title: Renal and cardiac sympathetic baroreflexes in hypertensive rabbits.
abstract: 1. The purpose of the present study was to assess the changes to renal sympathetic nerve activity (RSNA) baroreflexes during the development of hypertension after renal clipping in conscious rabbits. 2. Rabbits were fitted with a clip on the right renal artery or underwent a sham operation under halothane anaesthesia. A recording electrode was implanted on the left renal nerve 1 week before the experiment, 3 or 6 weeks after the initial operation. During the experiment, drug-induced ramp rises and falls in mean arterial pressure (MAP) were used to produce RSNA and heart rate (HR) baroreflex curves. The RSNA for each experiment was calibrated against maximum RSNA evoked by stimulation of baroreceptor-independent trigeminal afferents. 3. Mean arterial pressure was 20 and 36% higher 3 and 6 weeks after clip implantation, respectively. Renal sympathetic nerve activity baroreflex curves were reset rightwards accordingly, but the shape of the RSNA curves was differentially affected. 4. At both hypertensive periods, MAP-HR baroreflex gain was markedly reduced due to a reduction in curvature. The HR baroreflex range was increased. The RSNA baroreflex gain was reduced at 3 weeks, which was due to a 35% lower RSNA baroreflex range, but was similar to sham animals at 6 weeks. 5. The results show that, in established two kidney, one clip hypertension in rabbits, the sympathetic baroreflex is relatively well preserved but sensitivity of cardiac baroreflexes is attenuated. Therefore, the short-term inhibition of RSNA baroreflexes is not related to the level of blood pressure or the development of secondary changes, such as cardiac or vascular hypertrophy, but may be related to circulating angiotensin, which is known to increase at this time.
authors.affiliation: Neuropharmacology Laboratory, Baker Medical Research Institute, Melbourne, Victoria, Australia. Geoff.Head@baker.edu.au
authors.forename: G A
authors.initials: GA
authors.lastname: Head
authors.forename: S L
authors.initials: SL
authors.lastname: Burke
mesh_terms: D000818:Animals; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D005260:Female; D006321:Heart / Q000187:drug effects / Q000294:innervation* / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects / Q000294:innervation* / Q000503:physiopathology*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013566:Sympathomimetics / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D013566:Sympathomimetics; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine