Mechanisms for attenuated pressor responses to alpha-agonists in ovine pregnancy.

Attenuated pressor responses to angiotensin II and alpha-agonists normally occur during ovine pregnancy; however, for alpha-agonists it is not known to what extent this reflects alterations in cardiac output. We therefore compared peripheral and cardiac responses to alpha-agonists in pregnant (n = 6) and nonpregnant (n = 6) sheep, measuring mean arterial pressure, heart rate, and cardiac output before and during steady-state dose responses to norepinephrine (0.458 to 45.84 micrograms/min) and phenylephrine (1.29 to 129 micrograms/min). Both alpha-agonists caused dose-dependent increases in mean arterial pressure and systemic vascular resistance, more so in nonpregnant than pregnant sheep (p less than 0.01), and decreases in cardiac output and heart rate (p less than 0.01). In both nonpregnant and pregnant sheep the percent change in systemic vascular resistance generally exceeded the percent change in mean arterial pressure, reflecting decreases in cardiac output; however, at equivalent increases in percent change in mean arterial pressure and percent change in systemic vascular resistance, the fall in the percent change in cardiac output was greatest in pregnant sheep (p less than 0.05). Also, at similar increases in mean arterial pressure the percent change in heart rate was greatest in pregnant sheep (p less than 0.01). In contrast to angiotensin II, the attenuated pressor responses to alpha-agonists observed during ovine pregnancy are partly a result of reflex decreases in cardiac output mediated mainly through falls in heart rate.