THE EFFECT OF HYPERTENSIVE EPISODES AND CARDIAC-HYPERTROPHY ON THE CANINE CARDIAC BAROREFLEX

1. Left ventricular (LV) hypertrophy has been implicated in the reduction of baroreflex sensitivity present in hypertension. The aim of the current study was to investigate the mean arterial pressure-heart;ate reflex (MAP-HR) in a model which induced left ventricular hypertrophy but no sustained blood pressure elevation. 2. Five mongrel dogs were exposed to transient blood pressure elevation of between 20 and 30 mmHg, through hindlimb compression using a pneumatic pressure suit, for 7 h per day, 6 days per week for 6 weeks. Resting blood pressure was not altered by the 6 week hindlimb compression intervention. 3. Echocardiographically determined LV mass (mean+/-s.e.m.) was 116.0+/-7.4g prior to hindlimb compression (baseline) and elevated to 125.4+/-8.1 g (P=0.003) after 6 weeks of compression. A reduction in the early (E) to late (A) transmitral diastolic flow ratio (E/A) from 1.80+/-0.06 at baseline to 1.54+/-0.09 (P=0.037) after the 6 week intervention suggested that cardiac compliance was reduced. 4. The maximum gain of the MAP-HR reflex, studied using the 'steady-state' drug technique, when blood pressure was normal, showed a trend for reduction from 3.85+/-0.43 beats/min per mmHg at baseline to 3.10+/-0.45 beats/min per mmHg (P=0.067) after 6 weeks of compression. This gain reduction became significant after beta-adrenoceptor blockade with propranolol (3.13+/-0.55 vs 2.32+/-0.25 beats/min per mmHg P=0.039). Covariant analysis showed a significant inverse correlation between LV mass and maximum gain (r=0.96; P<0.001) during the 6 week compression period. 5. The MAP-HR reflex changes in this model mimic those present in hypertension and implicate cardiac hypertrophy as one possible mediator.