Baroreflex function in lifetime-captopril-treated spontaneously hypertensive rats.
- 1 January 1989
- journal article
- research article
- Published by Wolters Kluwer Health in Hypertension
- Vol. 13 (1) , 63-69
- https://doi.org/10.1161/01.hyp.13.1.63
Abstract
The effects of lifetime oral captopril treatment on baroreflex control of heart rate and lumbar sympathetic nerve activity were measured in 19-21-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). The sensitivity of baroreflex control of heart rate and lumbar sympathetic nerve activity were determined by the slopes of the relation between the change in mean arterial pressure (MAP) (mm Hg) versus the change in pulse interval (msec/beat) and the change in MAP versus the percent change in nerve activity, respectively. Untreated SHR had significantly higher MAP than WKY (157 .+-. 3 vs. 115 .+-. 3 mm Hg, p < 0.001) and exhibited a decreased baroreflex control of heart rate. Lifetime treatment with captopril prevented the development of hypertension in SHR (MAP = 110 .+-. 5 mm Hg) and increased the sensitivity of baroreflex function. The gains of the baroreflex control of heart rate for captopril-treated SHR and control SHR when MAP was raised or lowered by phenylephrine or nitroprusside were 2.38 .+-. 0.49 vs. 1.10 .+-. 0.33 msec/mm Hg (p < 0.05) and 0.74 .+-. 0.20 vs. 0.54 .+-. 0.09 (NS) msec/mm Hg, respectively. The sensitivity of the baroreflex control of lumbar sympathetic nerve activity was greater in captopril-treated SHR than in control SHR when MAP was increased or decreased (-1.03 .+-. 0.26 vs. -0.38 .+-. 0.11, p < 0.05; -0.84 .+-. 0.2 vs. -0.04 .+-. 0.58 (NS) mm Hg-1, respectively). Captopril-treated WKY also had lower MAP than control WKY (100 .+-. 2 vs. 115 .+-. 3 mm Hg, p < 0.001); however, no significant differences were observed in baroreflex functions between these two groups. These data indicate that lifetime oral captopril treatment enhances baroreflex control of heart rate and lumbar sympathetic nerve activity in SHR, and are consistent with the hypothesis that the brain renin-angiotensin system plays a role in the development and maintenance of hypertension in SHR by attenuating the buffering capacity of the baroreceptor reflex. However, it cannot be ruled out that the prevention of hypertension per se might be responsible for the results obtained.This publication has 4 references indexed in Scilit:
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