Why the study?
Does NO-synthase inhibition with l-NMMA affect renal hemodynamics differently in normotensive versus hypertensive subjects?
Does NO-synthase inhibition with l-NMMA affect renal hemodynamics differently in normotensive versus hypertensive subjects?
Basal nitric oxide synthesis in the renal vasculature is not impaired in patients with established essential hypertension.
Preserved basal renal NO activity in essential hypertension; leaves open therapeutic targeting in earlier or resistant disease.
OBJECTIVE: To examine the acute effects of NO-synthase inhibition on renal hemodynamics in normotensive and hypertensive subjects. METHODS: Changes of renal plasma flow (RPF) and glomerular filtration rate (GFR) in response to intravenous infusions of NG-monomethyl-l-arginine (l-NMMA) (3 mg/kg per 30 min) were measured in 32 normotensive and in 39 essential hypertensive patients by use of clearance technique. RESULTS: l-NMMA significantly decreased RPF in normotensive and hypertensive individuals (P < 0.001), while GFR was preserved. Changes of renal hemodynamic parameters were similar in hypertensive and normotensive subjects (deltaRPF: -88 +/- 89 versus -81 +/- 105 ml/min, P = NS; deltaGFR 1.6 +/- 8.2 versus 4.3 +/- 8.9 ml/min, P = NS) Furthermore, l-NMMA increased mean arterial pressure (deltaMAP 5.3 +/- 6.3 versus 6.0 +/- 6.1 mmHg, P = NS) and decreased heart rate (deltaHR -5.8 +/- 3.9 versus -4.1 +/- 3.8 beats/min, P = NS) to a similar extent in both groups. CONCLUSION: Basal NO synthesis of the renal vasculature is not impaired in patients with established essential hypertension.
No takes yet. Share an insight, caveat, or question.
Jacobi et al. (2002) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: