Stability and Inter‐relationships of Hormone, Haemodynamic and Electrolyte Levels in Heart Failure in Man

Abstract

Relationships between clinical status, haemodynamic measurements, hormone and biochemical indices, and maintenance diuretic dose in patients with chronic cardiac failure, are not clear. This study assessed such relationships and their stability under standardized conditions in 21 hospitalized patients. The daily maintenance dose of frusemide correlated closely and in a positive fashion with plasma levels of renin activity, angiotensin II and aldosterone (P less than 0.001), and to a lesser extent with plasma noradrenaline. Although there was some overlap, patients most incapacitated by their heart failure had the highest circulating levels of renin activity, angiotensin II, aldosterone and noradrenaline. Plasma aldosterone correlated closely with concomitant angiotensin II levels (r = 0.70, P less than 0.001) but not with its other secretagogues ACTH (as reflected by plasma cortisol) or plasma potassium. Close positive correlations between angiotensin II and plasma levels of urea and creatinine (P less than 0.01) were observed. Both renin and angiotensin II showed positive relationships with right heart pressures, but were inversely related to cardiac index and arterial pressure. These results show close relationships between clinical and haemodynamic indices on one hand, and hormones on the other. The renin-angiotensin system appears to be the primary regulator of aldosterone under these conditions, and its activity relates closely to haemodynamic measurements and to the degree of azotaemia.

The effect of angiotensin II and noradrenaline alone and in combination on renal sodium excretion in man.

“…The increase in plasma NA (mean 316 ± 51 pg m-1') and final levels achieved (Table 2) are slightly higher than those that might be expected in upright salt depleted subjects and are similar to those seen during submaximal exercise (Robertson et al, 1979;Romoff et al, 1979;Seidelin et al, 1987). These levels are also comparable with those found in patients with heart failure (Levine et al, 1982;Fitzpatrick et al, 1985). The results of our study show that these small increments of AII, or NA, alone produce a significant reduction in sodium excretion ( Figure 1 and Table 3).…”

“…The increase in plasma AII (mean 19 ± 5 pg ml-1 for all 14 infusions) and the final levels achieved by infusion (Table 2) are similar to those that would be expected in normal subjects on a low salt diet (Oelkers et al, 1974), or in some groups of patients with heart failure (Dzau et al, 1981;Fitzpatrick et al, 1985). Similarly the baseline plasma NA levels in our subjects were at the upper part of the normal range for resting supine subjects.…”

The circulating renin–angiotensin system during treatment with metoprolol or captopril in patients with heart failure due to non‐ischaemic dilated cardiomyopathy

“…The daily dose of furosemide in the present study was only in the region of 60 mg, and Fitzpatrick et al . [5] reported that a daily maintenance dose of furosemide lower than 80 mg had only a modest stimulatory effect on renin and aldosterone levels in patients with stable heart failure. However, they found increasing levels of renin, A II and aldosterone when increasing the daily maintenance doses of furosemide to above 80 mg. On the other hand, Anand et al .…”

“…One of these is the atrial natriuretic peptide (ANP) system [2–4]. Several studies have shown a good correlation between circulating ANP levels and cardiac filling pressures and have also demonstrated the effect of exercise on ANP levels [5–8].…”

Patients with acute heart failure treated with the CARRESS-HF diuretic protocol in association with canrenoate potassium: Tolerance of high doses of canrenoate potassium

“…High doses of loop diuretics are used in patients with acute heart failure (AHF) to achieve euvolaemia, blocking sodium-potassium-chloride cotransporter 2 (NKCC2) proteins at the apical surface of thick ascending limb cells and inhibiting potassium reabsorption [6,7]. Moreover, loop diuretics cause important potassium secretion at the distal nephron, where the principal cells take up sodium from the lumen through the epithelial sodium channel in exchange for potassium via sodiumpotassium-adenosine triphosphatase [8].…”