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THE ROLE OF ANGIOTENSIN CONVERTING ENZYME AND NITRIC OXIDE IN THE ENHANCED SYSTEMIC DEPRESSOR RESPONSES TO BRADYKININ IN PREGNANT RATS
Z. M. Chu 1 L. J. Beilin 1 , 2
  1 University Department of Medicine & West Australian Heart Research Institute, The University of Western Australia, Medical Research Foundation Building, Perth. Western Australia, Australia
Correspondence to   2 University Department of Medicine & West Australian Heart Research Institute, Medical Research Foundation Building, Rear 50 Murray Street, Perth 6000, Western Australia, Australia.
Copyright 1995 Blackwell Publishing Asia Pty Ltd
KEYWORDS
blood pressure, • bradykinin, • depressor responses, • pregnancy.

ABSTRACT

AbstractREFERENCES

1. In the present study we have examined the effects of angiotensin I converting enzyme (ACE) inhibition and nitric oxide (NO) synthesis inhibition on bradykinin (BK) depressor responses in pregnancy in both Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR).

2. Ramipril (10 mg/kg, i.v.) significantly reduced mean blood pressure (MBP) in all animals. Further administration of L-nitro-arginine (L-NOARG, 20 mg/kg, i.v.) increased MBP to a less extent in pregnant WKY and to a similar level in pregnant SHR compared with their non-pregnant controls (controls), respectively.

3. Systemic depressor responses to BK were increased in pregnant WKY and were unchanged in pregnant SHR as compared with their controls. Ramipril (10 mg/kg, i.v.) potentiated BK responses in all groups, and abolished the differences between pregnant and non-pregnant WKY. Further administration of L-NOARG (20 mg/kg, i.v.) did not further influence BK responses in all groups.

4. The results suggest that systemic depressor responses to BK are enhanced in pregnant WKY and unchanged in pregnant SHR. Decreased ACE activity may contribute to enhanced systemic depressor responses to BK in pregnant WKY.


Received 22 December 1994; revision 1 March 1995; accepted 3 March 1995.

DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1440-1681.1995.tb02051.x About DOI

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