EFFECT OF ANTIHYPERTENSIVE THERAPY ON ELECTROLYTES Jan Castenfors Electrolyte disturbances during antihypertensive therapy is mostly, as expected, caused by diuretic therapy, but some other antihypertensive agents may also affect salt and water balance. Peripheral vasodilatation with hydralazin and mi- noxidil as well as sympatholytic (a or ganglionic blocking) agents is known to cause retention of sodium and water, resulting in expansion of the extra cellular volume, which counteracts their antihypertensive ac- tion (McMahon 1978). The mechanism behind this retention of sodium and water, is still obscure, but is probably related to renal factors. These antihypertensive agents therefore mostly have to be used in combination with a diuretic agent to enhance their antihypertensive effect. Saluretic therapy with thiazide diuretics exerts its antihypertensive effect through an increased urinary excretion of sodium and water, but also results in an increased potassium excretion, which tends to decrease body potassium. Four months treatment with the diuretic agent mefruside induced a significant decrease in plasma potassium, however, potassium content in muscle tissue (biopsy technique) only showed a minor decrease (Bevegkd et al. 1977). On the other hand, four months mefruside therapy induced a significant increase in intracellular sodium content. sodium ion probably moves into the cell in exchange for the loss of potassium ion from the cell. These changes in intracellular sodium and potassium can be abolished with the potassium sparing diuretic drug amiloride (Bergstrom 1975). Potassium loss is also counteracted by using the aldosterone blocking drug spironolactone as diuretic agent. 13-receptor blockade alone has not been demonstrat- ed to influence electrolyte balance, However, some studies suggest (Hodler 1976)that 13-receptor blockade tends to increase urinary sodium excretion and decrease urinary potassium excretion during the first week of diuretic therapy with furosemide. This is also supported by own unpublished observations that 13- receptor blockade with timolol seems to interfere with the initial diuretic effect of amiloride, resulting in an increased sodium excretion and decreased potassium and water excretion. These effects may be due to a suppression of the renin mediated secondary aldos- teronism induced by diuretic therapy, and/or also by direct renal effects. 13-receptor blockade, thus can be expected to counteract potassium losses during diuretic therapy which adds another argument for this useful combination in antihypertensive therapy. REFERENCES Bergstrom J: The effect of hydrochlorothiazide and amiloride administered together on muscle electrolytes in nor- ma1 subjects. Acta Med Scand 197: 415-419, 1975. BevegArd S, Castenfors J. Danielson M & Bergstr6m J: Effect of saluretic therapy on muscle content of water and electrolytes in relation to hemodynamic variables. Acta Med Scand 202: 379-384, 1977. Hodler J: Metabolische Wirkungen der Betablocker. In: Die Betablocker - Gegenwart und Zukunft, pp 272-287. Ed: W Schweizer. Verlag Hans Huber. Bern 1976. McMahon F G: Management of essential hypertension. Fu- tura Publishing Company Inc. Mount Kisco. New York 1978. 61

EFFECT OF ANTIHYPERTENSIVE THERAPY ON ELECTROLYTES

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EFFECT OF ANTIHYPERTENSIVE THERAPY ON ELECTROLYTES

Jan Castenfors

Electrolyte disturbances during antihypertensive therapy is mostly, as expected, caused by diuretic therapy, but some other antihypertensive agents may also affect salt and water balance.

Peripheral vasodilatation with hydralazin and mi- noxidil as well as sympatholytic (a or ganglionic blocking) agents is known to cause retention of sodium and water, resulting in expansion of the extra cellular volume, which counteracts their antihypertensive ac- tion (McMahon 1978). The mechanism behind this retention of sodium and water, is still obscure, but is probably related to renal factors. These antihypertensive agents therefore mostly have to be used in combination with a diuretic agent to enhance their antihypertensive effect.

Saluretic therapy with thiazide diuretics exerts its antihypertensive effect through an increased urinary excretion of sodium and water, but also results in an increased potassium excretion, which tends to decrease body potassium. Four months treatment with the diuretic agent mefruside induced a significant decrease in plasma potassium, however, potassium content in muscle tissue (biopsy technique) only showed a minor decrease (Bevegkd et al. 1977). On the other hand, four months mefruside therapy induced a sig-

nificant increase in intracellular sodium content. sodium ion probably moves into the cell in exchange for the loss of potassium ion from the cell. These changes in intracellular sodium and potassium can be abolished with the potassium sparing diuretic drug amiloride (Bergstrom 1975). Potassium loss is also counteracted by using the aldosterone blocking drug spironolactone as diuretic agent.

13-receptor blockade alone has not been demonstrat- ed to influence electrolyte balance, However, some studies suggest (Hodler 1976) that 13-receptor blockade tends to increase urinary sodium excretion and decrease urinary potassium excretion during the first week of diuretic therapy with furosemide. This is also supported by own unpublished observations that 13- receptor blockade with timolol seems to interfere with the initial diuretic effect of amiloride, resulting in an increased sodium excretion and decreased potassium and water excretion. These effects may be due to a suppression of the renin mediated secondary aldos- teronism induced by diuretic therapy, and/or also by direct renal effects. 13-receptor blockade, thus can be expected to counteract potassium losses during diuretic therapy which adds another argument for this useful combination in antihypertensive therapy.

REFERENCES Bergstrom J : The effect of hydrochlorothiazide and amiloride administered together on muscle electrolytes in nor- ma1 subjects. Acta Med Scand 197: 415-419, 1975. BevegArd S, Castenfors J. Danielson M & Bergstr6m J: Effect of saluretic therapy on muscle content of water and electrolytes in relation to hemodynamic variables. Acta Med Scand 202: 379-384, 1977.

Hodler J: Metabolische Wirkungen der Betablocker. In: Die Betablocker - Gegenwart und Zukunft, pp 272-287. Ed: W Schweizer. Verlag Hans Huber. Bern 1976. McMahon F G: Management of essential hypertension. Fu- tura Publishing Company Inc. Mount Kisco. New York 1978.