Anesth Analg 2002;94:1304-1309
© 2002 International Anesthesia Research Society
OBSTETRIC ANESTHESIA
Pregnancy Alters Adrenergic Mechanisms in Uterine Arterioles of Rats
Steven Y. Wang, MD PhD,
Sanjay Datta, MD, and
Scott Segal, MD
Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts
Address correspondence and reprint requests to Steven Y. Wang, MD, PhD, c/o Scott Segal, MD, Department of Anesthesiology, Perioperative, and Pain Medicine, Brigham and Womens Hospital, 75 Francis St., Boston, MA 02115. Address e-mail to swang{at}communitymedical.org
Pregnancy is associated with altered vascular reactivity. However, the effect of pregnancy on the - and ß-adrenergic responses in the uterine microcirculation remains to be determined. In late-pregnant (Day 2021, n = 6) and virgin (n = 6) Sprague-Dawley rats, uterine radial arterioles (70120 µm in internal diameter) were isolated. We studied in vitro arteriolar responses in a pressurized, no-flow state with videomicroscopy. 2-Adrenergic activation relaxed uterine arterioles; this relaxation was increased with pregnancy and was inhibited after endothelial denudation or inhibition of nitric oxide synthase. Pregnancy significantly increased the contractile response to the 1-adrenoceptor agonist phenylephrine but decreased the relaxation to the ß-adrenoceptor agonist isoproterenol. The contractile response to the protein kinase C activator phorbol ester and relaxation responses to both the adenylate cyclase activator forskolin and the endothelium-independent cyclic guanosine monophosphate-mediated vaso- dilator nitroprusside were preserved. These results suggest that pregnancy enhances the 2-adrenoceptor-mediated relaxation of uterine arterioles, probably because of an increase in the release of nitric oxide. The 1-adrenergic response is upregulated, whereas the ß-adrenergic response is impaired, in the uterine microcirculation of pregnant rats.
IMPLICATIONS: Both - and ß-adrenergic responses are important mechanisms for the regulation of uteroplacental perfusion. By use of an in vitromicrovascular technique, we have shown pregnancy-associated alteration in adrenergic responses in the uterine microcirculation of the rat.
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