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To assess the effects of age on responsiveness of atrial natriuretic factor (ANF) release, and the possible contribution of cardiac sympathetic activity, in young (n = 8) and older normotensives (n = 7), the effects of cardiac volume load on plasma ANF, central venous pressure, and general hemodynamics were evaluated. Studies were performed after pretreatment with placebo or 80 mg propranolol. Cardiac volume loading increased central venous pressure by 3–5 mmHg (1 mmHg = 133.3 Pa); β-blockade did not affect this response. Cardiac volume load caused significant increases in heart rate (10–15 beats/min) and cardiac index (by 0.7–0.8 L∙min−1∙m−2) and decreases in plasma catecholamines. Propranolol attenuated the increases in heart rate and cardiac index. These hemodynamic responses did not differ significantly between the two groups of subjects. Cardiac volume load significantly increased plasma ANF, by 87 ± 21 pg/mL in the young normotensives and by 212 ± 33 pg/mL in the older normotensives (p

Twenty patients whose systemic hypertension was not controlled with chronic beta-blocker therapy were studied to evaluate the acute (first dose), short-term (4 weeks) and chronic (6 to 12 months) effects of the calcium antagonist felodipine on blood pressure (BP), left ventricular (LV) anatomy and function and on plasma norepinephrine. The first dose of felodipine rapidly reduced total peripheral resistance and BP, associated with significant increases in heart rate, cardiac output and plasma norepinephrine. During chronic therapy, at the end of the dosing interval (12 hours), significant decreases in BP persisted with minimal changes in the other variables. However, even after 1 year of therapy BP after dosing again rapidly decreased associated with 50 to 100% increases in plasma norepinephrine and small increases in heart rate and cardiac output. Despite the marked decreases in systolic BP, LV wall thickness and mass showed only small decreases (LV mass -- 17 +/- 7 g/m2 after 1 year) and significant LV hypertrophy persisted after 1 year. Both average systolic BP and plasma norepinephrine were significant determinants of LV mass over the duration of the study. It is concluded that during chronic treatment with the twice-daily tablet formulation of felodipine, major daily fluctuations in BP persist associated with persisting sympathetic hyperactivity. The latter may play a role in the modest regression of LV hypertrophy despite 30 to 40 mm Hg decreases in systolic BP for 1 year.

To determine whether hypertension occurring after heart transplant causes the development of cardiac hypertrophy, changes in pressure load (N = 13) and left ventricular anatomy (N = 11) were evaluated up to 1 year after heart transplant in a prospective longitudinal study. Pressure load was evaluated by 24-hour ambulatory blood pressure monitoring, and left ventricular anatomy and function were assessed by M-mode echocardiography under two-dimensional guidance. Body weight increased by 11 to 12 kg. Blood pressure showed a gradual increase during the first few months after transplant: diastolic pressure by 15 to 18 mm Hg and systolic pressure by 12 to 15 mm Hg, with hypertension persisting during the night. Nearly all patients required treatment with one or two antihypertensive drugs. The increase in blood pressure was related to increased total peripheral resistance with minor decreases in cardiac output. Both septal and posterior wall thickness and left ventricular mass (by 25 to 30 gm/m 2 ) decreased during the initial months after transplant and subsequently remained at "normal" levels (100 gm/m 2 ). The persistence of normal left ventricular mass may indicate either that the increases in daily pressure load and body weight were not sufficient to induce myocardial growth or that the latter was prevented by, for example, absence of cardiac sympathetic nerve activity.