Increase in vascular sensitivity to angiotensin II and norepinephrine after four-day infusion of 0.3 M sodium chloride in conscious kininogen-deficient brown Norway Katholiek rats.

Kininogen-deficient Brown Norway Katholiek (deficient BN-Ka) rats excreted a small amount of kinin in their urine, compared with normal BN Kitasato (normal BN-Ki) rats from the same strain. Intraarterial (i.a.) infusion (6 ml/kg/hr) of conscious deficient BN-Ka rats with 0.15 M NaCl did not increase mean arterial blood pressure (MBP) [from 103 +/- 2 (pre) to 93 +/- 6 mmHg (day 4)] and did not cause sodium accumulation in the serum, cerebrospinal fluid or erythrocytes, but 0.3 M NaCl infusion significantly increased MBP from 104 +/- 3 (pre) to 130 +/- 5 mmHg (day 4) with increased sodium levels in the serum, cerebrospinal fluid and erythrocytes. Infusion of 0.3 M NaCl in normal BN-Ki rats neither increased MBP nor accumulated sodium. The dose-response curve of the increase in MBP for angiotensin II injection (i.a., bolus, 1-1000 pmol/kg) in 0.3 M NaCl-infused deficient BN-Ka rats shifted to the left by a factor of 10 compared with that in 0.15 M NaCl-infused deficient BN-Ka rats, and that for norepinephrine injection shifted to the left by a factor of 30. Normal BN-Ki rats did not show any enhancement in MBP elevation with 0.3 M NaCl. These results suggest that the sodium accumulation attributable to a lack of kinin generation may be related to increased vascular reactivity to angiotensin II and norepinephrine.