title: Rabbits with a genetic impairment in baroreceptor reflex sensitivity show abnormal renal haemodynamics and proximal tubular sodium reabsorption in response to a saline infusion.
abstract: OBJECTIVE
  To compare renal haemodynamics and proximal tubular sodium reabsorption (PTSR) in response to an acute intravenous saline infusion in rabbits bred for genetic differences in cardiac baroreflex sensitivity (BRS). Rabbits with low BRS increase their blood pressure significantly on a high-salt diet, in association with an initial delay in sodium excretion. It was hypothesized that this could occur through an impaired baroreflex regulation of renal sympathetic nerve activity. This, in turn, would alter renal blood flow and PTSR.
  
  
  METHODS
  Experiments were performed in two groups of normotensive male rabbits (n = 10 per group), one of which had high BRS (> 5 beats/min per mmHg; group I) and one of which had low BRS (< 4 beats/min per mmHg; group II). Effective renal plasma flow (ERPF) was measured by para-aminohippuric acid clearance, and PTSR by the lithium clearance technique. Sodium, lithium, para-aminohippuric acid and glomerular filtration rate were measured from urine samples collected every 30 min (for 90 min) via an indwelling bladder catheter, during a control infusion of glucose (30 mg/ml) NaCl (1.8 mg/ml), and for 2 h after a threefold increase in NaCl.
  
  
  RESULTS
  Group I rabbits increased their ERPF by approximately 40%, in response to saline, and doubled their sodium and lithium clearances within the 2 h, but those in group II did not change their cation excretion or their ERPF significantly during this period. Blood pressure did not increase in either group.
  
  
  CONCLUSIONS
  A genetic impairment in BRS may be responsible for the inadequate depression of renal sympathetic nerve activity, which results in a failure to increase ERPF and suppress sodium reabsorption in the proximal tubule in response to salt loading.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Hebrew University Hadassah Medical Centre, Jerusalem, Israel.
authors.forename: M
authors.initials: M
authors.lastname: Razin
authors.forename: M
authors.initials: M
authors.lastname: Borosh
authors.forename: M
authors.initials: M
authors.lastname: Weinstock
mesh_terms: D000042:Absorption / Q000187:drug effects; D000818:Animals; D004305:Dose-Response Relationship, Drug; D006439:Hemodynamics / Q000187:drug effects; D007668:Kidney / Q000187:drug effects / Q000502:physiology; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D018021:Lithium Chloride / Q000494:pharmacology; D008297:Male; D011311:Pressoreceptors / Q000502:physiology*; D011817:Rabbits; D012018:Reflex / Q000502:physiology*; D012079:Renal Circulation / Q000187:drug effects*; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride / Q000494:pharmacology*
chemical_list: D012965:Sodium Chloride; D012964:Sodium; D018021:Lithium Chloride