Key result
Peptidic ANG receptor antagonists profoundly inhibit the tonic activity of cardiovascular but not respiratory neurons in the VLM, independent of ANG II or ANG-(1-7) receptors.
Peptidic ANG II receptor antagonists profoundly inhibit the tonic activity of cardiovascular neurons in the VLM independently of ANG II or ANG-(1-7) receptors.
Should not alter clinical use of ANG receptor antagonists; leaves open non-canonical actions on VLM cardiovascular neurons for validation in conscious models.
The peptidic ANG II receptor antagonists [Sar(1),Ile(8)]ANG II (sarile) or [Sar(1),Thr(8)]ANG II (sarthran) are known to decrease arterial pressure and sympathetic activity when injected into the rostral part of the ventrolateral medulla (VLM). In anesthetized rabbits and rats, the profound depressor and sympathoinhibitory response after bilateral microinjections of sarile or sarthran into the rostral VLM was unchanged after prior selective blockade of angiotensin type 1 (AT(1)) and ANG-(1---7) receptors, although this abolished the effects of exogenous ANG II. Unlike the neuroinhibitory compounds muscimol or lignocaine, microinjections of sarile in the rostral VLM did not affect respiratory activity. Sarile or sarthran in the caudal VLM resulted in a large pressor and sympathoexcitatory response, which was also unaffected by prior blockade of AT(1) and ANG-(1---7) receptors. The results indicate that the peptidic ANG receptor antagonists profoundly inhibit the tonic activity of cardiovascular but not respiratory neurons in the VLM and that these effects are independent of ANG II or ANG-(1---7) receptors.
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Potts et al. (2000) studied this question. Peptidic ANG II receptor antagonists (sarile or sarthran) was evaluated on Arterial pressure and sympathetic activity. Peptidic ANG receptor antagonists profoundly inhibit the tonic activity of cardiovascular but not respiratory neurons in the VLM, independent of ANG II or ANG-(1-7) receptors.
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