SYMPATHETIC-NERVE ACTIVITY IN CONSCIOUS RENAL HYPERTENSIVE RATS TREATED WITH AN ANGIOTENSIN-CONVERTING ENZYME-INHIBITOR OR AN ANGIOTENSIN-II ANTAGONIST

Citation
M. Niederberger et al., SYMPATHETIC-NERVE ACTIVITY IN CONSCIOUS RENAL HYPERTENSIVE RATS TREATED WITH AN ANGIOTENSIN-CONVERTING ENZYME-INHIBITOR OR AN ANGIOTENSIN-II ANTAGONIST, Journal of hypertension, 13(4), 1995, pp. 439-445
Citations number
30
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
02636352
Volume
13
Issue
4
Year of publication
1995
Pages
439 - 445
Database
ISI
SICI code
0263-6352(1995)13:4<439:SAICRH>2.0.ZU;2-S
Abstract
Objective: To assess in conscious two-kidney, one clip renal hypertens ive rats whether angiotensin converting enzyme (ACE) inhibition with l isinopril, angiotensin II receptor blockade with losartan or vasodilat ion with sodium nitroprusside have similar effects on intra-arterial m ean blood pressure, heart Fate and splanchnic nerve activity. Results: A bolus dose of lisinopril or losartan (both 10 mg/kg, intravenously) induced within 2 h an equal reduction in mean blood pressure, whereas sodium nitroprusside infused during the same period (at 10 mu g/min) lowered mean blood pressure, but less strongly. The heart rate was acc elerated significantly more during sodium nitroprusside infusion than during lisinopril or losartan treatment. Splanchnic nerve activity inc reased significantly only in those rats given sodium nitroprusside. No change in the parameters studied was observed in vehicle-treated rats . The doses of lisinopril and losartan were repeated after 12 and 24 h . Before administration of the fast dose, the mean blood pressure was still low. Administration of lisinopril or losartan again 24 h after t he initial dose had no further effect on the mean blood pressure, hear t rate or splanchnic nerve activity. Conclusion: These results obtaine d in rats with a renin-dependent form of hypertension show that blocka de of the renin-angiotensin system for 24 h produces an equivalent blo od pressure reduction irrespective of whether it is due to ACE inhibit ion or angiotensin II antagonism. The results also indicate that there is less reflex activation of sympathetic nerve activity when blood pr essure is lowered with a blocker of the renin-angiotensin system rathe r than with a direct vasodilator such as sodium nitroprusside.