Sodium renin-angiotensin system

The development of ascites is related to systemic arterial vasodilation that leads to the activation of the baroreceptors in the kidney and an activation of the renin-angiotensin system, with sodium and water retention and vasoconstrictor production. 

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. 

Mineralocorticoids are involved in controlling electtolyte and fluid levels.9,44 The primary mineralo-corticoid produced by the adrenal cortex is aldosterone. Aldosterone increases the reabsorption of sodium from the renal tubules. By increasing sodium reabsorption, aldosterone facilitates the reabsorption of water. Aldosterone also inhibits the renal reabsorption of potassium, thus increasing potassium excretion. Mineralocorticoid release is regulated by fluid and electrolyte levels in the body and by other hormones, such as the renin-angiotensin system. 

The short-term mechanism for BP control centres on the baroreceptor reflex. The long-term mechanism involves the renin-angiotensin system and body sodium control via aldosterone. 

Clinical signs of chronic renal failure primarily include (1) edema due to reduced renal perfusion leading to stimulation of the renin-angiotensin system, which stimulates aldosterone secretion leading to retention of sodium and water, (2) hypocalcemia with compensatory parathyroid activity and osteodystrophy, and (3) reduced red blood cell counts due to decreased synthesis of erythropoietin as a result of damage to the juxtaglomerular cells. 

This occurs in hypopituitarism. In theory the best treatment is corticotropin, but the disadvantages of frequent injection are such that hydrocortisone is preferred. Usually less hydrocortisone is needed than in primary insufficiency. Special sodium-retaining hormone is seldom required, for the pituitary has little control over aldosterone production which responds principally to plasma potassium concentration and to the renin-angiotensin system. Thyroxine and sex hormones are given when appropriate. The general conduct of therapy does not differ significantly from that in primary adrenal insufficiency. 

The pathophysiology of ciclosporin-induced hypertension is complex and not yet fully elucidated. Increased systemic vascular resistance subsequent to altered vascular endothelium function, renal vasoconstriction with reduced glomerular filtration and sodium-water retention, and/or increased activity of the sympathetic nervous system were suggested, while only a minor role or none was attributed to the renin-angiotensin system (10). However, hypertension often occurs before changes in renal function or sodium balance can be demonstrated, and ciclosporin nephrotoxicity alone does not explain ciclosporin-associated hypertension (8,11). 

The importance of volume control in patients with renal insufficiency extends beyond its effect on blood pressure. Accordingly, the addition of hydrochlorothiazide can overcome the blunting by a high sodium intake of the therapeutic efficacy of ACE inhibition on proteinuria (42). This presumably relates to volume-related activation of the renin-angiotensin system. 

Under conditions in which arterial pressure or body fluid volumes are sensed as subnormal, the renin-angiotensin system will be activated and plasma renin activity and angiotensin II levels will be elevated. These conditions include dietary sodium restriction or sodium depletion (such as during diuretic therapy), renal artery stenosis, and congestive heart failure. In each case, fluid and sodium will be retained until the pressure and volume are again sensed as normal. Note... 

In one of the earliest reports it was shown that not only captopril but also minoxidil caused GFR to decrease in a patient with a transplant renal artery stenosis [23], suggesting that it was the fall in blood pressure itself, which caused the reduced GFR. However, in other studies it was found that GFR decreased only during treatment with captopril and enalapril [24] whereas a fall in blood pressure during sodium nitroprusside [25] or minoxidil [26, 27], which do not directly interfere with the renin-angiotensin system, did not result in a decline in GFR. Furthermore, studies from Anderson et al. indicated that during infusion of... 

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