Explain The Steps To Angiotensin-Aldosterone

The other hormone that can be affected if diagnosed with Addison 's disease is aldosterone. Aldosterone belongs to a class of hormones known as mineralocorticoids. Aldosterone is used to maintain blood pressure and water and salt balance in the body by helping the kidney retain salt or release potassium (MedicineNet, 2011). If the aldosterone levels fall too low the kidneys are unable to regulate sodium and water levels that result in a drop of blood volume and blood pressure.

If the kidney functions properly it regulates the retention of fluids in the body. It balances the chemicals like potassium for the heart and muscle function. It can also maintain acid balance and proteins. Hormones in the kidney stimulate activity in the body, renin erythropoietin, and a form of vitamin D. Renin helps to control blood pressure. The kidney also releases the erythropoietin to help

Aldosterone is the mineralocorticoid steroid which is release from the adrenal gland, situated superior to the kidney. Aldosterone play a major role for the retention of water and sodium in the nephrone (10) in the patient with congestive heart failure, cirrhosis, and nephrotic syndrome (25). The level of the Aldosterone will increase in the patient of heart failure when angiotensin I receptors is activated by Angiotensin II leading to fluid overload (10).

Blood pressure in our blood vessels is monitored by the baroreceptors. These receptors send messages to the cardio regulatory center of the medulla oblongata to regulate our blood pressure every minute. In order for blood to be delivered to all organs and tissues, our cardiovascular system must always maintain adequate blood pressure. If the blood pressure drops too low, these organs will not receive an adequate of nourishing blood. Also if the pressure goes too high, the walls of the arteries will stretch and increased activity within the baroreceptor, information will then be sent through the nerves to the cardio regulatory center within the medulla which will responds by initiating the mechanisms that decrease the blood pressure to a normal

Heart rate and blood pressure can change with many different stimuli; any stimuli that result in an increase in sympathetic nervous system activity, such as emotional stress or physical exercise, should result in an increase in heart rate and/or blood pressure, assuming there are no other health problems at play. Similarly, activities that inhibit sympathetic nervous system activity help to decrease both heart rate and blood pressure (Powers and Howley, 2009, p. 178). However, there are extrinsic factors that can affect the two: for example, beta-blockers will stimulate vasodilation and thus a decrease in blood pressure (Powers and Howley, 2009, p. 183). The kidneys also plays a large role in cardiac regulation: secretion of norepinephrine by the adrenal glands leads to a more rapid heart rate, and higher levels of water retention by the kidneys leads to increased blood volume and thus increased blood pressure (Powers and Howley, 2009, p. 178).

In periods of extreme stress, the sympathetic nervous system will override autoregulation. An increase in sympathetic flow to the kidney will result in what two important effects that will aid maintenance of blood pressure?

Aldosterone falls in the class of hormone called mineralocorticoids, produces by the adrenal glands and is found near the kidneys. It sustains blood pressure, water and salt balance within the body. This procedure is assisting the kidneys to preserve sodium and excrete potassium in order to maintain a balance. If Aldosterone production falls, there isn’t enough regulation of salt and water balance (as aldosterone is being lost through urination) triggering blood pressure and blood volume to decline as a result of the kidneys not functioning properly. If body is in need of salt, water is not retained and adrenals release more Aldosterone and salt is reabsorbed from the tubule.

Baroreceptors activate the sympathetic nervous system, with an increase in heart rate and blood pressure and vasoconstriction, causing beta receptor downregulation, and further increased adrenergic tone with pathological activation of the renin-angiotensin-aldosterone-system (Johnson, 2014). Angiotensin II releases catecholamine and stimulates renin release, which raises tone and pressure on the heart, and leads to aldosterone secretion, also increasing the pressure load on the heart; water and sodium retention through the presence of vasopressin and aldosterone add to preload (Johnson, 2014). This model is used to explain the compensatory mechanisms employed to maintain cardiac reserve, the ability of the heart to respond to increased needs; additional neurohormonal changes involve natriuretic peptides, atrial natriuretic peptide, brain natriuretic peptide and endothelin 1 (Johnson, 2014; Porth,

Body: the regulation tof blood pressure. When your blood pressure increases, it is detected by the recepters in your blood vessels that sence the resistance of blood flow against the walls if the vessel. The receptors send a message to your brain, which sends a message to your heart and blood vessels. Your heart rate decreases and your blood vessels expand in diameter, which together decreases your blood

In an effort to increase cardiac output, the sympathetic nervous system is activated, through baroreceptors in the aortic arch, as an early compensatory mechanism which provides inotropic support and maintains cardiac output (Cadwallader, 2013; Yelle & Chaudhry, 2016). These compensatory mechanisms include increased heart rate, myocardial remodeling, and increased fluid volume. Chronic sympathetic activation eventually increases the stress placed on the heart and causes further weakening in cardiac function (Markaity, 2012; Yelle & Chaudhry, 2016).

There is a complex interrelationship among the cardiovascular system, the central nervous system (Na+, appetite and thirst regulation), the kidneys, and the tissue capillary beds distribution of extracellular fluid volume). Any change at any of these sites affects the function at other sites. There is a basic law of kidneys that Na+ excretion is directly proportional to mean arterial blood pressure (MABP). A marginal increase in MABP causes significant increase in Na+ excretion.

Hypertension affects all body systems, hypertension affects the cardiovascular system as the thickening of the arteries causes more pressure to build up in the walls

Angiotensin II stimulates blood flow by increasing a person's arterial blood pressure. High blood pressure destroys the glomerulus filtration by over spilling proteins. The increase in blood volume cause secretion of antidiuretic hormone and aldosterone which return cause sodium and fluid to build up in the kidney. Because the patient already has poor blood flow, the ACE inhibitors cause the arterial and venous blood pressure to decrease even

The cardiovascular system is one of the most important systems in the body and responsible for the delivery of oxygen, nutrients and the removal of wastes from cellular and tissue levels. These products are transported within the blood through an interconnected system of blood vessels throughout the body with the heart being the power and force to pump it to the body. With the interaction of the many body systems, the blood is able to be regulated, oxygen and nutrients are able to get to the tissues and cells, and lastly the waste products are able to be excreted and removed. The vascular endothelium is very important in the functioning of the cardiovascular system because of its vast functionality. When the vascular endothelium is in

Two mechanisms act by changing the resistance or diameter of afferent arterioles. When the afferent arteriole tighten, within the glomerular capillaries, the pressure decreases. Myogenic regulation is the first of the intrinsic mechanisms that are arteriole-related. Arteriole constriction is when there is an increase in stretch, as observed if pressure increases. To maintain GFR, constriction tends to limit the change in pressure all throughout the glomerular capillaries. The second arteriole-related intrinsic mechanisms, called tubuloglomerular feedback, involve the juxtaglomerular apparatus, where the afferent and efferent arterioles come in contact