Sodium and dopamine excretion in prehypertensive Dahl rats during severe hypervolaemia.

As opposed to the salt-resistant Dahl-R rat the salt-sensitive Dahl-S has a defective renal dopamine DA1 receptor that may be involved in its susceptibility to develop hypertension during a high salt diet. To compare the ability of prehypertensive Dahl-R and Dahl-S to respond to a severe isotonic sodium load, renal function was monitored during a severe form of acute isotonic volume expansion (10% VE). Mean arterial blood pressure before VE was similar in Dahl-R and Dahl-S and decreased in both strains by 6% during VE. The accumulated sodium excretion during VE in Dahl-R was 411 +/- 64 micromol 100 min(-1) g(-1) kidney wt (kw) which was not different from that in Dahl-S (420 +/- 95 micromol 100 min(-1) g(-1) kw). The accumulated dopamine excretion (a mirror of renal dopamine synthesis) during VE was also similar in Dahl-R (134 +/- 13 ng 100 min(-1) g(-1) kw) and Dahl-S (126 +/- 16 ng 100 min(-1) g(-1) kw). The excretion of DOPAC, the main metabolite of Dahl-S, glomerular filtration rate and systemic haematocrit did not differ between the strains before, during or after VE. To conclude, in spite of a defective renal DA1 receptor prehypertensive Dahl-S do not respond with an attenuated natriuretic or dopamine excretory response when subjected to a severe isotonic sodium load. The results do not support a sodium retaining role over a defective DA1 receptor in the salt-sensitive hypertension in Dahl-S.