Proximal Tubular Function in Essential Hypertensives on Beta-blocker Therapy with Atenolol

Abstract

Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured during waterloading and constant infusion of [131I]hippuran and [125I]iothalamate in 24 mild to moderate essential hypertensive patients before and after 3.5 months treatment with atenolol. Clearances of sodium and potassium were measured 2-3 hours post-dosing and renal vascular resistance (RVR) and filtration fraction (FF) were calculated. Measurement of clearance of lithium (CLi) and uric acid (Curic acid) was employed to investigate specifically proximal tubular function. Beta-blockade with atenolol produced a borderline significant decrement in RPF but no change in GFR, RVR and FF. There was a significant reduction in CLi, fractional proximal escape of sodium and water, Curic acid and an increase in absolute proximal reabsorption of sodium, indicating an inhibition of proximal tubular function. The distal tubular parameters exhibited changes tending to normalize excretion of sodium, but not water. Changes in RVR were inversely related to changes in CLi and Curic acid, suggesting unopposed alfa-adrenergic stimulation to be implicated in the renal counterregulation at a proximal tubular site following long-term administration of atenolol in essential hypertension.

A multicenter study of the association of serum uric acid, serum creatinine, and diuretic use in hypertensive patients

“…A total of 2187 patients were recruited and 42 patients (1.9%) were excluded due to insufficient information of SUA (9), prescription drug use (25), and missing questionnaire data (8). Thus, 2145 patients (1139 men, 1006 women) were included in the statistic analysis.…”

“…β-blockers are known to induce peripheral and renal vascular resistance. In a clinical investigation of essential hypertensive subjects, after 5 months treatment with β-blockers a decrease in renal plasma flow was associated with a significant reduction in uric acid clearance [25].…”

Metoprolol prevents sodium retention induced by lower body negative pressure in healthy men

“…Yet, a natriuretic effect of beta-receptor blockade has been reported in experimental congestive heart failure [6], in spontaneously hypertensive rats [19], and in patients with essential hypertension [20]. However, in other studies, the long-term administration of beta-blockers has been found to decrease renal plasma flow and/or urinary sodium excretion [21,22]. In our normotensive subjects, no significant change in renal hemodynamics was found after 1 week of administration, thereby confirming several previous observations [17,18,20].…”

Prevalence of hyperuricemia and its association with antihypertensive treatment in hypertensive patients in Taiwan

“…It seems that this could be due to diuretic-induced hyperuricemia resulting in renal failure. Nevertheless earlier studies have shown that diuretics and β-blockers may deplete renal blood flow and consequently decrease urate clearance [13,14]. A recent animal study showed, however, that hyperuricemia may directly induce renal dysfunction [15,16], and a clinical cohort observation study demonstrated that high serum uric acid levels are associated with a higher incidence of end-stage renal disease [17].…”