Restraint stress (RS) is an experimental model to study stress-related cardiovascular responses, characterized by sustained pressor and tachycardiac responses. We used pharmacologic and
surgical procedures to investigate the role played by sympathetic nervous system (SNS) and parasympathetic nervous system (PSNS) in the mediation of stress-evoked cardiovascular responses. Ganglionic blockade with
pentolinium significantly reduced RS-evoked pressor and tachycardiac responses. Intravenous treatment with
homatropine methyl bromide did not affect the pressor response but increased
tachycardia. Pretreatment with
prazosin reduced the pressor and increased the tachycardiac response. Pretreatment with
atenolol did not affect the pressor response but reduced
tachycardia. The combined treatment with
atenolol and
prazosin reduced both pressor and tachycardiac responses. Adrenal demedullation reduced the pressor response without affecting
tachycardia. Sinoaortic
denervation increased pressor and tachycardiac responses. The results indicate that: (1) the RS-evoked cardiovascular response is mediated by the autonomic nervous system without an important involvement of humoral factors; (2)
hypertension results primarily from sympathovascular and sympathoadrenal activation, without a significant involvement of the cardiac sympathetic component (CSNS); (3) the abrupt initial peak in the hypertensive response to restraint is sympathovascular-mediated, whereas the less intense but sustained hypertensive response observed throughout the remaining restraint session is mainly mediated by sympathoadrenal activation and
epinephrine release; (4)
tachycardia results from CSNS activation, and not from PSNS inhibition; (5) RS evokes simultaneous CSNS and PSNS activation, and heart rate changes are a vector of both influences; (6) the baroreflex is functional during restraint, and modulates both the vascular and cardiac responses to restraint.