PLASMA-CONCENTRATIONS AND COMPARISONS OF BRAIN AND ATRIAL-NATRIURETIC-PEPTIDE IN NORMAL SUBJECTS AND IN PATIENTS WITH ESSENTIAL-HYPERTENSION

We have developed a radioimmunoassay for the measurement of immunoreactive BNP (1-32) in human plasma. Simultaneous measurement of ANP have also been carried out to allow for direct comparison between circulating BNP and ANP. Plasma levels of immunoreactive BNP (means +/- SEM) were 1.1 +/- 0.1 pmol/l in 36 normal healthy subjects and were significantly elevated in 50 patients with essential hypertension (1.6 +/- 0.2 pmol/l, P < 0.02). Similarly, in patients with essential hypertension plasma levels of ANP were also significantly raised (5.5 +/- 0.6 pmol/l, P < 0.001) when compared with the group of normal healthy subjects (2.8 +/- 0.2 pmol/l). ANP was significantly higher than BNP in normal subjects and in patients with essential hypertension, with ANP/BNP ratios of 2.8 +/- 0.2 and 3.8 +/- 0.3, respectively, in these two groups. A major finding was a significant and positive association between plasma levels of both BNP and ANP within the healthy subjects (r = 0.49, P < 0.05, n = 36) and within the hypertensive subjects (r = 0.76, P < 0.001, n = 50). When all plasma values for BNP and ANP were taken together for both groups, there was an overall correlation coefficient of 0.65 (P < 0.001, n = 86). Both BNP and ANP had significant positive associations with age in hypertensive patients, with correlation coefficients of 0.53 (P < 0.001, n = 50) and of 0.53 (P < 0.001, n = 50) for BNP and ANP, respectively. After correction for age, both BNP and ANP showed positive associations with supine SBP (r = 0.35, P < 0.01, n = 50 for BNP) and (r = 0.32, P < 0.02, n = 50 for ANP) and standing SBP (r = 0.3, P < 0.02, n = 50 for BNP and r = 0.24, P < 0.05, n = 50 for ANP, respectively). These results suggest that BNP is cosecreted with ANP and may be released in response to the same physiological stimuli. Both BNP and ANP may be released into the circulation in hypertensive patients either as a result of an increased BP, or an inherent or aquired defect in the kidneys' ability to excrete sodium.