| Autor: |
Rubin, PC, Millar, JA, Sturani, S, Lawrie, C, Reid, JL |
| Zdroj: |
British Journal of Clinical Pharmacology; 1984, Vol. 17 Issue 6, p713-717, 5p |
| Abstrakt: |
The fall in blood pressure produced by captopril is not accompanied by a compensatory tachycardia. Angiotensin converting enzyme may participate in the metabolism of endogenous opioids and these substances can lower blood pressure without reflex tachycardia. It is therefore possible that the hypotensive effect of captopril involves an action on endogenous opioid metabolism. The influence of naloxone, an opiate receptor antagonist, on the cardiovascular effects of captopril has been studied in nine normal volunteers. Mean blood pressure following a 70 degrees head up tilt 1.5 h after captopril was significantly lower than following placebo, but the blood pressure following the combination of captopril and naloxone differed from neither the placebo nor the captopril values. Blood pressures (mm Hg) were: placebo 97.7 +/- 5.9; captopril 83.3 +/- 14.2; captopril + naloxone 89.6 +/- 11.8. Heart rate (beats/min) following a 70 degrees head up tilt at 1.5 h was the same on all three treatments: placebo 83.4 +/- 21.1; captopril 83.3 +/- 16.5; captopril + naloxone 83.6 +/- 11.8. Maximum systolic blood pressure achieved during isometric exercise following captopril + naloxone was intermediate between, and did not differ significantly from, pressures obtained on the other two treatment days. We conclude that co-administration of naloxone may attenuate the effect of captopril on blood pressure and that endogenous opioids could be involved in the actions of this drug. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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