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Increased sensitivity to bradykinin in pregnant rats
1Department of Obstetrics and Gynecology, Nagoya University School of Medicine, Japan.
Research Communications in Chemical Pathology and Pharmacology
|June 1, 1989
Summary
Late pregnancy in rats enhances the depressor response to bradykinin. However, the Kininase II enzyme, inhibited by captopril, does not appear to mediate this hypersensitivity during late pregnancy.
Area of Science:
- Pharmacology
- Physiology
- Reproductive Biology
Background:
- Bradykinin plays a role in cardiovascular regulation.
- Pregnancy can alter physiological responses to vasoactive substances.
- Kininase II (angiotensin-converting enzyme) metabolizes bradykinin.
Purpose of the Study:
- To investigate the effects of late pregnancy on the depressor response to bradykinin in rats.
- To determine the role of Kininase II in bradykinin hypersensitivity during late pregnancy.
Main Methods:
- Experiments were conducted on anesthetized rats (pentobarbital).
- Arterial and venous catheters were used for blood pressure monitoring and drug administration.
- The depressor response to graded doses of bradykinin was measured.
- The effects of captopril, a Kininase II inhibitor, were assessed in pregnant and nonpregnant rats.
Main Results:
- Late pregnancy (19-21 days) exhibited a hypersensitive depressor response to bradykinin.
- Captopril administration significantly increased the bradykinin-induced depressor response in both pregnant and nonpregnant rats.
- The parallel increase in response to bradykinin by captopril suggests Kininase II acts as a bradykinin-metabolizing enzyme in vivo.
Conclusions:
- Kininase II inhibition augments bradykinin's depressor effect in rats.
- The hypersensitivity to bradykinin observed in late pregnancy in rats is likely not mediated by Kininase II.