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Hypertension, Vol 5, 545-551, Copyright © 1983 by American Heart Association

ARTICLES

Elevated plasma catecholamines in hypertensives with primary glomerular diseases

M Ishii, T Ikeda, M Takagi, T Sugimoto, K Atarashi, T Igari, Y Uehara, H Matsuoka, Y Hirata, K Kimura, T Takeda and S Murao

Supine plasma concentration of norepinephrine (PNE), epinephrine (PE), and aldosterone (PA), plasma renin activity (PRA), and blood volume (BV) were measured in 25 normotensive and 11 hypertensive patients with biopsy-proven glomerulonephritis who had serum creatinine concentrations of less than 1.6 mg/dl, and in 20 normotensive control subjects. PNE and PE were measured according to the trihydroxyindol method using high pressure liquid chromatography. Renal clearances of p- aminohippurate (CPAH) and endogenous creatinine (Ccr) were also determined. Age, BV, and 24-hour urinary excretion of sodium were not significantly different in the three groups. Although all the measured variables were comparable between the control subjects and the normotensive nephritic patients, blood pressure, PNE, PE, PRA, and PA were significantly higher and CPAH and Ccr were significantly lower in the hypertensive nephritic patients than in the normotensive nephritic patients or the control subjects. In the pooled nephritic patients, mean blood pressure was significantly correlated with PNE (r = 0.76, p less than 0.001), PE (r = 0.34, p less than 0.05), PRA (r = 0.33, p less than 0.05), PA (r = 0.40, p less than 0.05) and CPAH (r = -0.51, p less than 0.01). Highly significant positive correlation was also observed between PNE and systolic pressure (r = 0.63, p less than 0.001) or diastolic blood pressure (r = 0.78, p less than 0.001). The results suggest that deterioration of renal function is an important factor in the development of hypertension even in non-azotemic patients with glomerulonephritis, and that increased activities of the sympathetic nervous system and the renin-aldosterone system participate, in part, in elevating blood pressure in the hypertensive nephritic patients. Mechanisms involved in the elevation of plasma concentrations of catecholamines and renal effects on the plasma catecholamines remain to be elucidated.

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