Neural regulation of cardiovascular function during inhibition of nitric oxide synthesis in anaesthetized rats

Abstract

Recent years have seen emergence of the role of nitric oxide (NO) in maintaining cardiovascular newlinehomeostasis. Deficient synthesis of NO is an important component not only of hypertension but newlinealso of cardiac autonomic dysfunction. However, the underlying mechanisms are not clearly newlinedefined. It is not known whether the hemodynamic and cardiac autonomic derangements newlineassociated with NO deficiency are due to interference of direct vasodilatory action of NO or newlineinvolve some neuro-humoral system. In order to clarify and fill in the existing gaps, we assessed newlinecardiac autonomic functions during acute and chronic inhibition of NO synthesis by NG-nitro-Larginine newlinemethyl ester (L-NAME) in adult Wistar rats. Baroreflex sensitivity (BRS) and heart newlinerate variability (HRV) were measured for assessment of cardiac autonomic functions. BRS was newlinedetermined from heart rate responses to changes in systolic arterial pressure achieved by newlineintravenous administration of hypertensive (phenylephrine) and hypotensive (sodium newlinenitroprusside) stimuli. Time and frequency domain measures of HRV were calculated from 5 newlineminute (min) electrocardiogram recordings. In the time domain, we determined the standard newlinedeviation of normal R-R intervals (SDNN) and square root of mean squared difference of newlinesuccessive R-R intervals (RMSSD). Spectral components of HRV were obtained by fast Fourier newlinetransform analysis. Frequency bands defined for spectral analysis were: total spectral power (P) newlinefrom 0 to 3 Hz, low frequency (LF) spectral power from 0.25 to 1 Hz and high frequency (HF) newlinespectral power from 1 to 3 Hz. LF to HF ratio (LF:HF) indicated sympathovagal balance. We newlinefurther evaluated the contribution of oxidative stress, sympathetic nervous system as well as newlinerenin-angiotensin system, to the changes in neural regulation of cardiovascular system during newlineinhibition of NO synthesis.