Abstract
Salivary gland function is regulated by both the sympathetic and parasympathetic nervous systems. Previously we showed that the basal sympathetic outflow to the salivary glands (SNASG) was higher in hypertensive compared to normotensive rats and that diabetes reduced SNASG discharge at both strains. In the present study we sought to investigate how SNASG might be modulated by acute changes in the arterial pressure and whether baroreceptors play a functional role upon this modulation. To this end, we measured blood pressure and SNASG discharge in Wistar–Kyoto rats (WKY-intact) and in WKY submitted to sinoaortic denervation (WKY-SAD). We made the following three major observations: (i) in WKY-intact rats, baroreceptor loading in response to intravenous infusion of the phenylephrine evoked an increase in SNASG spike frequency (81%, p<0.01) accompanying the increase mean arterial pressure (ΔMAP: +77±14mmHg); (ii) baroreceptor unloading with sodium nitroprusside infusion elicited a decrease in SNASG spike frequency (17%, p<0.01) in parallel with the fall in arterial blood pressure (ΔMAP: −30±3mmHg) in WKY-intact rats; iii) in the WKY-SAD rats, phenylephrine-evoked rises in the arterial pressure (ΔMAP: +56±6mmHg) failed to produce significant changes in the SNASG spike frequency. Taken together, these data show that SNASG increases in parallel with pharmacological-induced pressor response in a baroreceptor dependent way in anaesthetised rats. Considering the key role of SNASG in salivary secretion, this mechanism, which differs from the classic cardiac baroreflex feedback loop, strongly suggests that baroreceptor signalling plays a decisive role in the regulation of salivary gland function.
Published Version
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