Key Points
- To determine the physiological and pharmacological mechanisms mediating renal renin secretion during electrical stimulation of the brainstem.
- Delivered 5-minute electrical stimulation to the dorsolateral pons in anesthetized cats while measuring blood pressure, renal blood flow, and renin release.
- Compared responses between intact kidneys, contralateral surgically denervated kidneys, and kidneys locally infused with the alpha-adrenergic blocker phenoxybenzamine.
- Administered intravenous propranolol (1.3–3.0 mg/kg) to evaluate the involvement of beta-adrenergic receptor mechanisms.
- Pontine stimulation in intact kidneys increased arterial blood pressure by 40%, decreased renal blood flow by 28%, and increased the rate of renin release by >100%, whereas renal denervation completely abolished both the blood flow reduction and renin release.
- Phenoxybenzamine infusion blocked the 28% reduction in renal blood flow but did not diminish brain-stimulated renin release compared to the untreated contralateral kidney.
- Intravenous propranolol (1.3–3.0 mg/kg) completely abolished stimulation-induced renin release while further accentuating the decrease in renal blood flow.
Structured PICO
PPopulationAnesthetized cats
IInterventionElectrical stimulation of the dorsolateral pons for 5-minute periods, with or without phenoxybenzamine infusion or intravenous propranolol (1.3-3.0 mg/kg)
CComparatorContralateral denervated kidney or baseline state
OOutcomeRate of renin releasesurrogate
Brainstem stimulation-induced renin release is dependent on intact renal nerves and beta-adrenergic mechanisms, but independent of changes in renal blood flow or alpha receptors.