Autonomic neuroscience : basic & clinical
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Comparative Study
alpha-Adrenoceptor subtypes mediating regional kidney blood flow responses to renal nerve stimulation.
The mechanisms underlying the relative insensitivity of the renal medullary circulation to renal sympathetic nerve stimulation (RNS) remain unknown. Therefore, we tested the effects of systemic alpha(1)- and alpha(2)-adrenoceptor blockade on responses to electrical RNS in pentobarbitone anaesthetized rabbits. Renal blood flow (RBF), cortical laser Doppler flux (CLDF), and to a lesser extent medullary LDF (MLDF) were reduced by RNS in a frequency-dependent manner. ⋯ Rauwolscine markedly blunted renal vasoconstrictor responses to renal arterial guanabenz, but not phenylephrine. These data suggest that alpha(1)-adrenoceptors contribute to RNS-induced vasoconstriction in the renal cortex, but contribute less in vascular elements controlling medullary perfusion. Activation of alpha(2)-adrenoceptors appears to blunt RNS-induced renal vasoconstriction, but this mechanism does not underlie the relative insensitivity of medullary perfusion to RNS.
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Comparative Study
Enhanced cardiac vagal efferent activity does not explain training-induced bradycardia.
Studies of heart rate variability (HRV) have so far produced contradictory evidence to support the common belief that endurance training enhances cardiac parasympathetic tone. This may be related to the fact that most studies failed to specifically isolate the vagally mediated influence of respiration. This study used a cross-sectional comparison of endurance athletes (n=20; ATHL) exhibiting resting bradycardia and age-matched nonathletes (n=12; CRTL) to indirectly assess training effects on amplitude and timing characteristics of respiratory sinus arrhythmia (RSA). ⋯ RSA phase was not affected by training status or by changes in total breath duration. RSA amplitude was negatively related to breathing frequency in all groups (p<0.05), while the mean slope of the relationship (sensitivity) was not different between groups. In as much as RSA is an adequate marker of cardiac vagal efferent activity, these results add support to a contribution of a decrease in intrinsic heart rate to explain training-induced bradycardia.