Microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) has been shown to produce a dose-dependent increase in blood pressure and heart rate. We have tested the effect of subpressor infusions of ANG II (10 ng . kg-1 . min-1) in the NTS on reflex bradycardia after intravenous administration of the vasoconstrictor phenylephrine (1-12 micrograms) in normotensive urethan-anesthetized rats. ANG II within the brain is thought to contribute to the decreased baroreflex sensitivity in spontaneously hypertensive rats (SHR). The sensitivity of the baroreflex was significantly decreased by the infusion of ANG II (1.01 +/- 0.08) compared with control (2.41 +/- 0.51) in the normotensive animals. Baroreflex sensitivity was significantly decreased in SHR (0.40 +/- 0.21) compared with normotensive animals. We conclude that ANG II within the NTS can inhibit the function of baroreceptor reflexes in normotensive animals, suggesting that the endogenous peptide may perform an inhibitory role in the baroreflex arc, and this is further evidence that central ANG II is involved in blood pressure of SHR.

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Freely moving rats exhibit complex motor and cardiovascular responses to tactile stimulation (12.5 psi air puff, 100-ms duration). In naive Wistar-Kyoto rats, the behavioral response is characterized by a short-latency (25 +/- 1 ms) jumping event, the magnitude of which habituates to repeated stimuli. In a paradigm of consecutive tactile stimuli, each delivered at 30-s intervals, the arterial pressure (AP) response is consistent in profile (36.4 +/- 1.7 mmHg, initial stimulus) and habituates rapidly (15.4 +/- 2.2 mmHg, at 20th stimulus). Rates of habituation of the jumping behavior and AP increase are similar and significantly correlated (P less than 0.01), suggesting partial common mediation. Heart rate changes are bimodal and highly dependent on stimulus number. Initial stimuli elicit bradycardia (-42 +/- 7 beats/min), habituating to extinction by stimulus 10. A temporally delayed tachycardia becomes evident by trial 5 (19 +/- 5 beats/min) and persists unchanged throughout the remainder of the 30-stimulus session. Delayed tachycardia may represent activation of secondary autonomic mechanisms. The nature of cardiovascular responses elicited by the tactile stimulus suggests a somatomotor reflex mediated through the ventrolateral medulla. Adrenal enucleation exaggerated the magnitude of transient bradycardia and abolished extinction of bradycardia with repeated stimuli. Adrenal medullary secretion has only minor importance in direct mediation of the response, but this study suggests that adrenal function plays an important role in tonically setting the level of cardiac responsiveness to parasympathetic vs. sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

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