Antihypertensive monotherapy and cardiovascular responses to an acoustic startle stimulus

To determine contribution of the autonomic nervous system to cardiovascular reactivity to noise, acoustic startle stimulus (110 dB, 1-20 kHz, 0.150 s) was administered to 35 subjects (19 women, 16 men) with mild essential hyp ertension. Among these patients, 10 were unmedicated and 35 were receiving long-term monotherapy (10 were taking 100 mg atenolol, 5 were taking 10 mg prazosin, and 10 were taking 50 mg losartan daily). Polygraphic recordings were obtained in supine position. Blood pressure (BP) and heart rate (HR) l evels were stable until the noise was administered. In the unmedicated grou p BP and HR were elevated during the first 10 s. BP returned to resting lev els after this period. The calculated hemodynamic indexes showed a biphasic change in total peripheral resistance (TPR), with an overall vasoconstrict ion associated with the BP rise phase, preceding a delayed vasodilation. Th e lowest HR changes were observed in the P-blocker group with increases of 6 beats/min and 3 beats/min after the first and second noise stimulations, compared with 10 beats/min and 5 beats/min in the unmedicated group. Prazos in significantly reduced the BP rises to 7 mm Hg and 6 mm Hg for systolic B P and diastolic BP after the first stimulation compared with 22 mm Hg and 1 7 mm Hg in the untreated group (p < 0.01). The second stimulation after pra zosin determined -5 mm Hg and 1 mm Hg changes for systolic BP and diastolic BP respectively, compared to rises of 13 mmHg for systolic BP and 10 mmHg for diastolic BP in the untreated group (p < 0.01). The hemodynamic percent age changes resulting from the first stimulation indicated prazosin markedl y reduced the noise-induced rise in TPR (p < 0.05). No effect of P-blocker was detectable using percentage changes. The rises in BP were amplified in the losartan-treated subjects compared with the other groups. Because of a low resting TPR in this group, the percentage changes in TPR resulting from noise were amplified in the subjects treated with the AT, receptor antagon ist. In conclusion the acoustic startle stimulus appeared as a simple and r eliable procedure for inducing transient increases due to a rise in TPR. Ca rdiovascular responses differed according to the antihypertensive monothera py, with a limited effect of noise in the prazosin-treated group.