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Reply to this 2 discussion posts and Ask a question at the end of each one. 1. The first step that triggers this process is when the body detects low sodium levels, low blood pressure, or decreased blood flow to the kidneys. The second step is that, upon detection, the kidneys release an enzyme called renin, which then travels through the bloodstream. In the third step, renin converts a protein called angiotensinogen into angiotensin I. In the fourth step, angiotensin I is converted by an enzyme in the lungs called ACE into angiotensin II. In the fifth step, angiotensin II is responsible for vasoconstriction, ADH release, and aldosterone release. Lastly, with all these steps completed, blood volume increases, blood pressure rises, and blood vessels constrict. The pharmaceutical drug that will act on this system is Lisinopril. Basically this drug will act like a blocker to the enzyme ACE and it will stop angiotensin II to form. Therefore, we will have an outcome of lower blood pressure and it will help to treat high blood pressure and heart failure. RAAS affects renal regulation in the GFR because RAAS will help regulate GFR when the blood pressure is low. So that’s when angiotensin II comes in because it will help keep that blood flow in the kidneys. RAAS has an important part in helping to increase the blood volume and increase blood pressure as well. For reabsorption we will have aldosterone and it will help with the process of sodium reabsorption. As the sodium is being reabsorbed we will then have an increase in water reabsorption as well. This process goes hand and hand with increasing blood volume and increasing blood pressure. 2. The RAAS system is an endocrine system that plays an important role in regulating blood pressure, fluid balance, and sodium retention. This system has several steps, it starts with a drop of blood pressure or a decrease in blood flow to the kidneys which then triggers the specialized cells that are in the kidneys (aka juxtaglomerular cells) to release an enzyme called renin into the bloodstream. Renin acts as a protein called angiotensinogen which is produced by the liver, converting it to Angiotensin I. Angiotensin-converting enzyme which is known as ACE, found in the lungs which will then convert to angiotensin II. This will then become the key in RAAS as it exerts potent effects on blood vessels, causing them to constrict, leading to an increase in blood pressure. It also stimulates the release of aldosterone from the adrenal glands, enhancing sodium and water in the kidneys. It will then result in an increase in blood volume and blood pressure. A pharmaceutical drug that acts on this system are any ACE inhibitors such as Lisinopril. They intend to inhibit the activity of ACE, the enzyme that converts angiotensin I to angiotensin II. By doing so, ACE inhibitors lower the levels of angiotensin II in the body. The intended effect of Lisinopril is to dilate blood vessels, decrease blood pressure, and reduce the heart’s workload. This drug can be beneficial by managing conditions like heart failure or hypertension. In renal regulation, the RAAS system has effects. Angiotensin II vasoconstriction action narrows down blood vessels which leads to an increase in blood pressure. At the same time, aldosterone promotes sodium reabsorption in the kidneys, increasing blood volume. These combined result in an elevation of blood pressure and a restoration of fluid balance. However, it can also lead to an increase in GFR, as increased blood pressure can drive more blood through the glomeruli. This can enhance filtration, activation of RAAS can contribute to kidney damage over time, especially if blood pressure is consistently up.
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