Reflex changes in post- and preganglionic sympathetic adrenal nerve activity and postganglionic sympathetic renal nerve activity upon arterial baroreceptor activation and during severe haemorrhage in the rat.

Carlsson, S., Skarphedinsson, J. O., Delle, M., Hoffman, P. & Thoren, P. 1992. Reflex changes in post- and preganglionic sympathetic nerve activity and postganglionic sympathetic renal nerve activity upon arterial baroreceptor activation and during severe haemorrhage in the rat. Acta Physiol Scand144, 317–323. Received 19 August 1991, accepted 18 November 1991. ISSN 0001–6772. Department of Physiology, University of Goteborg, Sweden and Department of Physiology, University of Iceland, Reykjavik, Iceland. The aim of the study was to compare pre- (pre-aSNA) and postganglionic adrenal sympathetic nerve activity (post-aSNA) and postganglionic renal sympathetic nerve activity (rSNA) in rats during arterial baroreceptor activation and haemorrhage. Adrenal multifibre nerve activity was recorded in chloralose-anaesthetized Wistar rats. To test for pre-aSNA or post-aSNA in adrenal nerves, a ganglionic blocker, trimethaphan (10 mg kg-1), was administered i.v. If the nerve activity in the adrenal nerve decreased or increased the nerve was considered to contain predominantly post-or preganglionic fibres, respectively. In contrast, the renal nerves exhibit an almost pure postganglionic activity. Baroreceptor activity was tested by activation of baroreceptors, with an a-receptor agonist, phenylephrine, which was slowly infused (0.5–2 mUg kg-1 min-l), and to deactivate the baroreceptors the rats were bled down to 50 mmHg for 8 min. The experiments showed that all tested nerve types were baroreceptor dependent. There were no significant differences between the slopes relating nerve activity inhibition to increase in blood pressure (infusion of phenylephrine). During maximal inhibition there was a difference between the rSNA and pre-aSNA, 87 ± 4%, n=6, and 68±6%, n = 10 (P < 0.01) of the control value, respectively. The maximal inhibition of post-aSNA was 80 ± 3%, n=7, of the control value. During haemorrhage there was a difference between the nerve populations. Pre-aSNA responded with a marked increase within 1.5 rnin (159 ± 29% of control, n= 7) and was then maintained at that level until retransfusion. Post-aSNA responded with i transient increase, reaching 158 ± 19% of control after 1.5min but then decreased slowly during the next 3 min, reaching a value of 89 8 76 at 7.5 rnin of haemorrhage. Finally, rSNA (n = 7) responded with an initial increase (peak value 1.5 min 138 ± 16%) followed by an inhibition to a minimum of 74±12% of control. Our conclusion is that the postganglionic adrenal nerves respond in a similar way to postganglionic renal nerves during baroreceptor activation and also show the same pattern of response during haemorrhage. This might indicate that postganglionic fibres to the adrenal gland and postganglionic renal fibres to the kidney have the same target structures, i.e. blood vessels. and postganglionic adrenal fibres might therefore be of importance in adrenal blood flow regulation.