These data, when viewed collectively with the finding that, in PAN-NS rats, the natriuretic response resulting from inhibition of enhanced cellular cGMP catabolism was blunted when the D1R antagonist Sch-23390 was simultaneously administered, support the notion that renal dopamine and D1R contribute to the in vivo natriuretic effect associated with corrected resistance to ANP in experimental NS. Here, DRD1 is linked to polyarteritis nodosa.