The Cardiovascular System: Angiotensin

antidiuretic hormone (ADH) in the distal convoluted tubules. Therefore, resulted into ANP pathway turning off ADH, renin and aldosterone. At T=30 to T=90, there was increase in urine flow rate for drinking group which increased in plasma volume and blood, decreased in aldosterone concentration and plasma vasopressin (Evans, et al., 2009). Additionally, increment in urine flow rate, Atrial natriuretic peptide (ANP) attributed to the increase in the Glomerular filtration rate (GFR) and glomerular permeability; Atrial natriuretic peptide (ANP) had a direct contribution to the increase of radius and the large glomerular pores (Theilig, Wu. 2015). The Glomerular filtration rate (GFR) rate increased as the surface area of the capillaries increased.

It inhibits Na+K+ ATPase active transport raising cytosolic Na+ concentrtion and leading to the increasement of Ca2+ concentration in the sarcoplasmic reticulum by the reversival exchange of Na+ and Ca2+ in the myocardial cell. This increase in the contraction of the heart (32) and improve cardiac outpur , left ventricualr ejection fraction, stroke volume, pulmonary capilary wedge pressure and exercise tolerance (33). Secondly, digoxin produce vagus activation showing negavite chronotropic action in SA node and negative dromotropic action in AV node. This lead to a shift in automatic balance by dominating the positive iontropic action of the drugs digoxin (33). In this way digoxin is cosinder as a only available inotropic drug which increase cardiac output and decreae pulmoary capillary wedge preure with our increasing heart rate and without decreasing blood pressure

Renin keep the blood pressure at a normal level by intaking more water and solutes so that the filtration in our bodies can balance out. The juxtaglomerular apparatus cell answer to low blood pressure when angiotensin one is converting to angiotensin two.

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.

ACEI causes hyponatremia by blocking the conversion of angiotensin I to angiotensin II in the peripheral circulation but not in the brain where angiotensin I gets converted to angiotensin II [16]. Angiotensin II is known to stimulate the release of ADH resulting in hyponatremia [18].

In order to understand the role of ATRAP in humans, it is imperative to understand the role of the AT1 receptor itself. AT1 receptors are crucial elements of the renin-angiotensin system. They act as mediators for almost all physiological roles of angiotensin II (AngII). Inhibiting the binding of angiotensin II to AT1 receptors can effectively lower blood pressure of patients who are found to have hypertension. This observation demonstrates that AT1 receptors, more specifically those found in the kidneys, are important factors in the cause of hypertension in humans (Chen & Coffman, 2015). After understanding regulation model, the function of

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.

When the heart begins to fail, mechanisms are activated to compensate for the impaired function and maintain the cardiac output. The primary compensatory mechanisms are Frank –Starling mechanism, neuroendocrine responses including activation of the sympathetic nervous system and the renin- angiotensin-aldosterone system, and ventricular hypertrophy. Decreased cardiac output initially stimulates aortic baroreceptors, which in turn stimulate the SNS. SNS stimulation produces both cardiac and vascular responses through the release of norepinephrine. Norepinephrine increases heart rate and contractility by stimulating cardiac beta- receptors. Cardiac output improves as both heart rate and stroke volume increase. Norepinephrine also causes arterial

The major health problem selected for this project was hypertension (Harrison et al, 2011). It is identified as a cardio vascular disease risk factor such as dementia, chronic kidney disease, coronary heart disease, and stroke (NICE, 2011). It can be missed easily, as in various instances it is asymptomatic as well as it is also known as a silent killer. The Hypertension is thought to be a disease of vascular regulation ensuing from arterial pressure control mechanisms malfunction (extracellular fluid volume, rennin-angiotensin-aldosterone system, and CNS) that results in elevation of BP by means of enhanced peripheral vascular resistance, and cardiac output. There are 2 basic hypertension types. Around 90 to 95 percent of the individuals have primary hypertension which is linked with change in lifestyle as well as needs medical treatment. On the other hand, 5-10% has secondary hypertension which is linked with various other diseases for instance pregnancy, thyroid, and renal (Haslam and James, 2005). It is estimated that around 1 in 20 adults will have increased BP of 160/100 mmHg and above that results in either more than one predisposing aspects (Gemmell et al, 2006).

Renin inhibitors are effective in treating hypertension because they block the activity of an enzyme secreted within the kidney called renin. Renin inhibitors blocks the activation of angiostensinogen. Without the activation of angiostensinogen, blood vessels will relax and widen. This will cause a decrease in blood pressure. The blood volume decrease as well through the diuretic and natriuretic effects with helps treat hypertension.

Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) are a group of drugs that belong to the antihypertensive drug class. There are currently 10 ACE inhibitors that are available. ACE inhibitors can be taken either by themselves or can be combined with a calcium channel blocker or a thiazide diuretic to enhance the treatment This group of drugs is often used as a first line of treatment to treat both heart failure and hypertension. Some of these drugs include; benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), and fosinopril (Monopril) (Lilley, p. 348).

The cardiovascular system is formed by the heart and the vasculature, a close system of vessels, which include arteries, arterioles, capillaries, venules, veins and lymph vessels.

The purpose of this essay is to discuss the role that sodium and potassium play in blood pressure regulation.

http://www.sharinginhealth.ca/biology/blood_pressure.html Cardiac output – HR X SV HR control by sympathetic NS SV = EDV – ESV INCREASE AND DECREASE AFFECTS CO OTHER FACTORS 1. Activation of Baroreceptors: located in the aorta and carotid (Pressoreceptors) arteries; detect changes in arterial

The cardiovascular system can be split into three different parts: the blood, the heart, and the blood vessels. They all work within the cardiovascular system in their own individual ways and each has their own unique characteristics and functions within the system.