Influence of short-term versus prolonged cardiopulmonary receptor stimulation on renal and preganglionic adrenal sympathetic nerve activity in rats.
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 microg IV); Prolonged mechanical (15 min): volume expansion (0.9% NaCl, 5% body weight) and hemorrhage, to modulate LVEDP; Prolonged chemical: PBG infusion (32 microg/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.
Ditting
T
T
Department of Nephrology Medicine IV, Friedrich-Alexander University Erlangen-Nürnberg, Loschgestrasse 8, 91054 Erlangen, Germany.
Hilgers
K F
KF
Scrogin
K E
KE
Linz
P
P
Veelken
R
R
D000311:Adrenal Glands / Q000294:innervation*; D000818:Animals; D001339:Autonomic Fibers, Preganglionic / Q000187:drug effects / Q000502:physiology*; D001645:Biguanides / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume / Q000502:physiology; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D006339:Heart Rate / Q000187:drug effects; D006706:Homeostasis / Q000502:physiology; D007668:Kidney / Q000294:innervation*; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012018:Reflex / Q000502:physiology; D017366:Serotonin Receptor Agonists / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D014628:Vagotomy; D017725:Ventricular Pressure / Q000502:physiology
D001645:Biguanides; D017366:Serotonin Receptor Agonists; C008846:phenyl biguanide