Sympathetic Neural Blockade by Thoracic Epidural Anesthesia Suppresses Renin Release in Response to Arterial Hypotension

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Abstract
The renin-angiotensin and vasopressin systems, in addition to the sympathetic system, are important backup mechanisms for maintaining arterial blood pressure during circulatory challenges. We tested the hypothesis that preganglionic sympathetic blockade by thoracic epidural anesthesia interferes with the functional integrity of the renin-angiotensin system. Renin concentrations were assessed in awake non-sedated patients in response to induced arterial hypotension both before and during sympathetic blockade by thoracic epidural anesthesia (n = 10). Heart rate (electrocardiogram) and mean arterial blood pressure (electromanometry) were recorded continuously. Active renin (radioimmunoassay), vasopressin (radioimmunoassay), and osmolality (osmometry) in arterial blood were measured intermittently: (1) at baseline, (2) during a hypotensive challenge (15 min) induced by sodium nitroprusside (titrated to decrease mean arterial blood pressure by at least 25%) with the sympathetic system intact, (3) during recovery, (4) with epidural anesthesia alone (sensory blockade T1-T11), and (5) during a second hypotensive challenge and sympathetic blockade with sodium nitroprusside titrated to the same mean arterial blood pressure as with the sympathetic system intact. With the sympathetic system intact hypotension almost doubled renin concentration (34 ± 32 SD to 60 ± 58 pg ml-1, P = 0.019), while vasopressin concentration remained unchanged. In contrast, during sympathetic blockade and despite identical hypotension (mean arterial blood pressure 68 ± 8 vs. 67 ± 5 mmHg), renin concentration did not change (35 ± 27 vs. 35 ± 29 pg ml-1, P = 0.5), whereas vasopressin concentration increased (4.6 ± 2.5 to 13.4 ± 9.4 pg ml-1, P = 0.01). Osmolality remained unchanged. Our results Indicate a key role of renal sympathetic fibers in mediating renin release during hypotension in humans, and that epidural anesthesia interferes with the functional integrity of the renin-anglotensin system.

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