Why the study?
Do converting enzyme inhibitors cause pressure-independent resetting of baroreflex control of sympathetic outflow in normotensive and hypertensive rats?
Do converting enzyme inhibitors cause pressure-independent resetting of baroreflex control of sympathetic outflow in normotensive and hypertensive rats?
Converting enzyme inhibitors cause a pressure-independent resetting of baroreflex control of sympathetic outflow, which may contribute to their antihypertensive effects.
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ACE inhibitors may reset baroreflex sympathetic control independently of pressure in rats; leaves open relevance to human hypertension.
The current study was performed to determine whether baroreflex resetting after acute administration of converting enzyme inhibitors (CEIs) was dependent on the concomitant decrease in mean arterial pressure (MAP). Reflex changes in lumbar sympathetic nerve activity (LSNA) due to increases and decreases in MAP [i.v. phenylephrine (PE) and nitroprusside infusions] were determined in normotensive and renal hypertensive (1-kidney, 1-clip) anesthetized WKY rats 1) before (control), 2) 15 min after intravenous captopril (2 mg/kg) or enalaprilat (300 micrograms), and 3) 15 min after MAP was returned to pre-CEI levels with intravenous PE. CEIs decreased MAP and caused a leftward shift of the MAP-LSNA curve toward a lower operating pressure range in all hypertensive and in one group of normotensive rats. The baroreflex curve remained shifted to the left even after MAP was restored to pre-CEI levels by infusion of PE. Thus CEIs cause a pressure-independent resetting of baroreflex control of sympathetic outflow within 15 min. This effect of CEIs is most likely due to elimination of a central nervous system effect of circulating angiotensin II and could contribute to the antihypertensive actions of this class of compounds.
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Heesch et al. (1996) studied this question.
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