Nine patients with untreated essential hypertension (mean casual blood pressure 173/109 +/- 14/7 mm Hg) (+/- SD) were studied in the control state and after 16 weeks of treatment with nifedipine, 10 mg orally every 8 hours. Direct arterial blood pressure monitored continuously over 24 hours showed that nifedipine significantly reduced systolic and diastolic blood pressure throughout the day and the night. The variability of blood pressure was not altered by nifedipine therapy. There was no significant change in heart rate after nifedipine therapy. Chronic nifedipine therapy increased forearm blood flow and decreased forearm vascular resistance, consistent with its action as a vasodilator. The absolute blood pressure responses to tilt, handgrip and cold were reduced, but the percent increase in pressure was not altered by therapy. Plasma renin activity was not altered by chronic nifedipine therapy. At each study, the sensitivity and setting of the baroreflex response to i.v. phenylephrine was measured. After chronic nifedipine therapy there was resetting of the sinoaortic baroreflex and an increase in its sensitivity. Successful control of blood pressure with nifedipine led to a significant reduction in the left ventricular mass index.

SUMMARY Sixteen untreated black patients with mild-to-moderate hypertension and no evidence of target organ damage were matched for age, sex, casual blood pressure (BP), and socioeconomic status with 16 white hypertensives. All patients were studied under standardized conditions in the hospital where they underwent continuous intraarterial ambulatory monitoring of BP and assessment of BP control mechanisms. BP characteristics over prolonged periods of recording were similar for both groups, as were sinoaortic baroreflex activity and pressor response to isometric and dynamic exercise and to cold. Fasting cholesterol and triglyceride levels in both groups were similar. Resting plasma renin activity (PRA) was significantly lower in blacks, but no difference was observed in resting plasma norepinephrine levels. Urinary excretion of Na + and K + was also similar in both groups. Thus, results showed that casual BPs matched for black and whites, and recorded over a prolonged period, were similar in pattern, variability, and response to pressor stimuli. It appears that, if BP contributes to the different patterns of morbidity in blacks and whites, it is more likely to be the actual level of BP rather than differences in BP characteristics. (Hypertension 4: 817-820, 1982) KEY WORDS • ambulatory blood pressure • reflex cardiac control * atheroma T HE observation that the black population in North America has a higher blood pressure (BP) than the white population 1 2 has excited much interest. Associated with the higher BP is an increased incidence of target organ damage in blacks manifested as left ventricular hypertrophy (LVH), 3 cerebrovascular accidents/ and changes in optic fundi. 5The pathophysiological basis for raised BP in blacks and whites may differ, and reduced levels of plasma renin activity (PRA), 6 resting heart rate (HR), 7 and dopamine beta-hydroxylase (DBH) 8 could reflect differences in activity of the central nervous system. In addition, pathological studies have shown a different distribution of atheroma in the arteries of blacks and whites, 9 ' l0 the former having an increased deposition in the cerebral arteries, but conversely the coronary arteries are relatively spared, and this might be related to different BP characteristics and control between the groups.The purpose of this report is to compare the responses of matched black and white hypertensive pa-

1. Continuous intra-arterial ambulatory monitoring of blood pressure was recorded in 46 patients with mild to moderate hypertension under standardized conditions. M-mode echocardiography was performed after recording and left ventricular mass index calculated by standard formulae. 2. Systolic blood pressure from continuous recording was significantly correlated with left ventricular mass index (mean 24 h: r = 0.543, n = 45, P less than 0.001). Diastolic blood pressure exhibited a weaker but still significant correlation with left ventricular mass index (mean 24 h: r = 0.318, n = 45, P less than 0.05). Casual systolic blood pressure was significantly correlated with left ventricular mass index (r = 0.476, n = 46, P less than 0.001) but casual diastolic blood pressure did not correlate with left ventricular mass index (r = 0.245, n = 46). Awake blood pressure variability, age, resting plasma renin activity and resting plasma noradrenaline levels did not have a significant correlation with left ventricular mass index. 3. Nine patients were treated for 16 weeks with once-daily timolol and repeat ambulatory monitoring and M-mode echocardiography was performed with the same protocol. 4. Once-daily timolol provided good 24 h control of blood pressure and repeat echocardiography showed a reduction in left ventricular mass index in that group of patients (t = 2.59, P less than 0.05).

