Changes

The maintenance of normal pressures within the arterial and venous circulations is essential for the maintenance of normal fluid homeostasis. The '''Starling hypothesis''' describes the state whereby the equilibrium of fluid exchange across the capillary wall (between the blood and the interstitial fluid) is determined by the hydrostatic pressures and oncotic pressures that exist across the capillary wall. This fluid exchange is controlled by the capillary blood pressure, the interstitial fluid pressure and the colloid osmotic pressure of the plasma. Normally there is a net loss of fluid from the capillary at the arteriolar end, and a net gain at the venous end, resulting in almost perfect fluid balance being maintained. Any net fluid movement from the intravascular to the extracellular space can be compensated for by lymphatic drainage. Low blood pressure results in fluid moving from the interstitial space into the circulation, helping to restore blood volume and blood pressure.

The maintenance of normal pressures within the arterial and venous circulations is essential for the maintenance of normal fluid homeostasis. The '''Starling hypothesis''' describes the state whereby the equilibrium of fluid exchange across the capillary wall (between the blood and the interstitial fluid) is determined by the hydrostatic pressures and oncotic pressures that exist across the capillary wall. This fluid exchange is controlled by the capillary blood pressure, the interstitial fluid pressure and the colloid osmotic pressure of the plasma. Normally there is a net loss of fluid from the capillary at the arteriolar end, and a net gain at the venous end, resulting in almost perfect fluid balance being maintained. Any net fluid movement from the intravascular to the extracellular space can be compensated for by lymphatic drainage. Low blood pressure results in fluid moving from the interstitial space into the circulation, helping to restore blood volume and blood pressure.

===Hormonal Responses===

==Hormonal Responses==

Hormonal responses exist for the purpose of both lowering and raising blood pressure. They act in various ways, including vasoconstriction, vasodilation and alteration of blood volume.

Hormonal responses exist for the purpose of both lowering and raising blood pressure. They act in various ways, including vasoconstriction, vasodilation and alteration of blood volume.

====Renin-Angiotensin-Aldosterone System (RAAS)====

===Renin-Angiotensin-Aldosterone System (RAAS)===

The juxtaglomerular apparatus of the kidneys plays an important role in the control of blood volume and blood pressure - renin is released from this area. The stimulus for renin release into the circulation includes;  

The juxtaglomerular apparatus of the kidneys plays an important role in the control of blood volume and blood pressure - renin is released from this area. The stimulus for renin release into the circulation includes;  

*local baroreceptors in the afferent renal arteriole - a drop in renal blood flow stimulates renin release

*local baroreceptors in the afferent renal arteriole - a drop in renal blood flow stimulates renin release

'''NOTE''' This system is responsible for the long-term maintenance of blood pressure, but is also activated very rapidly in the presence of hypotension.

'''NOTE''' This system is responsible for the long-term maintenance of blood pressure, but is also activated very rapidly in the presence of hypotension.

====Vascular Hormal Effects====

===Vascular Hormal Effects===

Angiotensin II is a potent vasoconstrictor (causing an increase in mean arterial pressure), which also causes the direct stimulation of sodium retention in the proximal convoluted tubule of the kidney, via its increased synthesis and release of aldosterone. Aldosterone stimulates reabsorption of sodium and chloride, and secretion of potassium and protons. Initially, effects are advantageous by protecting perfusion to essential vascular beds and expanding the circulation fluid volume, and therefore increasing contractility by the Starling mechanism. Disadvantages include increased systemic vascular resistance, therefore increased myocardial work and increased myocardial oxygen demand. Expanded circulation fluid volume ultimately results in congestion of vascular beds when the Starling mechanism is not effective in the failing heart. Angiotensin II and aldosterone have effects at the level of the gene involving altered expression, which may lead to a progression of the myocardial dysfunction present. They therefore play a role in the regulation of hypertrophy and fibrosis.

Angiotensin II is a potent vasoconstrictor (causing an increase in mean arterial pressure), which also causes the direct stimulation of sodium retention in the proximal convoluted tubule of the kidney, via its increased synthesis and release of aldosterone. Aldosterone stimulates reabsorption of sodium and chloride, and secretion of potassium and protons. Initially, effects are advantageous by protecting perfusion to essential vascular beds and expanding the circulation fluid volume, and therefore increasing contractility by the Starling mechanism. Disadvantages include increased systemic vascular resistance, therefore increased myocardial work and increased myocardial oxygen demand. Expanded circulation fluid volume ultimately results in congestion of vascular beds when the Starling mechanism is not effective in the failing heart. Angiotensin II and aldosterone have effects at the level of the gene involving altered expression, which may lead to a progression of the myocardial dysfunction present. They therefore play a role in the regulation of hypertrophy and fibrosis.