[Role of sympathetic nerve fibers in hemodynamic responses to stress in rats].

Hemodynamic responses to acute stress exposure were studied in normotensive control (C) and chronically sympathectomized (S) rats. Male Sprague-Dawley rats received daily sc injections of either saline (C) or guanethidine (S) from 1 to 13 weeks of age. Doppler flow probes were then implanted for the measurement of blood velocity in the sub-diaphragmatic aorta, superior mesenteric artery and distal aorta (hindquarters). After 10 days of recovery and 24 hours before the study, the caudal artery was cannulated. In the conscious freely moving rats, mean arterial pressure (MAP), heart rate (HR) and indices of regional blood flows and vascular conductances (G as blood flow/MAP ratio) were recorded beat to beat, before and during emotional stress (jet of air for 2 min). In basal conditions, mean values of MAP and HR were similar in C (107 +/- 2 mmHg; 399 +/- 8 bpm, n = 9) and S (106 +/- 3 mmHg; 384 +/- 12 bpm, n = 7) rats. The effects of stress on MAP, HR, aortic (AoG), mesenteric (MeG) and hindquarters (HqG) vascular conductances are expressed as percentage changes from baseline (delta): [table: see text] These results highlight the role of vascular sympathetic nerves in pressor responses and systemic and mesenteric vasoconstrictions induced by stress in the rat. They also indicate that vasodilatation in the hindquarters vascular bed is not secondary to withdrawal of sympathetic vasoconstrictor tone but rather to active phenomena which do not involve the stimulation of vascular beta 2-adrenoceptors by neuronal catecholamines nor the release of vasodilator cotransmitters from the sympathetic nerve endings.