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The D allele of the angiotensin-converting enzyme (ACE) gene has been linked with diabetic nephropathy and IgA glomerulonephritis and with faster renal disease progression. The association of this allele with nephroangiosclerosis has been scarcely investigated. We have tested this association in 45 hypertensive patients (all whites) with well defined nephroangiosclerosis (diagnosis established on the basis of renal biopsy in all cases) and moderate to severe renal failure. As studies of genetic association of small size often produce conflicting results, besides a control group of 343 Italian patients with essential hypertension and normal renal function, we elected to use also a very large control group of race-matched subjects taken from a meta-analysis of 27,565 whites. The proportion of patients with the D allele (64%) was higher in patients with nephroangiosclerosis than that in Italian hypertensives (54%) and in whites (54%). DD and DI genotypes were more prevalent in patients than in control groups. The dominant model (DD and DI v II: nephroangiosclerosis v Italian controls: chi2 = 6.19, P = .012; nephroangiosclerosis v whites chi2 = 6.86, P = .009) fitted the data better than the codominant and the recessive model (P < or = .022). The D allele is associated with nephroangiosclerosis with a dominant effect in the sample of patients studied. Although intervention studies are needed to see whether these findings imply a causal association, our data suggest that this allele may at least act as disease marker in nephroangiosclerosis.

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Discrete brain sections were obtained from rats once or repeatedly (once a day for 5 days) given i.p. nifedipine, verapamil or diltiazem at doses ranging from 5 to 20 mg/kg. The biogenic amines and metabolites in the hypothalamus, brain stem, hippocampus, striatum, cortex and thalamus-midbrain were determined by high performance liquid chromatography with electrochemical detection. The drug-induced changes, displaying regional specificity and differences according to the various com pounds, suggested that: (a) serotonergic systems were activated, especially in fasted rats or after repeated treatment; (b) the dopaminergic system of the striatum was inhibited by nifedipine which did reduce the HVA levels and the HVA/DA, as well as the DOPAC/DA, ratio. These effects disappeared after repeated treatment. It was also speculated that the data obtained could be of great interest in view of the possi ble use of calcium antagonists to treat disorders of the central nervous system.