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

抄録

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. Intra-arterial (i.a.) infusion (6 ml/kg/hr) of conscious deficient BN-Ka rats with 0.15 M NaCI 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 NaCI 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 NaCI 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 NaCI-infused deficient BN-Ka rats shifted to the left by a factor of 10 compared with that in 0.15 M NaCI-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 NaCI. 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.