Marked Blood Pressure Responses to Norepinephrine, Epinephrine, and Angiotensin II in Borderline Hypertension with a Parental History of Hypertension

Summary

The hemodynamic responses to norepinephrine, epinephrine, and angiotensin II were investigated in borderline essential hypertensives with a positive parental history of hypertension and normotensives. Intravenous infusion of norepinephrine at the rate of 0.2 μg/kg per minute was administered for 5 min to 12 normotensives and 14 hypertensives, and angiotensin II, at the rate of 0.02 μg/kg per minute, was given for 5 min to 14 subjects of both groups. Both norepinephrine and angiotensin II raised the blood pressure and total vascular resistance with accompanying reductions in stroke volume and cardiac output, which indicated that the rise in blood pressure was caused by the elevation of vascular resistance. Epinephrine infusion (0.2 μg/kg per minute for 5 min) in 10 subjects in both groups raised blood pressure with an increased stroke volume and cardiac output associated with a reduction in vascular resistance, which indicated the rise in blood pressure was caused by the increased cardiac output. The absolute rise in blood pressure during infusion of these three agonists was greater in the hypertensives than in the normotensives. The percentage rise in both stroke volume and cardiac output and the percentage reduction of vascular resistance during epinephrine infusion were smaller in the hypertensives than in the normotensives, but not during norepinephrine or angiotensin II infusion. In conclusion, the marked blood pressure responses to the agonists were observed in borderline essential hypertensives, which suggests that the hyperresponses may possibly carry an abnormality in the contractile responses of vascular smooth muscle. This abnormality may be transferred by a hypertension gene from parents to offspring.