ABSTRACTS

PRELOM AND AFTERLOAD REDUCTION DURING ANGIOTENSIN II BLOCKADE WITH THE CONVERTING ENZYME INHIBITOR. A.P. Niarchos, MD, T.G. Pickering, MD, D.B. Case, MD, J.M. Wallace, MD, A. Morganti, MD, J.E. Sealey, DSc, and J.H. Laragh, MD, FACC. Cardiovascular Center, The New York Hospital-Cornell Medical Center, New York, N.Y. 10021

The hemodynamic effects of the converting enzyme inhibi- tor (CEI, SQ20881) were investigated in 7 normotensive patients (group I) with normal plasma renin activity

(PRA), in 5 hyperten$ives with normal PR4 (group II), and in 5 hypertensives with high PRA (group III). No signi- ficant hemodynamic changes were observed during CEI admin- istration in group I. In group II a 16% decrease (p<.OS) was observed in stroke index (SI), and cardiac index (CI) which resulted in a 12% decrease (p<.OOOS) in mean arter- ial pressure (MAP), but without change in total peripheral resistance (TPR). In group III the 19% decrease in MAP (p<.OOO5) was due to a significant fall in TPR (by 30%, p<.OO5); in this group SI and CI were significantly in- creased (by 14%, p<.O5). There were no compensatory changes in heart rate (HR) neither in group II nor in group III. These results indicate that: 1) in hyperten- sive patients with high PBA, CEI decreases MAP by de- creasing TPR; in this group SI and CI are increased; 2) in hypertensives with normal PRA, CEI decreases MAP by reducing CT, an effect which is the result either of venodilatation or decreased myocardial contractility; 3) acute angiotensin II blockade concurrently modulates baroreceptor mediated responses in HR as evidenced by the lack of expected increase in HR during hypotension.

THE INTERACTION BETWEEN SYMPATHETIC NERVOUS SYSTEM, RENIN- ANGIOTENSIN AND SODIUM BALANCE IN BLOOD PRESSURE MAINTEN- ANCE DURING TILT IN ESSENTIAL HYPERTENSIVE PATIENTS. A. Morganti, MD, 3. Lopez-Ovejero, MD, J.E. Sealey, DSc, T.G. Pickering, MD, A.P. Niarchos, MD, J.H. Laragh, MD, FACC. Cardiovascular Center, The New York Hospital- Cornell Medical Center, New York, N. Y. 10021

The effect of a 30 min 65“ head up tilt on BP, HR and plasma renin activity (PRA) was evaluated in 7 essential hypertensive patients (EHT) on 100 mEq sodium diet before and after 0.12 rag/kg propranolol i.v. Before propranolol mean BP was unchanged during tilt while HR increased by 23.5 + 1.7 beats/rein and PRA by 2.9 + 0.9 ng/ml/h. During propranolol 3 patients fainted after a mean of 20 min tilt. In those who did not faint BP fell by 18.0 2 10.6 mmHg and HR increased by only 9.5 + 4.2 beats/min, that is a 63% + 16 blockade of the HR response. The PRA increase was abolished by propranolol in all but the one patient who had the highest pretreat- ment PRA increase (6.7 ng/ml/h) and the least effective blockade of the HR response during tilt (19%). In 4 of the patients studies were repeated after sodium deprivation and sodium loading. On both diets before pro- pranolol mean BP was again unchanged during tilt, HR had similar increases (28.7 + 9.3 vs. 28.0 + 8.7 beats/min) while PRA always increased more after sodium deprivation (mean 3.4 k 2.3 vs. 1.2 + 0.5 ng/ml/h). After propranolol all sodium depleted patients developed hypotension and fainted whereas BP decreased in only 2 after sodium load- ing (mean 8.6 + 4.4 mmHg); HR increases were similarly blunted (57% + 10 vs. 51% + 11 blockade) and PRA increases wers again abolished. These data show that PRA increases during tilt in EHT are mainly B-adrenergically mediated and suggest that the renin-angiotensin system is an ad- junctive pathway supporting BP during tilt. This support is inversely related to the state of sodium balance.

