Aldosterone

product of cardiac output and total peripheral vascular resistance. To maintain a balance between these factors, there are four control systems that play a role: the arterial baroreceptor system, regulation of body fluid volume, the renin angiotensin aldosterone system, and vascular autoregulation (Beeman, 2013, p. 337). Arterial baroreceptors are responsible for monitoring the levels of arterial pressure. When these baroreceptors sense a rise in arterial pressure, they counteract by slowing down the cardiac

Comprising of the kidneys, ureter, bladder and urethra, the urinary system is responsible for the filtration, reabsorption and/or removal of dissolved organic substances and materials from the human blood stream. Fed directly by the aortic and superior vena cava blood vessels, the kidneys are the first point of the urinary system. The kidneys produce the urine which drains into, and is stored in the bladder through the ureter before being excreted through the urethra as waste, and out of the body

agents. Current pharmacological treatments for HF that target the renin-angiotensin-aldosterone system include ACE inhibitors and Angiotensin II receptor blockers (ARBs). ACE inhibitors such as Captopril block activity of the enzyme ACE and therefore the conversion of angiotensin I to angiotensin II (the most bio active product of the RAAS), thus inhibiting the actions of angiotensin II and leading to decreased aldosterone production, decrease blood volume and reduced hypertension. ACE inhibitors also

In order to study the kidney 's regulation of plasma volume, osmolality, and pH, the changes in urine flow rate, specific density, and urine pH of adult human subjects were measured. Subjects were assigned one of four beverage options: water, Gatorade, Coke, or nothing. Beverages of different compositions were used to study what effects does fluid intake have on urine volume and composition. Subjects fasted five hours prior to the experiment, in which the subjects were required to void and test their

Urinary System: Anatomy Review 1. Name the organs in the urinary system: 1. 2 kidneys 2. 2 ureters 3. bladder 4. uethra 2. The kidneys are retroperitoneal (behind the peritoneum), lying against the dorsal body wall in the upper abdomen. 3. The adrenal gland sits atop the kidneys. Blood vessels enter and leave the kidney at the renal cortex. 4. The functional units of the kidney are the nephrons. They are called renal pyramids if they are located mainly in the cortex. They are called renal

Congenital Adrenal Hyperplasia (CAH) is a family of autosomal recessive disorders caused by impairment of biosynthesis of cortisol, aldosterone, and androgens. More than 85-90% of CAH is due to 21-hydroxylase deficiency. This is due to the defect in 2 genes-CYP21P and CYP21. 90% of the mutated forms causing 21-hydroxylase deficiency and they all recombination between CYP21 and CYP21P. Clinically they all are divided into two forms deficiency are described- the classical form, which is subdivided

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

inhibiting the activity of the angiotensin converting enzyme. Since angiotensin II is a vasoconstrictor, the lack of the protein allows blood vessels to remain dilated which decreases blood pressure. In addition, the lack of angiotensin II decreases aldosterone release which further lowers the blood pressure and puts less strain on the heart. Angiotensin II has been shown to be involved in the myocardial

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

Nicpon-Marieb, 1997). Prolonged overstimulation of the adrenal glands results in the release of their steroid hormones; glucocorticoids and mineralocorticoids from the outer cortex of the adrenals. The secretion of mineralocorticoids, in particular aldosterone result in the retention of sodium and water by the kidneys, and increased blood pressure and volume, while glucocorticoids secreting result in an increased blood glucose level, while fats and proteins (from muscles) are broken down for energy, thus