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Electrical stimulation of the aortic depressor nerve in conscious rats still causes a hypotensive effect after blockade of the autonomic nervous system and nitric oxide production
Author(s) -
Durand Marina de Toledo,
Castania Jaci Airton,
Salgado Maria Cristina Oliveira,
Salgado Helio Cesar
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.956.5
Subject(s) - bradycardia , medicine , stimulation , blockade , anesthesia , atropine , vasodilation , blood pressure , prazosin , sympathetic nervous system , heart rate , receptor , antagonist
Previous observations indicated that α 1 ‐ adrenergic receptor blockade did not blunt, completely, the hypotensive response to electrical stimulation of the aortic depressor nerve (ADN) in conscious normotensive and L‐NAME hypertensive rats. In the present study it was examined whether the reflex bradycardia played a role in the above hypotensive response. Rats received catheters into the femoral artery and vein and a pair of electrodes around the ADN under pentobarbital anesthesia. ADN stimulation (1mA, 2 ms, 5 to 90 Hz) was applied during 20s, before and after triple pharmacological blockade (prazosin + atropine + atenolol). The hypotensive response to ADN stimulation was greater in L‐NAME hypertensive (‐26±4 to ‐70±10 mmHg; N=6) as compared to normotensive (‐21±3 to ‐54±2 mmHg; N=8) rats, while the bradycardic responses were similar (‐40±12 to ‐147±39 bpm and ‐17±3 to ‐94±19 bpm). After the triple pharmacological blockade the bradycardic response was abolished. Nevertheless, the hypotensive response was not completely blunted and the significant remnant fall in mean arterial pressure was similar in normotensive (12±2 to 27±2 mmHg) and L‐NAME hypertensive rats (13±2 to 27±3 mmHg). These results show that the bradycardic response did not affect the residual fall in pressure induced by ADN stimulation and suggest the activation of a non‐adrenergic vasodilatory mechanism which does not involve nitric oxide.