Restraining effects of captopril on sympathetic excitatory responses in dogs: a spectral analysis approach

Abstract

This study was planned to clarify the effects of captopril administration on the autonomic control of the circulation in conscious dogs and in dynamic conditions using spectral analysis of R-R interval and systolic arterial pressure (SAP) variabilities. Changes in sympathovagal balance modulating the sinoatrial (SA) node were inferred, respectively, from the low (LFR-R)- and high-frequency (HFR-R) components of R-R variability; LFSAP furnished a marker of sympathetic vasomotor control. Increases in sympathetic activity were induced by three different experimental maneuvers [bilateral carotid occlusion (BCO), coronary artery occlusion (CAO), and dynamic exercise] capable of increasing sympathetic outflow to the SA node and to the vessels. Studies were performed both before and after intravenous captopril administration. During BCO, only LFSAP increased from 4.3 +/- 1.5 to 19.7 +/- 4.1 mmHg2; during CAO, both LFR-R and LFSAP increased, respectively, from 3 +/- 1 to 21 +/- 2 normalized units (nu) and from 4.1 +/- 1.3 to 7.2 +/- 1.5 mmHg2. Dynamic exercise at 2 and 4 km/h progressively raised LFR-R from 8 +/- 2 to 58 +/- 7 and 75 +/- 5 nu, respectively; LFSAP showed a parallel trend increasing from 2.5 +/- 0.7 to 8.04 +/- 1.9 and 12.7 +/- 2.2 mmHg2. In all experimental conditions, captopril significantly (P < 0.05) blunted the increase of LFSAP. A restraining effect on LFR-R was apparent only with CAO. Spectral analysis of cardiovascular variabilities indicates that, in the conscious dog, acute captopril administration has an important inhibitory effect on cardiac sympathetic excitatory mechanisms as well as on sympathetic vasomotor control.

Respiratory-related heart rate variability in progressive experimental heart failure

“…This is in keeping with the known predominant resting vagal tone in resting dogs (32). With the onset of mild left ventricular systolic and diastolic dysfunction, there were major decreases of total RRI power and HF RRI variability, suggesting a significant contribution of decreased parasympathetic nervous system modulation in early heart failure pathophysiology.…”

582 Respiratory-related heart rate variability in progressive experimental heart failure

“…In the present experiments, the baseline power density spectrum of heart rate was characterized by a predominance of the HF parasympathetically mediated region. This is in keeping with the known predominant resting vagal tone in resting dogs (32). With the onset of mild left ventricular systolic and diastolic dysfunction, there were major decreases of total RRI power and HF RRI variability, suggesting a significant contri-bution of decreased parasympathetic nervous system modulation in early heart failure pathophysiology.…”

Time course of sympathovagal imbalance and left ventricular dysfunction in conscious dogs with heart failure

“…These adverse reactions are assumed to be related to reflex-mediated sympathoexcitation. Unlike these vasodilators, angiotensin-converting enzyme inhibitors have been documented to improve sympathovagal imbalance and to exert beneficial influences on hemodynamics and long-term clinical outcome in patients with chronic heart failure (6,28,31,32). Recently, several large clinical trials have demonstrated that direct interference with the sympathetic nervous system by using a ␤-blocker improves symptoms and cardiac function in patients with dilated cardiomyopathy (23,34).…”