Release of renin and angiotensin II into plasma and lymph during hyperchloremia.

Renal vascular resistance (RVR) was related to intrarenal release of renin (RR) and angiotensin II (ANG II) during increases in plasma osmolality (Posmol) or chloride (PCl). Intrarenal infusions of 1.232 M solutions given to in situ kidneys increased Posmol by 7-18%. Hypertonic dextrose (n = 8) reduced RVR (P less than 0.005) but increased RR into plasma (P less than 0.01) and increased lymph renin (LR) (P less than 0.05). The response to hypertonic Na acetate (n = 5) was similar, but hypertonic NaCl (n = 9) increased RVR (P less than 0.02) without changing RR. During infusion of arachidonic acid (AA), hypertonic NaCl increased RVR (P less than 0.02) but decreased RR into plasma and decreased LR (P less than 0.05). Overall group mean changes in RVR were inversely related to LR (r = -0.96; P less than 0.01). An increase in PCl of 12 +/- 1 mmol/l was induced in denervated kidneys by changing an intrarenal 0.616 M infusion of Na acetate to NaCl. Hyperchloremia increased RVR from 14 +/- 2 to 19 +/- 2 mmHg . ml-1 . min-1 . kg-1 (P less than 0.01), reduced GFR from 1.4 +/- 0.1 to 1.1 +/- 0.1 ml . min-1 . kg-1 (P less than 0.01), and reduced ANG II (pg/ml) in renal venous plasma (55 +/- 6 to 35 +/- 6; P less than 0.05) and lymph (366 +/- 111 to 209 +/- 53; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)