Medical Research Societyi S o l a t e d i n a q u i e t rooin; a d o c t o r [ O J K I then e n t e r e d t h e room and me83sured blood p r e s s u r e c o n v e n t i o n a l l y and a t t h e same time i n t h e o t h e r arm.T h i s r a i s e d Bosoinat blood p r e s s u r e i n a l l h y p e r t e n s i v e p a t i e n t s , ~y an average of 18/16 [ s y s t o l i c / d i a s t o l i c ) , 5/6 and 1/3 mHg on t h e 1 s t . 3rd and 5 t h days of admission r e s p e c t i v e l y .S i g n i f i c a n t and s i m i l a r d e c r e a s e s occured i n mean ward blood p r e s s u r e [17/13 from 1 s t t o 5th day) and i n t h e alarm r e a c t i o n ( 1 7 / 1 2 from 1 s t t o 5th d a y ] .There was i n a d d i t i o n i n i n d i v i d u a l s u b j e c t s a s i g n i f i c a n t c o r r e l a t i o n between t h e d e c l i n e i n ward blood p r e s s u r e and t h e r e d u c t i o n i n t h e alarm r e a c t i o n [ r = 0.927, p <0.01 f o r s y s t o l i c ) .I n c o n t r o l s u b j e c t s t h e alarm r e a c t i o n , t h e d e c r e a s e i n t h e alarm r e a c t i o n and t h e f a l l i n ward blood p r e s s u r e were s i g n i f i c a n t l y less than i n h y p e r t e n s i v e s .These r e s u l t s suggest t h a t a t t e n u a t i o n of t h e alarm r e a c t i o n i s l a r g e l y r e s p o n s i b l e f o r t h e f a l l i n blood p r e s s u r e which o c c u r s when p a t i e n t s w i t h u n t r e a t e d hypertension a r e a d m i t t e d t o h o s p i t a l . D e p a r t m e n t of C a r d i o v a s c u l a r Medicine, East Birmingham Hospital, BirminghamNifedipine, a calcium a n t a g o n i s t a n d p o t e n t vasod i l a t o r , h a s s h o w n g r e a t potential as a n antih y p e r t e n s i v e a g e n t alone (Olivari MT e t l . , C i r culation 1979; 2: ( 5 ) ) or i n combination with 6-blockade ( C o r e a L e s Acta T h e r a p e u t i c a 1980; 6: 177-189). W e report t h e results of t r e a t m e n t with nifedipine f o r a mean p e r i o d of 15 w e e k s ( r a n g e 12 w e e k s to 18 w e e k s ) assessed by continu o u s ambulatory i n t r a -a r t e r i a l p r e s s u r e r e c o r d i n g under s t a n d a r d i z e d conditions as d e s c r i b e d previously by this D e p a r t m e n t (Watson RDS M.H y p e r t e n s i o n 1980; 5: ( 2 ) ) .9 patients with untreated e s s e n t i a l h y p e r t e n s i o n , mean c a s u a l B P 1 7 3 / 1 0 9 g 4 / 7 mmHg ( S D ) w e r e s t u d i e d in the c o n t r o l state a n d t h e n following t r e a t m e n t with nifedipine 1 0 mg p.0. t d s . A t e a c h s t u d y t h e sensitivity a n d s e t t i n g of the baroreflex r e s p o n s e t o i n t r a v e n o u s p h e n y l e p h r i n e w a s m e a s u r e d u s i n g the method of S m y t h HS e t . ( C i r c . R e s . 1969; 24: 1 0 9 ) . R e p e a t monitoring s h o w e d s i g n i f i c a n t r e d u c t i o n s in 24 h o u r B P (153/98Y9/11 ( S D ) mmHg t o 1 3 3 / 8 5 4 3 / 8 (SD)mmHg, p