No abstract

The high frequencies of the TT genotype and T allele in Chinese populations may contribute to the high prevalence of albuminuria in patients with type 2 diabetes. The possibility of synergism between the AGT TT genotype and the ACE D allele should also be explored.

1. The response of venous plasma natriuretic peptides (atrial natriuretic peptide, ANP, and brain natriuretic peptide, BNP) plasma cyclic guanosine monophosphate (cGMP) and vasoactive hormones to dynamic exercise has been studied in 16 subjects undergoing diagnostic exercise tolerance for ischaemic heart disease (IHD), and in five healthy control subjects. 2. In patients with IHD, plasma ANP increased 3-fold (mean 16 +/- 2.5 pmol/L pre-exercise, 51 +/- 11 pmol/L after exercise, P < 0.01). Increase in plasma BNP (10.5 +/- 1.6 pmol/L pre-exercise, 13 +/- 2 pmol/L after exercise, P < 0.01) was proportionately much less than ANP but more sustained. In exercising normal subjects, plasma ANP levels doubled (P < 0.01) but there was no significant change in plasma BNP levels. 3. In patients with IHD, there was a significant correlation between levels of plasma ANP and BNP before exercise (r = 0.97, P < 0.001) as well as during exercise (r = 0.79, P < 0.001). 4. Hormone responses in patients with positive exercise tests did not differ significantly from those with negative tests. 5. Although resting levels of plasma ANP and BNP in IHD are correlated, the findings indicate different mechanisms of secretion. The low BNP/ANP ratio in response to acute dynamic exercise presumably reflects the predominance of ANP in pre-secretory atrial stores.

Acute myocardial infarction (MI) results in activation of neurohormonal systems and increased plasma concentrations of myocardial enzymes and structural proteins. We hypothesized that plasma levels of N-terminal pro-brain natriuretic peptide (NT-BNP) would respond more vigorously after MI than those of other natriuretic peptides. We also sought to compare this response with that of the established myocardial injury markers troponin T (TnT), myoglobin and creatine kinase MB (CK-MB). We obtained multiple blood samples for measurement of atrial natriuretic peptide (ANP), N-terminal pro-ANP, brain natriuretic peptide (BNP) and NT-BNP along with CK-MB, TnT and myoglobin in 24 patients presenting to the Coronary Care Unit within 6 h of onset of MI. Multiple samples were obtained in the first 24 h, then at 72 h, 1 week, 6 weeks and 12 weeks. NT-BNP increased rapidly to peak at 24 h and exhibited greater ( P <0.001) absolute increments from baseline compared with BNP and ANP, whereas NT-ANP did not change from baseline. Proportional increments in NT-BNP were also greater than those for the other natriuretic peptides ( P <0.05). Natriuretic peptide levels reached their peak around 24 h, later than peak TnT, CK-MB and myoglobin (peak between 1-10 h), and NT-BNP and ANP remained elevated on average for 12 weeks. Our present results, with detailed sampling of a cohort of acute MI patients, demonstrate greater absolute and proportional increments in NT-BNP than ANP or BNP with sustained elevation of these peptides at 12 weeks.