A single intake of alcohol has a depressor effect on BP that lasts for several hours after drinking, while repeated intakes for 7 days have both depressor and pressor effects according to the differences in time intervals after the last drink. This study suggests that the chronic effects of alcohol on BP might be overestimated when based on casual BP measurements alone.

SUMMARY The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (JI = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteronism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 ± 7 to 113 ± 7 mm Hg (p<0.025) in primary aldosteronism but not in renovascular hypertension (130 ± 6 to 128 ± 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated v-intercept of the curve was shifted rightward in both primary aldosteronism (111 ± 7 vs 87 ± 4 mm Hg; p<0.025) and renovascular hypertension (128 ± 5 vs 95 ± 2 mm Hg; p<0.025) and the slope was depressed in primary aldosteronism (16 ± 1 vs 40 ±17 [mEq/day]7mm Hg; p < 0.025) but not in renovascular hypertension (130 ± 75 vs 40 ± 13 [mEq/day]/mm Hg). After operation, the renal function curves in primary aldosteronism and renovascular hypertension were normalized. The rightward shift of the curve in renovascular hypertension probably was due to an increase in renal vascular resistance caused by the stenotic renal vascular lesion as well as to increased resistance caused by stimulation of the reninangiotensin system. The rightward shift in primary aldosteronism presumably was due to enhancement of renal tubular sodium reabsorption by aldosterone; the depressed slope likely resulted from suppression of the renin-angiotensin feedback mechanism by the excess aldosterone and resultant volume expansion. Thus, an abnormal renal function curve seems to have played a major role in the genesis of each of these forms of secondary hypertension. (Hypertension 10: 11-15, 1987) KEY WORDS • arterial pressure-natriuresis relationship hypertension • primary aldosteronism pathogenesis • renovascular B ASED on the hypothesis of Guyton and colleagues, 1 -2 the renal function curve (pressurenatriuresis relationship) must always be affected in the genesis of hypertension regardless of the factors that initiate the hypertension process (if the From the Department of Medicine, National Cardiovascular Center, Osaka, Japan.Supported by a research grant for cardiovascular diseases (59C-8) from the Ministry of Health and Welfare.Presented in part at the 1 lth Scientific Meeting of the International Society of Hypertension, Heidelberg, West Germany, 1986. Address for reprints: Dr. Genjiro Kimura, Division of Nephrol...

1. The effects of dietary sodium on blood pressure and levels of sodium, other electrolytes and noradrenaline (NA) in the cerebrospinal fluid (CSF) and blood of 15 patients with essential hypertension were studied. The CSF and blood sampling was carried out after 7 days of a high salt intake (16-18 g/day) and after 7 days of a low salt intake (1-3 g/day). 2. Blood pressure and sodium concentrations in CSF and serum were significantly higher in the high salt period than the low salt period (CSF Na+ concentration: 147.7 +/- 0.4 mmol/L vs 145.3 +/- 0.5 mmol/L; P less than 0.001). Levels of CSF pressure and potassium or calcium concentrations were not different between the two periods. Plasma NA and plasma renin activity (PRA) were lower and CSF NA levels tended to be lower in the high salt period. 3. The levels and the changes in sodium and NA in CSF were not significantly different between the salt-sensitive (n = 8) and the non-salt-sensitive (n = 7) subjects, but the changes in plasma NA and PRA were smaller in the salt-sensitive subjects. 4. These results indicate that the sympathetic nervous system is less suppressed in salt-sensitive subjects during high salt intake. This may be due to altered neural responsiveness to sodium loading rather than being greater increases in sodium concentration in the central nervous system.

The manifestations of Takayasu's arteritis of the aorta were studied in 84 patients. The extent of the involvement of the aorta was classified on aortographic examination in 54 patients and from the clinical manifestations in 30. Involvement of the aorta was classified as: (1) arch type in 47 cases; (2) extensive type (whole aorta and its branches involved) in 27 cases; and (3) descending thoracic and abdominal type (only descending thoracic and abdominal aortas involved) in 10 cases. The three types resembled one another in clinical manifestations and laboratory findings except for ischemic signs which varied with the type of lesion and a slight difference in the ratio of male to female patients. Generalized, cardiac and pulmonary symptoms were noted by about two thirds of the patients in the early stage. About one third complained of local pain. The erythrocyte sedimentation rate and C-reactive protein were high values during the active stage of this disease. The hemagglutination test using tannic acid-treated erythrocytes was positive in five of seven cases. It is not clear yet that circulating anti-arterial antibodies are the direct cause of Takayasu's arteritis.