Renin—angiotensin—aldosterone system Renin—angiotensin—aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water imbalance in the body such as hypotensionlow distal tubule sodium concentration, decreased blood volume and high sympathetic tone trigger the release of the enzyme renin from the cells of juxtaglomerular apparatus in the kidney.
Renin—angiotensin—aldosterone system Renin—angiotensin—aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water imbalance in the body such as hypotensionlow distal tubule sodium concentration, decreased blood volume and high sympathetic tone trigger the release of the enzyme renin from the cells of juxtaglomerular apparatus in Caso cooper pharmaceutical kidney.
Renin activates a circulating liver derived prohormone angiotensinogen by proteolytic cleavage of all but its first ten amino acid residues known as angiotensin I. ACE is found in the pulmonary circulation and in the endothelium of many blood vessels.
Bradykinin increases because of less inactivation by ACE. Under normal conditions, angiotensin II has these effects: Vasoconstriction narrowing of blood vessels and vascular smooth muscle hypertrophy enlargement induced by ATII may lead to increased blood pressure and hypertension.
Further, constriction of the efferent arterioles of the kidney leads to increased perfusion pressure in the glomeruli.
It contributes to ventricular remodeling and ventricular hypertrophy of the heart through stimulation of the proto-oncogenes c-fosc-junc-myctransforming growth factor beta TGF-Bthrough fibrogenesis and apoptosis programmed cell death.
Stimulation by ATII of the adrenal cortex to release aldosteronea hormone that acts on kidney tubules, causes sodium and chloride ions retention and potassium excretion. Sodium is a "water-holding" ion, so water is also retained, which leads to increased blood volume, hence an increase in blood pressure.
Stimulation of the posterior pituitary to release vasopressin antidiuretic hormone, ADH also acts on the kidneys to increase water retention. This allows the kidney to excrete sodium ions along with obligate water, and retain potassium ions.
This decreases blood volume, leading to decreased blood pressure. Epidemiological and clinical studies have shown ACE inhibitors reduce the progress of diabetic nephropathy independently from their blood pressure-lowering effect.
ACE inhibitors have been shown to be effective for indications other than hypertension even in patients with normal blood pressure.
Such therapy, of course, requires careful and gradual titration of the dose to prevent the effects of rapidly decreasing blood pressure dizziness, fainting, etc. ACE inhibitors have also been shown to cause a central enhancement of parasympathetic nervous system activity in healthy volunteers and patients with heart failure.
The other reported adverse effects are hepatotoxicity and effect on the fetus. Patients starting on an ACE inhibitor usually have a modest reduction in glomerular filtration rate GFR that stabilizes after several days.
However, the decrease may be significant in conditions of decreased renal perfusion, such as renal artery stenosis, heart failure, polycystic kidney disease, or volume depletion. Therefore, renal function should be closely monitored over the first few days after initiation of treatment with ACE inhibitor in patients with decreased renal perfusion.
When the three drugs are taken together, the risk of developing renal failure is significantly increased. Suppression of angiotensin II leads to a decrease in aldosterone levels.
Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors can cause retention of potassium. Some people, however, can continue to lose potassium while on an ACE inhibitor. This leads to cardiac dysfunction and neuromuscular consequences, such as muscle weakness, paresthesia, nausea, diarrhea, and others.
Close monitoring of potassium levels is required in patients receiving treatment with ACE inhibitors who are at risk of hyperkalemia.CONSOLIDATED MINI CATALOGUE. BA= Color Box Art Available for an additional $ FL= Film is in Foreign Language.
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