Renin-angiotensin—aldosteron system

Blood Pressure Control Renin-Angiotensin-Aldosteron System... 

Renin-Angiotensin-Aldosterone System ACE Inhibitors Nuclear Factor-icB... 

When the temporal sequence of adjustments of blood pressure is analysed it seems, that CNS mechanisms (e.g., baroreflexes) will provide regulation of the circulation within seconds to minutes. Other mechanisms, such as the renin-angiotensin-aldosterone system and fluid shifts, occur over minutes to hours. Only the... 

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

Renin-Angiotensin-Aldosterone System Epithelial Na+ Channels ACE Inhibitors... 

The renin-angiotensin-aldosterone system (RAAS) generates the peptide hormone angiotensin II and subsequently the mineralocorticoid aldosterone, which both exert considerable impact on blood pressure ( blood pressure control) and fluid homeostasis, and... 

Describe the pathophysiology of heart failure as it relates to neurohormonal activation of the renin-angiotensin-aldosterone system and the sympathetic nervous system. 

Development and progression of heart failure involves activation of neurohormonal pathways, including the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). 

As previously discussed, increased portal pressure triggers the release of nitric oxide to directly vasodilate the splanchnic arterial bed and decrease portal pressure. Unfortunately, nitric oxide also dilates the systemic arterial system, causing a decrease in blood pressure and a decrease in renal perfusion by lowering the effective intravascular volume. The kidney reacts by activating the renin-angiotensin-aldosterone system, which increases plasma renin activity, aldosterone production, and sodium retention. This increase in intravascular volume furthers the imbalance of intravascular oncotic pressure, allowing even more fluid to escape to the extravascular spaces. 

Diuretics are often required in addition to the sodium restriction described previously. Spironolactone and jurosemide form the basis of pharmacologic therapy for ascites. Spironolactone is an aldosterone antagonist and counteracts the effects of activation of the renin-angiotensin-aldosterone system. In hepatic disease not only is aldosterone production increased, but its half-life is prolonged because it is hepatically metabolized. Spironolactone acts to conserve the potassium that would be otherwise excreted because of elevated aldosterone levels. 

The zona glomerulosa is responsible for the production of the mineralocorticoids aldosterone, deoxycorticosterone, and 18-hydroxy-deoxycorticosterone. Aldosterone promotes renal sodium retention and excretion of potassium. Its synthesis and release are regulated by renin in response to decreased vascular volume and renal perfusion. Adrenal aldosterone production is regulated by the renin-angiotensin-aldosterone system. 

Aldosterone A hormone produced in and secreted by the zona glomerulosa of the adrenal cortex. Aldosterone acts on the kidneys to reabsorb sodium and excrete potassium. It is also a part of the renin-angiotensin-aldosterone system, which regulates blood pressure and blood volume. 

Renin-angiotensin-aldosterone system (RAAS) The hormonal system controlled mainly by the kidneys and adrenal glands that regulates blood pressure, blood volume, and electrolyte balance. 

Campbell BC, Meredith PA, Scott JJC. 1985. Lead exposure and changes in the renin-angiotensin-aldosterone system in man. Toxicol Lett 25 25-32. 

Lee DBN. 1989. The effect of lead on blood pressure, vascular contractility and the renin-angiotensin-aldosterone system in the rat. Washington, DC Veterans Administration, Research and Development. 

Although the kidneys are not considered endocrine glands per se, they are involved in hormone production. Erythropoietin is a peptide hormone that stimulates red blood cell production in bone marrow. Its primary source is the kidneys. Erythropoietin is secreted in response to renal hypoxia. Chronic renal disease may impair the secretion of erythropoietin, leading to development of anemia. The kidneys also produce enzymes. The enzyme renin is part of the renin-angiotensin-aldosterone system. As will be discussed, these substances play an important role in the regulation of plasma volume and therefore blood pressure. Other renal enzymes are needed for the conversion of vitamin D into its active form, 1,25-d i hyd ro xyv itamin D3, which is involved with calcium balance. 

Nesiritide is manufactured using recombinant techniques and is identical to the endogenous B-type natriuretic peptide secreted by the ventricular myocardium in response to volume overload. Consequently, nesiritide mimics the vasodilatory and natriuretic actions of the endogenous peptide, resulting in venous and arterial vasodilation increases in cardiac output natriuresis and diuresis and decreased cardiac filling pressures, sympathetic nervous system activity, and renin-angiotensin-aldosterone system activity. 

---