Lymphocyte β2‐adrenoceptors and adenosine 3′:5′‐cyclic monophosphate during and after normal pregnancy

Abstract

The β2‐sympathomimetics, used to inhibit preterm labour, bind predominantly to β2‐adrenoceptors, activating adenylate cyclase to form adenosine 3′:5′‐cyclic monophosphate (cyclic AMP), a messenger substance which inhibits the enzyme cascade triggering smooth muscle contraction. β2‐Adrenoceptor density and cyclic AMP formation can be used as markers of β2‐adrenergic effect. The present study addresses the influence of pregnancy on the β‐adrenoceptor system. β2‐Adrenoceptor density and cyclic AMP concentrations (basal and evoked by isoprenaline) in circulating lymphocytes were determined at three points in gestation (16, 29 and 37 weeks) and 9 weeks post partum in 22 normal pregnancies. (−)‐[125Iodo]‐cyanopindolol was used as the ligand to identify a homogeneous population of β2‐adrenoceptors on lymphocytes. B‐ and T‐cell fractions were estimated from the same samples. β2‐Adrenoceptor density decreased significantly during gestation until week 37 (P < 0.01), then increased post partum (P < 0.005). Cyclic AMP concentrations (basal and evoked by isoprenaline) were significantly lower after 16 weeks of gestation than post partum (P<0.05). The results, which cannot be explained in terms of a shift in the lymphocyte (B‐ and T‐cell) ratio, indicate that β‐adrenoceptor density and function are reduced in normal pregnancy and only return to normal post partum. These findings may be of significance in devising future tocolytic therapy with β2‐adrenoceptor agonists. 1993 British Pharmacological Society