Angiotensin sodium retention

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. 

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. 

Angiotensin-II AT, Human cDNA Artherosderosis, cardiac hypertrophy, congestive heart failure, hypertension, myocardial infarction, renal disease, cancer, diabetes, obesity, glaucoma, cystic fibrosis, Alzheimer s disease, Parkinson s disease Smooth muscle contraction, cell proliferation and migration, aldosterone and ADH release, central and peripheral sympathetic stimulation, extracellular matrix formation, tubular sodium retention, neuroprotection... 

Celecoxib is contraindicated during pregnancy, since COX-2 levels must be maintained for ovulation and onset of labor. COX-2 seems to be involved into the regulation of the renin-angiotensin system, and both celecoxib and rofecoxib use are associated with transient sodium retention. 

The benefit of glucocorticoid therapy is often limited by several adverse reactions, including cardiovascular disorders such as hypertension and atherosclerosis. Plasma volume expansion due to sodium retention plays a minor role, but increased peripheral vascular resistance, due in part to an increased pressor response to catecholamines and angiotensin II, plays a major role in the pathogenesis of hypertension induced by glucocorticoid excess. However, the molecular mechanism remains unclear. 

Pathophysiology In HF patients, the levels of aldosterone are elevated, even in the presence of ACE inhibitors or angiotensin-receptor blockers (34,35). Aldosterone has detrimental effects in HE such as causing potassium and magnesium loss, sodium retention, baroreceptor dysfunction, and myocardial fibrosis it also decreases the neuronal uptake... 

The active ingredients of licorice inhibit the breakdown of mineralocorticoids by inhibiting 11-beta-hydroxysteroid dehydrogenase type 2, and its adverse effects relate mainly to mineralocorticoid excess, with sodium retention, potassium loss, and inhibition of the renin-angiotensin-aldosterone system (36). 

ACE-I block the conversion of angiotensin 1 to angiotensin II, which causes vasoconstriction and stimulates the production of aldosterone synthesis. Thus, ACE-1 promote vasodilatation and decrease sodium retention, consequently lowering blood pressure. The inhibition of angiotensin-converting enzymes also blocks the breakdown of bradykinins. The increase in bradykinin level leads to additional vasodilatation effects. However, the increase in bradykinin is also responsible for adverse effects such as cough and angioedema. 

MOA ACE-l block the conversion of angiotensin 1 to angiotensin II, promoting vasodilatation and decreasing sodium retention. 

Angiotensin-converting enzyme (ACE) inhibitors Decrease the release of aldosterone, reducing sodium retention and resulting in improved renal blood flow and decreased fluid volume by dilating dilate venules and arterioles. 

In shock the excessive peripheral vasoconstriction may be caused by circulating angiotensin and not, as proposed by Nickerson (N5), by catecholamines alone. Secretion of ACTH may possibly stimulate renin secretion. Laparotomy in the rabbit per se causes a marked increase in plasma renin activity. Such change is in contrast to the results in rabbits subjected only to blood sampling and anesthesia (M2). Increased plasma activity could stimulate the secretion of aldosterone leading to postoperative sodium retention (L4, M14). 

ACE inhibitors decrease arterial tone by decreasing the production of angiotensin II and increasing bradykinin. In addition, a decrease in sodium retention by aldosterone is seen, which limits fluid retention and decreases blood volume. This in turn decreases ventricular filling and myocardial stretch. 

B. Effects Angiotensin II is a potent arteriolar vasoconstrictor and stimulant of aldosterone release. All directly incTeases peripheral vascular resistance and, through aldosterone, causes renal sodium retention. All also facilitates the release of norepinephrine from adrenergic nerve endings via presynaptic heteroreceptor action. All of these effects are mediated by the angiotensin AT, receptor, a G, -coupled receptor. 

The renin—angiotensin—aldosterone and sympathetic nervous systems are the main homeostatic effectors of vasoconstriction and sodium retention, paralleled by vaso-pressin/adiuretin activation. They all act synergistically but, at the same time, are balanced by counter-regulatory vasodilator and natriuretic mechanisms, particularly the natriuretic peptides and the NO system, also interplaying with endothelial redox systems, inflammatory cytokines and growth factors (Kaplan, 2002). 

Systolic dysfunction, or decreased contractility, can be caused by dilated cardiomyopathies, ventricular hypertrophy, or a reduction in muscle mass. Diastolic dysfunction, or restriction in ventricular filling, can be caused by increased ventricular stiffness, mitral or tricuspid valve stenosis, or pericardial disease. Both ventricular hypertrophy and myocardial ischemia can contribute to increased ventricular stiffness. Angiotensin II causes and/or exacerbates heart failure by increasing systemic vascular resistance, promoting sodium retention. 

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