Urinary Excretion Of Free Dopamine Research Articles

Urinary Dopamine Excretion in Normotensive Subjects wiht or without Family History of Hypertension

To define the role of the renal dopaminergic system in the pathogenesis of essential hypertension, urinary free dopamine excretion was examined in 23 normotensive subjects who had one or more first-degree relatives with essential hypertension, and also in 36 matched control subjects without any such family history. The group urinary dopamine excretion and urinary sodium excretion were not different. However, a significant urine dopamine-sodium relationship was apparent in the controls but not in the relatives due to relatively high dopamine output in those with lower sodium excretion. The two groups were similar as regards blood pressure (BP), plasma renin activity (PRA), prolactin and catecholamines. These findings demonstrate an alteration in the urine dopamine-sodium relationship in some normotensive subjects with genetic risk of hypertension.

Sympathetic nerve activity, plasma renin activity and water-sodium balance in obese patients with essential hypertension.

Studies were conducted to evaluate the role of water-sodium metabolism on the hypertensive mechanisms in obese patients with essential hypertension (EHT). The obesity index correlated positively with the mean arterial pressure, plasma volume, extracellular fluid volume or total exchangeable sodium, and negatively with plasma noradrenaline concentration or plasma renin activity in EHT. Hypotensive effects of sodium restriction (Na 35 mEq, K 75 mEq) or the natriuretic response to infused dopamine (3 micrograms/kg/min) was remarkable in obese EHT. Fractional excretion of sodium (FENa), which reflects the renal tubular reabsorption of sodium, was significantly lower in obese EHT than that in non-obese or mildly obese EHT. Urinary excretion of free dopamine (UDA) had a positive relationship with simultaneously measured urinary excretion of sodium or FENa. In addition, UDA correlated positively with the obesity index in patients whose weight was under 115% of the ideal weight. On the contrary, the relation between the two parameters was significantly negative in patients whose weight was over 115% of the ideal weight. These findings suggest that the expansion of body fluid volume and sodium, which might result from the blunted natriuretic ability, at least in part, due to an attenuation of the renal dopaminergic activity, play an important role of the hypertensive mechanisms in obese EHT.

Physiologic responses to chronic dietary tyrosine supplementation in DOCA-salt-treated rats.

The antihypertensive effect of chronic administration of L-tyrosine (Tyr) was investigated in a two-part study. In the first experiment, adult male Sprague-Dawley rats were assigned to 1 of 4 treatment groups: control diet plus unilateral nephrectomy (Nphx) and 0.15 M NaCl (Sal) as the sole drinking solution (C-CTRL); control diet plus deoxycorticosterone acetate (DOCA, 268 micrograms/rat/day), Nphx, and Sal (C-DOCA); control diet supplemented with 2.5% L-p-Tyr plus Nphx and Sal (Tyr-CTRL), and Tyr plus DOCA, Nphx, and Sal (Tyr-DOCA). Systolic blood pressure (SBP) increased within 2 weeks after initiation of treatment with DOCA-salt and remained elevated throughout the duration (8 weeks) of the study (p less than 0.001). Dietary administration of Tyr to DOCA-treated rats failed either to affect SBP in normotensive rats or the elevation of SBP in DOCA-treated rats. Dietary supplementation with Tyr induced a significant elevation in urinary excretion of free dopamine (week 1, 3, 5, and 7) and a decreased excretion of free norepinephrine (week 1) without regard to DOCA treatment. Metabolic responsiveness (change in colonic temperature) and cardiovascular responsiveness (change in heart rate) to subcutaneous administration of the beta-adrenergic agonist, isoproterenol, were significantly prolonged while alpha 2-adrenoceptor number (cerebral cortical membranes; 3H-yohimbine binding) was reduced in rats receiving Tyr. In the second experiment, similar rats were assigned to 1 of 3 treatment groups: control diet plus Nphx and Sal, control diet plus Nphx, DOCA and Sal, and Tyr plus DOCA, Nphx, and Sal; however, Tyr was not started until DOCA-salt-induced hypertension developed (4 weeks). Neither acute (2.5 h post-meal) nor chronic (4 weeks) effects of administration of Tyr on SBP were noted. Thus, the Tyr-induced changes observed in these studies include a chronic increase in free dopamine, and a transient decrease in norepinephrine, excretion. No significant effects of Tyr on blood pressure of DOCA-salt-treated rats were observed.

Failure of renal dopamine response to salt loading in chronic renal disease.

Eight patients with chronic glomerulonephritis and five age-matched normal volunteers were given additional sodium chloride by mouth under conditions of metabolic balance. Whereas in the normal volunteers plasma renin activity was suppressed and urinary excretion of free dopamine increased, in the patients dopamine was not mobilised and plasma renin activity was not completely suppressed. Abnormal retention of sodium and water in glomerulonephritis may be due partly to a failure to mobilise dopamine in the kidney. Specific renal dopamine agonists may be natriuretic and hypotensive in chronic glomerulonephritis.

Effect of inhibition of prostaglandin synthesis on urinary free dopamine excretion in women.

1. The effect of inhibition of prostaglandin synthesis on urinary excretion of free dopamine, a catecholamine thought to act as a renal natriuretic hormone, was examined in six normal women. 2. The volunteer subjects were treated with indomethacin (2 mg day-1 kg-1) for 7 days. This regimen produced an immediate and significant but transient decrease in urinary sodium excretion, averaging about 80 mmol over a period of 3 days. 3. Urinary dopamine excretion during the control period was not different from that during the entire period of indomethacin treatment. 4. It is concluded that indomethacin does not affect urinary dopamine excretion. The change in intrarenal nervous release of dopamine in response to the sodium retention induced by indomethacin may have been too small to make a significant contribution to total urinary dopamine excretion.