The renin-angiotensin-aldosterone system can be inhibited in orderto reduce high blood pressure. Usually, the angiotensin-convertingenzyme, which converts angiotensin I to angiotensin II, is inhibitedby drug therapy. Why would this enzyme be an effective point todisrupt the system?
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The renin-angiotensin-aldosterone system can be inhibited in order
to reduce high blood pressure. Usually, the angiotensin-converting
enzyme, which converts angiotensin I to angiotensin II, is inhibited
by drug therapy. Why would this enzyme be an effective point to
disrupt the system?
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Solved in 2 steps
- The rate at which the Na+K+ pump operates is not constant but is controlled by a combined effect of changes in ICF Na+ concentration and ECF K+ concentration. Do you think the changes in both ICF Na+ and ECF K+ concentration following a series of action potentials in a neuron would accelerate, slow down, or have no effect on the Na+K+ pumps in this cell?ANP (atrial natriuretic peptide) can be considered to act against (in opposition to) the reninangiotensin-aldosterone-system (RAAS). What then does ANP try to achieve?Describe in detail the renin-angiotensinogen pathway
- Diuretics can be prescribed to combat high blood pressure. Thiazide is one of the most common. Describeits mechanism of action (they physiology of what the drug does) and how it combats high blood pressure. The action of the diuretic Thiazide can also cause the activation of the renin-angiotensin system. Explain this system (starting with renin) and whyit would be counterproductive to the reason you prescribed Thiazide for a patient. i only need answer for the question 2 Please!Renin is secreted in response to hypovolemia or to an increase in the osmolality of the blood. Provide three possible mechanisms by which these conditions may stimulate rennin secretion. What are the consequences of increased rennin secretion that lead to increased aldosterone secretion? Present this sequence of events. Why are angiotensin converting enzyme inhibitors (ACEIs) used as a common therapy for hypertension? How do they influence blood pressure? Are plasma levels of renin elevated or depressed in a patient with Conn’s disease? Why?A patient has essential hypertension, and with a healthy lifestyle and medication, he is able to maintain normal blood pressure on a single antihypertensive medication. The medication he takes is called an angiotensin converting enzyme inhibitor, or ACE inhibitor, which blocks the activation of angiotensin II. Describe at least two mechanisms by which angiotensin II targets the kidneys to increase extracellular fluid volume and, therefore, increase blood pressure.
- Physiology of angiotensin II in humans Angiotensin I is enzymatically converted to angiotensin II by ACE. Angiotensinogen II acts on the adrenal cortex to cause the release of storage vesicles containing aldosterone. Angiotensin II is a peptide hormone that is made in advance and stored in vesicles. Physiology of angiotensin II in humans Question 24 options: Angiotensin I is enzymatically converted to angiotensin II by ACE. Angiotensinogen II acts on the adrenal cortex to cause the release of storage vesicles containing aldosterone. Angiotensin II is a peptide hormone that is made in advance and stored in vesicles.Present the rationale for clinical applications of renin-angiotensin inhibitors. What are the major side effects?Define renin-angiotensin-aldosterone mechanism
- Hyperaldosteronism (excessive aldosterone release) can be caused by many disease states including tumours in the adrenal gland. By now, we should be familiar with how this will affect sodium balance and blood pressure, but how would hyperaldosteronism affect potassium levels and why? Select one potassium effect (a or b) and one cause (c-f). a. The patient will become hyperkalemic. O b. The patient will become hypokalemic. O c. Aldosterone increases sodium reabsorption in the proximal tubule. Increased sodium reabsorption increases water reabsorption, which then establishes a concentration gradient to increase potassium reabsorption. Od. Aldosterone increases sodium reabsorption in the collecting duct. Increased sodium reabsorption increases water reabsorption, which then establishes a concentration gradient to increase potassium reabsorption. O e. Aldosterone increases sodium reabsorption in the collecting duct by increasing expression of EnaCs, sodium/potassium exchangers, and…Give the steps in the renin angiotensin pathway from start to finish.An inadequate (low) dietary intake of NaCl will cause A) increased angiotensin II production