attached  Peer responses, 150 words each response, 1 citation only for one of the responses only. Due Monday the

attached 

Peer responses, 150 words each response, 1 citation only for one of the responses only.

Due Monday the 30th before midnight

Student #1:

Sophia

 

1. RAAS stands for Renin-Angiotensin-Aldosterone System. It is a system of hormones, proteins, and enzymes that stabilizes and regulates a person’s blood pressure and blood volume. There are steps involved in the RAAS system. Step one, is that when a person’s blood pressure is falling, the kidneys release an enzyme called renin to the bloodstream. Next, the renin divides a protein called angiotensinogen, one of the pieces being named Angiotensin I, which is inactive. This protein is again broken into pieces and one of them is called Angiotensin II, which is an active hormone. This hormone makes the arterioles of the blood stream constrict. This constriction triggers the release of aldosterone, which releases vasopressin. These two hormones being released makes the kidneys retain more sodium while also excreting potassium. This sodium retention creates more water to be held in the body, which increases blood pressure and volume. (Cleveland Clinic, 2022). 

 

1. An example of a pharmaceutical drug that acts on the RAAS system is an ACE inhibitor, for example, Lisinopril. This drug cuts off the RAAS system directly by dilating the blood vessels and ceasing the production of Angiotensin II. These ACE drugs still have the same outcome as the RAAS system, but just without all the same steps. (NM, 2019)

 

1. The RAAS system affects renal regulation, specifically glomerular filtration rate, blood volume, and blood pressure in the following ways. For GFR, RAAS reduces the glomerular filtration rate by constricting the glomerular afferent arterioles. This can cause there to be a decrease in renal blood flow. It affects blood volume by increasing it, which is caused by the increase in sodium reabsorption. Finally, RAAS affects blood pressure by regulating it in the form of increasing the sodium and water retention in the renal system. (Ma et al., 2022)

 

References

 

Ma, K., Gao, W., Xu, H., Liang, W., & Ma, G. (2022). Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome. 
Journal of the Renin-Angiotensin-Aldosterone System
2022(3239057), 1–8.

NM, R. (2019, May 1). 
What are ACE Inhibitors and Where are they Used? News-Medical.net. 
to an external site.

Cleveland Clinic. (2022). 
Renin-Angiotensin-Aldosterone System (RAAS): What It Is. Cleveland Clinic.

Student #2:

Mia

The renin-angiotensin-aldosterone system (RAAS) begins when low blood pressure or low sodium levels stimulate specialized cells in the kidneys to release renin. Renin converts angiotensinogen, a protein produced by the liver, into angiotensin I. Angiotensin I is then converted into angiotensin II by the angiotensin-converting enzyme (ACE), primarily in the lungs. Angiotensin II has several effects: it constricts blood vessels, increasing blood pressure, and stimulates the adrenal glands to release aldosterone. Aldosterone promotes sodium and water reabsorption in the kidneys, further increasing blood volume and blood pressure. This complex system helps maintain blood pressure and fluid balance in the body.

An example of a pharmaceutical drug that acts on this system would be diuretics, as discussed in the textbook Human Physiology by Silverthorn, Dee Ungluab. Diuretics are medications that promote the excretion of water and electrolytes through the kidneys, primarily by inhibiting the reabsorption of ions in the renal tubules. By targeting specific segments of the nephron, diuretics disrupt the normal processes of ion reabsorption, leading to increased sodium and chloride excretion (Silverthorn, 641). This disruption causes an osmotic effect, drawing more water into the renal tubules and resulting in enhanced urine output. Consequently, this leads to a reduction in blood volume and pressure, making diuretics effective in managing conditions like hypertension and edema. The overall impact on the kidneys is a significant alteration in fluid balance, emphasizing the crucial role of ion reabsorption in regulating water retention and excretion. 

The endocrine system plays a critical role in renal regulation by influencing glomerular filtration rate (GFR), blood volume, blood pressure, and reabsorption through various hormones. For instance, the release of renin from the juxtaglomerular cells in response to low blood pressure initiates the renin-angiotensin-aldosterone system (RAAS), which increases blood pressure and promotes sodium reabsorption in the kidneys (Silverthorn 638). Aldosterone stimulates the distal tubules to reabsorb sodium, leading to water retention and an increase in blood volume. Additionally, antidiuretic hormone (ADH) regulates water reabsorption in the collecting ducts, concentrating urine and further affecting blood volume and pressure. These hormonal signals work together to maintain homeostasis, adjusting GFR to ensure adequate kidney function while balancing fluid and electrolyte levels in the body.

 

Reference: Silverthorn, D. U. (2016). 
Human physiology: An integrated approach. Pearson education. 

 

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