Tonic cardiovascular effects of angiotensin II in the ventrolateral medulla.

Abstract

The rostral and caudal parts of the ventrolateral medulla play a major role in the control of blood pressure. Both regions contain a high density of receptor binding sites for angiotensin II, and it has been shown previously that microinjection of angiotensin II into the rostral ventrolateral medulla causes a rise in blood pressure. The aims of this study were to determine the cardiovascular effects of microinjection of angiotensin II and its specific antagonist T here is considerable evidence that angiotensin II (Ang II) in the brain may play a role in hypertension. For example, it is well established that Ang II can influence fluid and electrolyte balance and arterial blood pressure via an action on circumventricular organs and the nucleus tractus solitarius (for review, see Reference 1). Recently, it has also been demonstrated that microinjection of Ang II into sites within the rostral part of the ventrolateral medulla (VLM) or application of the peptide to the nearby ventral surface results in an increase of blood pressure. -3 Furthermore, the sites at which Ang II microinjection produces the largest pressor responses correspond very closely to the location of Ang II receptor binding sites.2 These sites are confined to a highly localized region referred to as the subretrofacial nucleus, which contains sym-

Angiotensin and baroreflex control of the circulation

“…However, we did not observe any change in blood pressure or RSNA by giving an effective dose of Sarile (10 pmol) to urethane-anesthetized rabbits. This contrasts the findings of other groups that found a marked reduction in blood pressure with this agent or with [Sar 1 ,Thr 8 ]-Ang II (41,45). A recent study suggests, however, that this effect is not related to the blockade of Ang II receptors (46).…”

“…Andreatta and colleagues (40) suggested that the RVLM may contain a reninangiotensin system since Ang I applied to the ventral surface of the brainstem of the cat produced an increase in blood pressure after conversion to Ang II. Sasaki and Dampney (41) found that the sites which produced the greatest increase in blood pressure in the RVLM were also the sites containing the highest concentration of Ang receptors. We initially mapped various dorsal and ventral sites with microinjections of Ang II and found that marked pressor responses were observed only when Ang II was administered into a discrete region of the RVLM corresponding to the subretrofacial nucleus.…”

Baro-excited neurons in the caudal ventrolateral medulla (CVLM) recorded using the whole-cell patch-clamp technique

“…Muratani et al 26 and Alzamora et al 27 obtained similar results. As the baro-excited CVLM neurons formed synapses with the RVLM neurons, these previous results [25][26][27] support our present data. However, the findings of their studies and ours do not answer the question as to whether Ang-II activates the baro-excited CVLM neurons directly.…”

“…However, the findings of their studies and ours do not answer the question as to whether Ang-II activates the baro-excited CVLM neurons directly. Considering the results of previous studies, [25][26][27] we cannot deny the possibility that Ang-II may have activated non-baroexcited CVLM neurons and that these neurons in turn sent synaptic activity to the baro-excited CVLM neurons.…”

“…Sasaki and Dampney 25 showed that Ang-II microinjected in the RVLM region increased peripheral sympathetic nerve activity, whereas injection of the peptide in the CVLM region decreased the peripheral sympathetic activity. These results indicate that the CVLM neurons, Whole-cell patch-clamp of baro-excited CVLM neurons N Oshima et al which form inhibitory synapses with the RVLM neurons, were activated by Ang-II.…”