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Mean arterial pressure (MAP), heart rate (HR) and splanchnic sympathetic nerve activity were recorded in conscious, 4 months old, male spontaneously hypertensive rats (SHR; n = 9) and matched normotensive Wistar—Kyoto (WKY) rats (n = 8). 2. The reflex bradycardia and reflex inhibition of splanchnic sympathetic nerve activity were studied in each animal during baroreceptor activation. MAP was raised 30–50 mmHg above control with slow, intra-arterial infusion of noradrenaline (1 μg min−1 kg−1 body wt.). There was a significant negative linear correlation between MAP and splanchnic nerve activity and between MAP and HR in all experiments during noradrenaline infusion. 3. The baroreceptor sensitivity with respect to heart rate control was greatly reduced in SHR compared with WKY rats, being 1.5 ± 0.1 beats min−1 mm−1 Hg and 3.7 ± 0.4 beats min−1 mm−1 Hg respectively (P 0.001). 4. However, baroreceptor sensitivity with respect to control of splanchnic nerve activity, defined as percentage nerve inhibition per mmHg of MAP rise, did not differ statistically between the two groups: 1.8 ± 0.2%/mmHg for SHR and 2.0 ± 0.3%/mmHg for WKY rats. 5. It is suggested that the baroreceptor control of sympathetic ourflow is intact in conscious 4 months old SHR with early established hypertension. 6. It is also suggested that the impaired baroreceptor control of heart rate seen in SHR, and in human essential hypertension, is mainly due to an increased activity of the hypothalamic ‘defence area’, which can selectively block the efferent vagal component of the reflex bradycardia elicited from baroreceptor activation.
Ricksten et al. (1981) studied this question.