RABBITS WITH A GENETIC IMPAIRMENT IN BARORECEPTOR REFLEX SENSITIVITY SHOW ABNORMAL RENAL HEMODYNAMICS AND PROXIMAL TUBULAR SODIUM-REABSORPTION IN RESPONSE TO A SALINE INFUSION

Objective: To compare renal haemodynamics and proximal tubular sodium reabsorption (PTSR) in response to an acute intravenous saline infusio n in rabbits bred for genetic differences in cardiac baroreflex sensit ivity (BRS). Rabbits with low BRS increase their blood pressure signif icantly on a high-salt diet, in association with an initial delay in s odium excretion. It was hypothesized that this could occur through an impaired baroreflex regulation of renal sympathetic nerve activity. Th is, in turn, would alter renal blood flow and PTSR. Design: Experiment s were performed in two groups of normotensive male rabbits (n = 10 pe r 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). Effect ive renal plasma flow (ERPF) was measured by para-aminohippuric acid c learance, 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 indwell ing 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. Resu lts: Group I rabbits increased their ERPF by approximately 40%, in res ponse to saline, and doubled their sodium and lithium clearances withi n the 2 h, but those in group II did not change their cation excretion or their ERPF significantly during this period. Blood pressure did no t increase in either group. Conclusions: A genetic impairment in BRS m ay be responsible for the inadequate depression of renal sympathetic n erve activity, which results in a failure to increase ERPF and suppres s sodium reabsorption in the proximal tubule in response to salt loadi ng.