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Am J Physiol Regul Integr Comp Physiol (December 21, 2001). doi:10.1152/ajpregu.00472.2001
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Articles in PresS, published online ahead of print December 21, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00472.2001
Submitted on August 6, 2001
Accepted on November 12, 2001

Enhanced vascular effects of the Ca2+channel agonist Bay K8644 in pregnant rabbits

Rocco C Venuto1, Gail P Brown2, Marion Schoenl1*, and Gyorgy Losonczy3

1 Schools of Medicine and Biomedical Science, University at Buffalo, State University of New York, Buffalo, NY, USA
2 School of Nursing, University at Buffalo, State University of New York, Buffalo, NY, USA
3 Department of Pulmonology, Semmelweis University Medical School, Budapest, Hungary; Schools of Medicine and Biomedical Science, University at Buffalo, State University of New York, Buffalo, NY, USA

* To whom correspondence should be addressed. E-mail: mschoenl{at}acsu.buffalo.edu.

Hemodynamic studies were performed to determine if blunting of vascular pressor responsiveness to vasoconstrictors during pregnancy may be due to impaired L-type voltage-dependent calcium channels (L-VDCC). Bay K8644 (BAY), an L-VDCC agonist, was infused in pregnant and non-pregnant anesthetized, acutely instrumented rabbits (10, 20, 40 and 60 µg/kg) and pregnant and non-pregnant conscious, chronically instrumented rabbits (10, 25, and 50 µg/kg). BAY infusions resulted in greater elevation of mean arterial pressure in both anesthetized pregnant (n=6) versus non-pregnant (n=6) (p<0.05) and conscious pregnant (n=10) versus non-pregnant (n=10) rabbits (p<0.05). Fractional increase over baseline of total peripheral resistance index was greater in pregnant (36±5% to 78±14%) versus non-pregnant rabbits (14±4% to 52±6%) (p<0.02). Cardiac output index did not differ. There was a single high affinity L-VDCC antagonist aortic binding site with similar number and affinity in pregnant (n=7) and non-pregnant (n=7) rabbits. Conclusion: Stimulation of L-VDCC induces greater pressor responses in pregnant rabbits with heightened peripheral vasoconstriction. This does not appear to be due to a change in L-VDCC receptor parameters.






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