Sodium depletion with antihypertensives

Potassium restriction was also associated with sodium retention and with calcium depletion in various studies. The converse is also true, giving one good explanation as to why potassium works so well. The mineral causes the body to excrete more sodium in the urine, the same mode of action achieved with antihypertensive drugs called thiazide diuretics. Potassium seems to correct salt sensitivity as well. 

Drug-Drug Interaction Lithium. Telmisartan 40 mg per day was added into the antihypertensive regimen of a 52-year-old schizophrenic woman who had been on lithium 900 mg and haloperidol 20 mg per day. Her lithium level increased to 2.6 meq/L from a range of between 0.83 meq/L and 1.02 meq/L prior to the introduction of telmisartan urea and creatinine increased from normal baseline values to 76 mg/dL and 4.6 mg/dL, respectively, and potassium level was 7.0 mmol/L. Following haemodialysis, her laboratory results retiuned to normal, symptoms abated and lithium was replaced with valproic acid [18 ]. The exact mechanism of this interaction is not known however, it is thought that activation of ATI results in increasing sodium reabsorption at the proximal convoluted tubules which subsequently results in reduction in aldosterone secretion. This ultimately causes hyperkalemia and hyponatraemia. Sodium depletion may cause increase in lithium reabsorption from the proximal convoluted tubules. 

Patients at increased risk of NSAID-induced gastrointestinal adverse effects (e.g., dyspepsia, peptic ulcer formation, and bleeding) include the elderly, those with peptic ulcer disease, coagulopathy, and patients receiving high doses of concurrent corticosteroids. Nephrotoxicity is more common in the elderly, patients with creatinine clearance values less than 50 mL/minute, and those with volume depletion or on diuretic therapy. NSAIDs should be used with caution in patients with reduced cardiac output due to sodium retention and in patients receiving antihypertensives, warfarin, and lithium. 

It is usually recommended that ACE inhibitors be continued peri-operatively in common with other antihypertensives. There is some evidence that postoperative haemodynamic stability is improved and renal function protected. Pretreatment with ACE inhibitors may reduce tachyphylaxis to sodium nitroprusside and help to prevent rebound hypertension. On the other hand, there is evidence that ACE inhibitors may predispose to hypotension during anaesthesia and that they reduce cerebral blood flow during any period of systemic hypotension. Furthermore, the response to and recovery from hypotensive episodes due to blood loss or circulatory depletion may be impaired. At present, the advice concerning these drugs would be to continue therapy up to and including the day of operation. Another rare side-effect of ACE inhibitors is angioneurotic oedema, which has occasionally been seen complicating intubation. 

Therapeutic uses Thiazide diuretics decrease blood pressure in both the supine and standing positions postural hypotension is rarely observed, except in elderly, volume-depleted patients. These agents counteract the sodium and water retention observed with other agents used in the treatment of hypertension (for example, hydralazine). Thiazides are therefore useful in combination therapy with a variety of other antihypertensive agents including (3-blockers and ACE inhibitors. Thiazide diuretics are particularly useful in the treatment of black or elderly patients, and in those with chronic renal disease. Thiazide diuretics are not effective in patients with inadequate kidney function (creatinine clearance less than 50 mls/min). Loop diuretics may be required in these patients. 

Hydrochlorothiazide/triamterene is a diuretic combination. Hydrochlorothiazide inhibits reabsorption of sodium and chloride in the ascending loop of Henle and early distal tubules. Triamterene interferes with sodium reabsorption at the distal tubule. The combination provides additive diuretic activity and antihypertensive effects and minimizes potassium depletion. They are indicated in the treatment of edema or hypertension in patients who have, or are at risk of developing, hypokalemia. 

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