Plasma noradrenaline and dopamine in renin‐mediated hypertension

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Abstract
Summary. Noradrenaline (NA) and dopamine (DA) have opposite effects on the kidney; NA causes vasoconstriction and increased sodium reabsorption while DA promotes vasodilation and natriuresis.In 15 patients investigated for renin‐mediated hypertension measurements of plasma renin activity (PRA), NA and DA concentrations were made in arterial and renal venous blood from both kidneys before and after acute stimulation of renin release by i.v. dihydralazine.Nine patients had unilateral renin secretion and were classified as renin‐positive, while the remaining six patients were renin‐negative. Renin‐positive patients had higher arterial and renal venous PRA, NA and DA levels than the negative ones. In the renin‐positive group V‐A differences for NA and DA were present on both sides despite unilateral secretion of renin. NA but not DA levels were higher in the renin‐secreting kidney, which can partly be explained by the reduced plasma flow to the involved kidney.After dihydralazine the arterial NA and DA rose similarly in renin‐positive and renin‐negative patients, while PRA rose only in the renin‐positive cases. In the renin‐positive patients where stimulation of renin secretion caused a marked increase of the PRA gradient on the affected side only, renal gradients for NA and DA increased bilaterally. The increase in DA was more pronounced than that of NA yielding a rise in DA/NA ratio on the affected side. Arterial PRA was positively correlated to the plasma concentrations of NA and DA. V‐A differences for PRA and NA or DA were positively correlated on the involved renin‐secreting side.In summary, patients with renin‐dependent hypertension have elevated plasma NA and DA concentrations. Stimulation of renin release by dihydralazine increases the DA/NA ratio in arterial and renal venous blood indicating release of ‘precursor dopamine’ from noradrenergic fibres and/or activation of dopaminergic nerves. There seems to be a relationship between renal nerve activity and renin release in renin‐dependent hypertension.