Key result
Renal denervation blunts compensatory tachycardia and vasopressin release after hemorrhage, prolonging post-bleed hypotension.
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To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 +/- 16 to 207 +/- 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 +/- 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 +/- 6.4 ng ANG I . ml-1 . h-1) compared with intact lambs (4.0 +/- 1.1 ng ANG I . ml-1 . h-1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 +/- 8 to 197 +/- 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 +/- 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.
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Smith et al. (1998) studied Hemorrhage in conscious newborn lambs (n=13). Bilateral renal denervation vs. Intact renal nerves was evaluated on Cardiovascular (blood pressure, heart rate) and endocrine (plasma renin activity, arginine vasopressin) responses to 20% hemorrhage. Bilateral renal denervation in newborn lambs prevented the heart rate and vasopressin increases (15 pg/ml vs 11 to 197 pg/ml in intact lambs) and prolonged hypotension after 20% hemorrhage.
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