The study suggests that the diminished cardiovagal response in the baroreflex of hypertensive rats is likely due to an alteration on the input side, as parasympathetic cardioinhibitory mechanisms of the nucleus ambiguus are not significantly altered.
Animal data implicate upstream input alterations in hypertensive baroreflex impairment; leaves open translation to human mechanisms.
The distribution and reactivity of cardiac parasympathetic neurons in the ventral medulla of hypertensive rats (spontaneously hypertensive rats [SHR] and stroke-prone spontaneously hypertensive rats [SHRSP]) were compared with age matched normotensive rats (Wistar and Wistar-Kyoto [WKY]). Rats were anesthetized withα- chloralose and urethane. L-glutamate (Glu, 10 mM, 11 nl) was microinjected into the medulla to map the distribution of the cardioinhibitory neurons in and around the nucleus ambiguus (NA). The distribution pattern of the bradycardiac sites was similar in the four strains of rats. Differences in the maximal bradycardiac responses were not statistically significant either. In comparison, hypertensive rats had significantly larger depressor responses to Glu microinjected into the caudal ventrolateral medulla. Taken together, the results suggest that the ventral medulla of hypertensive rats has enhanced sympathetic reactivity, whereas the parasympathetic cardioinhibitory mechanisms of the NA of hypertensive rats are not significantly altered. Therefore, the diminished cardiovagal response in the baroreflex of hypertensive rats may be due to an alteration on the input side.
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Chiou et al. (2000) studied this question.
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