EFFECTS OF ANTIHYPERTENSIVE THERAPY (AlD) ON CARDIOVAS- CULAR RESPONSES TO EXERCISE

Won Ro Lee, MD; Lay M. Fox, MD, FACC; Lawrence M. Slotkoff, MD, Georgetown University and District of Columbia General Hospital, Washington, D.C.

The effects of AHI on exercise induced changes in heart rate (HR), systolic pressure (SP), diastolic pressure @P), and rate pressure product (RPP), an index to total tension generated, were evaluated by graded treadmill exercise (TM) to subjective maximal tolerance (SM) in 15 mild to moderate hypertensive patients (12 males and 3 females) before (C) and during AHT. Both hydrochlorothi- azide (HCTZ) and alpha methyl dopa (AMD) were used for AHT individually for 4 weeks given in random fashion. Each subject served as his own control. Neither KTZ nor AMD changed HR response to T?L Both IXX'Z and AMD reduced resting SP and DP to comparable levels (SP: C 155 an@; HCTZ 134, p<O.OOl; AMD 130, pLO.001. DP: C 104; KTZ 93, pLO.001; AMD 90, pcO.001). There was no change in BP re- sponse to TM or to recovery during HCTZ. PMD, however, reduced SP and DP at the initial stage (SP: C 194; AMD 173, ~0.01. DP: C 108; AMD 102, p~O.01) and at % (SP: C 218; AMD ZOO, p<O.O5. DP: C 111; AMD 102, pCO.05). SP and DP were significantly less compared with C at all levels of early recovery phase of 'I'M during AMD (Post-TM 1 min: SP C 189, AMD 165, ~~0.01; DP C 101, AMD 92, p< 0.05. Post-TM 3 min: SP C 160, AMD 140, pcO.001; DP C 104, AMD 93, p40.01. Post-TM 5 min: SP C 150, AMD 131, pCo.001; DP C 103, AMD 89, p'O.001). RPP was significant- ly reduced by AMD. Neither HCTZ nor AMD changed the to- tal duration of TM tolerance. Whereas HCTZ failed AMD significantly reduced pressure response i.e. tension gen- erated during exercise presumably reducing myocardial oxygen demand without reducing work capacity.

ECHOCARDIOGRAPHIC ASSESSMENT OF LEFT VENTRICULAR RE- SPONSE TO EXTREMES OF SALT INTAKE IN NORMO-TENSIVE MAN Arthur E. Weyman, M.D., F.A.C.C., Friedrich C. Luft,M.D., Richard Bloch, M.D., Raymond H. Murray, M.D., Myron Weinberger, M.D., Jane Marshall, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana Left ventricular performance in response to extremes of salt intake was evaluated echocardiographically in 8 nor- mal men (ages 29 to 40). In addition to their normal diet patients were given 4 levels of daily sodium intake as follows: 10 mEq x 7 days; 300 mEq x 3 days; 800 mEq x 3 days; 1500 mEq (800~0, 700 iv) x 3d. K+ intake was 75 mEq/day. Parameters studied included end diastolic volume (EDV), end systolic volume (ESV), stroke VO~UIII~

(SV), cardiac output (CO), heart rate (HR), urinary sodi- um excretion (UNaV) and mean arterial blood pressure (MABP). Results (mean + SD) are: Na+ intake (mEq/d) 10 300 800 1500 EDV - cc 125+16 - 136+18 142+19 153+15 ESV - cc 3977 44+6 3977 3577 SV - cc/Beat 86+12 93713 10611 115710 CO L/&n 5.3+0.5 5.9T1.2 5.871 6.971.8 HR Beats/min 62Tl5 63+13 58+9 6OT15 UNaV (mEq/d) 12+4 265+68 702762 14427100 - - -

MABP (mmHg) 83+6 84+7 90+8 99+9 With increasing l&els of salt intaKe significant in-

creases in EDV (P = d.001) SV (P = <.OOl) and CO (P = <.025) were observed. HR and ESV did not change signif- icantly. Both SV and CO correlated with urinary NA excretion r = 0.58, P( .OOl, and r = 0.42, P< 0.02. Since the observed changes in MABP cannot be explained by an increase in systemic vascular resistance these data suggest that increased MABP at increasing salt loads is due to the observed increase in CO and SV.

Fdxuaw 1474 The American Journal of CARMotOGY Volume 41 403