Key Points
- This study aims to assess the sustained impact of renal nerve activity on sodium excretion during chronic angiotensin II hypertension.
- Conducted in five conscious dogs with unilateral renal denervation and urinary bladder division for separate urine collection.
- Sodium retention was examined during a 10-day intravenous infusion of ANG II at a rate of 5 ng.kg(-1).min(-1).
- Measured mean arterial pressure and urinary sodium excretion ratios from Den and Inn kidneys over the study period.
- On days 8-10 of ANG II infusion, mean arterial pressure increased by +30 +/- 3 mmHg and sodium balance was achieved.
- Sodium excretion was significantly greater from Inn compared to Den kidneys (day 10 Den/Inn sodium = 0.56 +/- 0.05).
- Despite a decrease in Den/Inn for sodium and related metabolites, cGMP levels remained unchanged, suggesting a distinct mechanism at play.
Structured PICO
Does chronic ANG II infusion cause sustained suppression of renal sympathetic nerve activity in conscious dogs?
PPopulation5 conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders
IInterventionIntravenous infusion of ANG II for 10 days at a rate of 5 ng.kg(-1).min(-1)
CComparatorInnervated kidneys (within-subject control) and pre-infusion control measurements
OOutcomeRatio of urinary sodium excretion from denervated and innervated kidneys (Den/Inn) and mean arterial pressure (MAP)surrogate
Baroreflex suppression of renal sympathetic nerve activity is sustained during chronic ANG II hypertension, which may play an important role in attenuating the rise in arterial pressure.