Circulatory and renal effects of β-adrenergic-receptor stimulation in pregnant sheep

Abstract The effects of β-adrenergic-receptor stimulation with ritodrine on systemic and pulmonary hemodynamics and on renal handling of water and electrolytes were studied in unanesthetized, chronically instrumented pregnant sheep. Each animal was studied during control, ritodrine, and recovery periods, each lasting 60 minutes, with the use of three different modes of hydration. β-Receptor stimulation produced a significant increase in heart rate and cardiac output and a decrease in systemic vascular resistance. Pulmonary arterial and wedge pressures tended to increase. These circulatory effects were similar for the three types of hydration and they persisted after cessation of infusion. In terms of its renal effects, β-receptor stimulation elicited a profound decrease in urine flow and in the excretions of sodium and potassium, irrespective of the mode of hydration. The antidiuresis and antinatriuresis were accompanied by no changes in plasma osmolality and sodium concentration, whereas plasma potassium levels decreased. All of these effects persisted for 60 minutes after the cessation of infusion. In the water-loaded experiments, the antidiuresis seemed to be related to increased antidiuretic hormone secretion; in the saline-loaded experiments, however, both the antidiuresis and antinatriuresis appeared to be related to increased renal reabsorption. The changes in renal hemodynamics seemed to have an insignificant role. The amount of fluid retained in the body was greater when ritodrine was infused with saline solution than with dextrose solution. These cardiovascular and renal studies suggest that a circulatory overload may be the major factor in the pathogenesis of pulmonary edema observed during β-adrenergic-receptor stimulation.