increased blood volume. Carried in the blood to the kidney, ANF activates guanylyl cyclase in the cells of collecting ducts. The resulting rise in [cGMP] triggers increased renal excretion of Na+ and consequently of water driven by change in osmotic pressure. Water loss reduce the blood volume countering the stimulus that initially lead to ANF secretion. Vascular smooth muscle also have an ANF receptor guanylyl cyclase ; on binding to this receptor, ANF causes relaxation (vasodilation) of blood vessels which increases blood flow and hence decrease blood pressure.

Role of Vasopressin:

The hyperosmolarity (increase in fluid Na+ concentration) and hypovolemia (decrease in fluid blood volume) are detected by  osmoreceptors or baroreceptors, sensory cell that monitor changes in Na+ concentration or volume (pressure) respectively of blood. Integration of this information within the hypothalamus results in the release of hormone, vasopressin from the neurons that are components of the posterior pituitary gland. This hormone is also referred to as anti-diuretic hormone (ADH) (or more specifically arginine vasopressin). AVP is released into the blood and acts on certain cells of kidney collecting tubules to cause water reabsorption. Vasopressin also causes the contraction of certain smooth muscles of the vasculature, which results in partial restoration of blood pressure.

Role of NO (Nitric oxide):

A distinctly different type of guanylyl cyclase is a cytosolic protein with a tightly associated heme group, an enzyme activated by nitric oxide. Nitric oxide is produced from arginine by Ca2+ dependent NO synthase present in mammalian tissue, and diffuse from its cell of origin into nearby cells. NO is sufficiently non-polar to cross plasma membrane without carrier.

NO induced relaxation of cardiac muscle is the same response brought about by nitroglycerin and other nitro vasodilators taken to relieve angina pectoris, the pain caused by contraction of heart deprived of oxygen because of blocked coronary arteries. Nitric oxide is unstable and its action is brief, within seconds of its formation it undergoes oxidation to nitrite to nitrate. Nitro vasodilators produce long lasting relaxation of cardiac muscle because they break down over several hours, yielding a steady stream of NO. NO can dilate the smooth muscle of the blood vessels. With this dilation, the vessels can relax and allow blood to flow easily through them and quite possibly lower blood pressure.