Intracerebroventricular administration of hypertonic sodium chloride solution reduces the sensitivity of the baroreceptor heart reflex in anaesthetized rats
A Brattström1, E Appenrodt, A Brattström
1Institute of Physiology, Medical School, Magdeburg, FRG.
Insights
Intracerebroventricular infusion of hypertonic saline in rats elevates blood pressure and impairs baroreflex regulation. This suggests central sodium sensitivity contributes to hypertension by reducing the baroreflex buffering capacity.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
Background:
- Intracerebroventricular (i.c.v.) administration of hypertonic sodium chloride solutions is known to increase blood pressure (BP) and shorten heart period (interbeat-interval, IBI).
- Impairment in baroreflex regulation is hypothesized to be involved in this process.
Purpose of the Study:
- To investigate the effect of i.c.v. infusion of isotonic and hypertonic sodium chloride solutions on baroreceptor-heart reflex (BHR) sensitivity in anesthetized rats.
Main Methods:
- Anesthetized rats underwent i.c.v. infusion of isotonic or hypertonic (0.6 M, 1.0 M) sodium chloride solution for 15 minutes.
- Acute BP rises were induced using i.v. pressoric agents (phenylephrine, methoxamine).
- BHR sensitivity was assessed by measuring the reflex prolongation of IBI (delta ms/mm Hg).
Main Results:
- i.c.v. infusion of isotonic sodium chloride did not alter BHR sensitivity.
- Hypertonic sodium chloride infusion elevated BP, shortened IBI, and significantly impaired BHR sensitivity.
- The BHR was also observed to be reset during hypertonic saline infusion.
Conclusions:
- Increased central sensitivity to sodium chloride can elevate BP and impair the baroreflex buffering capacity.
- This impairment may contribute to the development of hypertension.
Abstract:
Intracerebroventricular (i.c.v.) infusion of hypertonic sodium chloride solution increased blood pressure (BP) and shortened heart period (interbeat-interval: IBI) that is why an impairment in baroreflex regulation is believed to be part of that process. Therefore, in anaesthetized rats (1.35 g urethane/kg BW) the baroreceptor-heart reflex (BHR) was tested before and during i.c.v. infusion (15 min) of isotonic or hypertonic (0.6 M, 1.0 M) sodium chloride solution by inducing an acute BP rise by i.v. pressoric agents (phenylephrine, methoxamine). The evoked reflex prolongation of the IBI was taken to estimate the sensitivity of that BHR (delta ms/mm Hg). Whilst i.c.v. infusion of isotonic sodium chloride solution did not affect BHR sensitivity, hypertonic sodium chloride solution not only elevated BP and shortened IBI but also reset and impaired the BHR. Therefore, an increased central sensitivity to sodium chloride might not only increase BP but also impair the buffering capacity of the BHR against this rise and in this way support development of hypertension.
