| pubmed-article:2625505 | pubmed:abstractText | Sympathetic nerve and/or adrenal medulla contributions to stress-induced cardiovascular responses were investigated by factoring out their influence using adrenal demedullation (DMED) and/or chemical sympathectomy with guanethidine (GUAN). Rats divided into 4 groups [sham-operated/saline (SHAM/SAL), SHAM/GUAN, DMED/SAL and DMED/GUAN] were injected i.p. over 4 weeks with either saline or GUAN (25 mg/kg/day). At the end of this treatment period, blood pressure (BP) and heart rate (HR) were monitored via carotid catheter prior to and during restraint in conscious rats. Treatments did not alter basal BP or HR when compared to controls. Restraint increased HR (delta 72 bpm) and systolic, diastolic and mean BP (delta approximately 20 mm Hg) in control animals. Restraint-induced HR change was significantly greater in DMED/SAL animals (delta 88 bpm), but less in SHAM/GUAN animals (delta 40 bpm) than in controls. DMED/GUAN was not different from SHAM/GUAN alone in altering HR response to stress, supporting the greater influence of sympathetic nerves over adrenal medulla in controlling HR. Chronic GUAN abolished normal pressor responses to restraint stress. DMED increased diastolic blood pressure response to stress. However, in DMED/GUAN rats, not only did stress fail to increase blood pressure but rather stress produced hypotension (delta - 34 mm Hg MAP), demonstrating the role of adrenal medulla in maintaining BP during stress. Differential effects of the various treatments on diastolic and systolic pressure suggest that the treatments had effects on peripheral vasculature. These results demonstrate that sympathetic nerves and adrenal medulla have important influences on cardiovascular function during stress and that in the absence of either, the other system may partially compensate.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
