Renal and preganglionic adrenal sympathetic nerve activities (RSNA, ASNA) are regulated differentially. Various cardiopulmonary receptor (CPR) stimulation procedures were performed to distinguish short-term and prolonged as well as mechanical and chemical stimulatory effects on RSNA and ASNA.
In anesthetized male Sprague-Dawley rats blood pressure, heart rate, left ventricular end-diastolic pressure (LVEDP), RSNA and ASNA were recorded. CPRs were stimulated as follows: Short-term mechanical: LVEDP changes (±4, ±6, ±8 mmHg) via aortic and caval vein occlusion; Short-term chemical: phenylbiguanide (PBG-bolus, 0.1, 1, 10 μg IV); Prolonged mechanical (15 min): volume expansion (0.9% NaCl, 5% body weight) and hemorrhage, to modulate LVEDP; Prolonged chemical: PBG infusion (32 μg/min IV, for 15 min); Stimulations were done with 1) all afferents intact, 2) bilateral cervical vagotomy (VX), 3) VX + SAD (sino-aortic denervation; short-term protocols and hemorrhage).
1) Short-term mechanical stimuli decreased RSNA (-52 ± 12%) and ASNA (-37 ± 13%). 2) PBG-bolus decreased RSNA (-54 ± 12%) but increased ASNA (+40 ± 13%). 3) Volume expansion decreased RSNA (-55 ± 7%), ASNA was unaffected. 4) PBG infusion persistently decreased RSNA (-60 ± 6%) but just shortly increased ASNA (+120 ± 15%); VX abolished all responses. 5) Hypotensive hemorrhage decreased RSNA (-39 ± 9%) but increased ASNA (+42 ± 9%). VX abolished RSNA response; ASNA response only disappeared with VX + SAD.
Short-term mechanical CPR stimulation uniformly decreased sympathetic activities, whereas chemical stimulation had opposing effects on renal and adrenal sympathetic responses. All prolonged stimuli decreased RSNA, whereas ASNA was virtually unaffected: Sympathetic out.ow is differentially controlled not only with regard to target organs or afferent receptors but also stimulus time pattern.