Changes

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

*cardiac and arterial baroreceptors responsd to reduced local perfusion - beta-1 mediated effect via innervation of the juxtaglomerular apparatus (JGA)  

*cardiac and arterial baroreceptors responsd to reduced local perfusion, initiating beta-1 mediated effects via innervation of the juxtaglomerular apparatus (JGA)  

*decreased chloride delivery to the macula densa is detected by chemoreceptors - a drop in glomerular filtration rate (GFR) detected as a drop in chloride presented at the macula densa leads to increased reabsorption in the proximal convoluted tubule.

*decreased chloride delivery to the macula densa is detected by chemoreceptors - a drop in glomerular filtration rate (GFR) detected as a drop in chloride presented at the macula densa leads to increased reabsorption in the proximal convoluted tubule.

'''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.

'''Effects of Hormones''':

====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.