Hemodynamic and endocrine changes associated with potassium supplementation in sodium-loaded hypertensives.

Abstract

SUMMARY To clarify the mechanism by which potassium (KC1) protects against the blood pressure rising action of sodium (NaCl), we studied the effects of KC1 loading in patients with idiopathic hypertension who, after a period of NaCl restriction, partook of a high NaCl diet. Eleven patients who had taken the KC1 supplement (96 mEq/day) during the high NaCl period showed lesser mean blood pressure (MAP) rise with changes in NaCl intake from 25 to 250 mEq/day than 12 patients who had not taken the KCI supplement (p < 0.001). With a high NaCl diet, the KCl-supplemented patients retained less NaCl, gained less weight, and showed a lesser increase in plasma volume and cardiac output than the non-KCl-supplemented ones. Overall, the increase in blood pressure levels during the high Na diet correlated directly either with changes in plasma volume (p < 0.05) or with changes in cardiac output (p < 0.01). The results suggest that KCI may prevent a rise in blood pressure with NaCl loads in hypertensive patients by attenuating the increase in cardiac output, mainly as a result of the natriuresis. Furthermore, plasma norepinephrine was measured to estimate the sympathetic activity, since the sympathetic nervous system is known to control urinary NaCl excretion. From the low NaCl diet to Day 3 of the high NaCl diet, plasma norepinephrine was significantly (p < 0.01) decreased in the KCl-supplemented patients, whereas it remained unchanged in the non-KCl-supplemented ones. Concomitantly, urinary Na excretion was significantly greater in the early period of NaCl loading in the KCl-supplemented group as compared to the other group. Taken together, these results suggest that lower levels of norepinephrine measured in the plasma of the KCl-supplemented patients in the early NaCI-loading phases of the study are indicative of reduced adrenergic neural activity, which might be involved not only in the attenuation of increased cardiac output, but also in the responses of the kidney to shift the pressure-natriuresis relationship toward normal, leading to the natriuresis. (Hypertension 6: 184-192, 1984) KEY WORDS • sodium • potassium • norepinephrine • cardiac output N UMEROUS animal studies have presented evidence that the mechanisms by which excess salt (NaCl) intake increases blood pressure may include augmentation of sympathetic nerve activity and release of norepinephrine from adrenergic nerve endings.1 : Studies in humans also suggest that an excess of dietary NaCl may augment not only the vascular responsiveness to catecholamines,-1 but also the sympathetic nerve activity in hypertensive patients. 4 Recently, several investigators found hyperactivity of the sympathetic nervous system in hypertensive patients, who showed a considerable increase in blood pressure with NaCl loads.5 -6 Since sympathetic nerve activity is known to influence urinary Na

Sodium-to-Potassium Ratio and Blood Pressure, Hypertension, and Related Factors

“…Twenty-two cross-sectional studies , 1 observational cohort study (37), and 18 RCTs [conducted in 13 hypertensive populations (38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50), 1 prehypertensive/hypertensive population (8), and 4 normotensive populations (50)(51)(52)(53)] were included in this review. Of note, classification of prehypertension status in the DASH diet RCT was based on blood pressure >120/80 mm Hg.…”

“…One crossover RCT included both hypertensive and normotensive adults but reported the results by hypertension status (50). There were 7 parallel-arm RCTs (38,39,41,42,44,45,47) and 6 crossover RCTs (40,43,46,(48)(49)(50) conducted in hypertensive populations only (Table 1). These RCTs enrolled subjects from Australia (41), Austria (49), India (38), Italy (40,42,44,45), Japan (47), New Zealand (48), The Netherlands (43), the United Kingdom (46,50), and the United States (39).…”

“…Sample sizes ranged from 9 (49) to 522 (39), with retention rates >89% (reported in 10 RCTs) (38,39,42,43,(45)(46)(47)(48)(49)(50). Six RCTs were conducted in a double-blind fashion (39,40,42,43,45,46), 2 RCTs were single-blind (physician or study staff) (38,50), 4 RCTs were not blind due to the nature of the intervention (41,44,48,49), and 1 RCT did not report on blinding (47). Study durations ranged from 6 to 180 d in the parallel-arm RCTs (39,47) and from 14 to 84 d per intervention/control period in the crossover RCTs.…”

“…Six RCTs were conducted in a double-blind fashion (39,40,42,43,45,46), 2 RCTs were single-blind (physician or study staff) (38,50), 4 RCTs were not blind due to the nature of the intervention (41,44,48,49), and 1 RCT did not report on blinding (47). Study durations ranged from 6 to 180 d in the parallel-arm RCTs (39,47) and from 14 to 84 d per intervention/control period in the crossover RCTs. All but 1 RCT (38) in hypertensive subjects examined the excretion of sodium and potassium with the use of 24-h urine specimens.…”

“…Methods for measuring dietary intake varied among the few RCTs that reported this information (38,39,41), and only 2 RCTs in hypertensive subjects reported the use of food composition tables (38,41); information on the nutrient database was not reported in the remaining RCTs (Table 1). Six RCTs in hypertensive populations examined blood pressure outcomes only (38,39,41,42,44,49), whereas 7 examined both blood pressure outcomes and renin-angiotensin variables (40,43,(45)(46)(47)(48)50). None of the RCTs in hypertensive populations examined arterial stiffness, the augmentation index, or endothelial dysfunction.…”