Why the study?
Do converting enzyme inhibitors (teprotide or captopril) affect efferent sympathetic postganglionic nerve activity to the kidney in rats?
Do converting enzyme inhibitors (teprotide or captopril) affect efferent sympathetic postganglionic nerve activity to the kidney in rats?
Converting enzyme inhibitors induce efferent sympathetic excitation to the kidney in rats, independent of baroreceptor or renorenal reflexes, potentially contributing to increased renin secretion.
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ACE inhibitors may increase renal sympathetic outflow in rats independent of reflexes; leaves open relevance to human renin secretion or therapy.
Experiments were designed to evaluate the effect of converting enzyme inhibitors on autonomic nervous system function in the rat. 2. Arterial blood pressure, heart rate, efferent postganglionic sympathetic activity and afferent nerve activity from the right renal nerves were recorded in anaesthetized, spontaneously breathing, non diuretic rats, either with an intact spinal cord or with a spinal cord transected at the T6 level, before, during and after intravenous injections of 0.5--1.0 mg/kg of teprotide or captopril. 3. After injection of drugs, efferent sympathetic nerve activity markedly increased and reached its peak value 4 min later, both in rats with an intact spinal cord (101 +/- 21% mean +/- SE, above the control discharge) and with a spinal cord transected at the T6 level (166 +/- 41%, above the control). 4. Afferent activity from the renal nerve, on the other hand, did not consistently change during converting enzyme blockade. 5. The results indicate that the efferent sympathetic excitation cannot be due either to a baroreceptor or to a renorenal reflex. This excitation might be responsible, at least in part, for the increase in renin secretion which follows the blockade of angiotensin-converting enzyme.
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Recordati et al. (1981) studied this question.
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