Effects of pregnancy and progesterone metabolites on arterial
baroreflex in conscious rats.
Masilamani, S. and Heesch, C. M.
Department of Physiology, The Ohio State University, 302 Hamilton
Hall, 1645 Neil Ave., Columbus, OH 43210-1218, Telephone: (614) 292
-0824, FAX: (614) 202-4888
APStracts 3:0381R, 1996.
Previous experiments in anesthetized rats suggested that
sympathoexcitatory responses were attenuated in pregnant (P) rats.
The major progesterone metabolite, 3-[alpha]-hydroxy
-dihydroprogesterone (3[alpha]-OH-DHP), is elevated in pregnancy and
reportedly potentiates central GABAergic mechanisms, while the
3[beta] isomer (3[beta]-OH-DHP) is inactive. This study obtained
baroreflex curves in conscious rats by recording reflex changes in
renal sympathetic nerve activity (RSNA) and heart rate (HR) due to
perturbations in mean arterial pressure (MAP) [iv phenylephrine (PE)
and nitroprusside (NTP)]: in P rats, and in virgin (V) rats before
(control), and 15 min after infusion (iv) of 3[alpha]-OH-DHP or
3[beta]-OH-DHP. Baseline MAP was lower in P rats (P=102+/-2 mm Hg vs.
V=124+3 mm Hg). Compared to V rats, P rats exhibited less
"sympathetic reserve" to respond to a hypotensive challenge
as evidenced by decreased maximum NA and decreased slope of RSNA
baroreflex responses to NTP. However, HR baroreflex curves were
similar in P and V rats. Acute iv administration of 3[alpha]-OH-DHP
to conscious V rats mimicked the effects of pregnancy. Baroreflex
sympathoexcitatory responses were decreased while baroreflex control
of HR was unaffected. The 3[beta] isomer of DHP had no affect on NA
or HR baroreflex responses. These results suggest that pregnancy may
have differential effects on baroreflex control of sympathetic
outflow and HR, and the major metabolite of progesterone, 3[alpha]
-DHP, may contribute to this adaptation of pregnancy.
Received 16 January 1996; accepted in final form 18 October 1996.
APS Manuscript Number R22-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996