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Renal denervation does not prevent development of angiotensin‐dependent hypertension in rabbits
Author(s) -
Head Geoffrey A,
Moretti JohnLuis,
Burke Sandra L,
Evans Roger G
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1182
Subject(s) - denervation , medicine , mean arterial pressure , sodium nitroprusside , adenosine , vasodilation , angiotensin ii , endocrinology , sympathetic nervous system , blood pressure , anesthesia , nitric oxide , heart rate
We determined whether renal nerves contribute to the development of Angiotensin II (Ang)‐dependent hypertension, and whether depressor responses to vasodilators were enhanced. Basal mean arterial pressure (MAP) and the maximum falls in MAP to ganglion blockade, sodium nitroprusside (SNP) and adenosine were initially determined in conscious rabbits before denervation of both kidneys or sham‐denervation. Measurements were made 2 weeks later and again after 2 and 4 weeks infusion with Ang II (50 ng/kg/min) or saline. MAP was 73 mmHg and falls in MAP −18±2 mmHg, −23±2 mmHg and −22±2 mmHg after pentolinium, SNP and adenosine, respectively. MAP was 10±2mmHg lower 2 weeks after renal denervation (P<0.01). Ang treatment increased MAP by 31±6mmHg and 29±6mmHg in denervated and sham‐denervated rabbits after 2 weeks and MAP was similarly elevated in both groups at 4 weeks. There was an enhancement of the depressor response to ganglion blockade after 2–4 weeks of treatment (by 65%). Responses to SNP and adenosine were doubled after 2–4 weeks of Ang treatment. Thus the development of Ang dependent hypertension is not dependent on the renal nerves. However, the renal nerves have a role in maintaining MAP in normal animals. The enhanced depressor responses to both vasodilators and ganglion blockade, suggest a vascular amplifier phenomenon rather than enhanced contribution from the sympathetic nervous system.