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M Balali-Mood

Publications and source records attributed to M Balali-Mood.

11 recordsLinked to original sources
PubMed1990

Ethnic differences in the renal sodium dopamine relationship. A possible explanation for regional variations in the prevalence of hypertension?

Over the last three years we have carried out studies on the urine output of both sodium and dopamine in five different ethnic groups: whites, Ghanaians, Zimbabweans, Iranians and Thais. Sodium was measured by ion specific electrode and dopamine by HPLC with electrochemical detection (using epinine as an internal standard). In several groups salt loading studies were also carried out. The five ethnic groups differed substantially with regard to the correlation between their urinary sodium and dopamine outputs. Three groups (whites, Thais and Zimbabweans) showed a strong positive correlation (P less than .001) and this may reflect their traditionally salt rich diet. In two groups (Ghanaians and Iranians) there was no correlation and this may reflect a salt scarce environment. Taken together with our previously reported studies showing that normotensive Ghanaians do not mobilize dopamine on salt loading, this would suggest that certain ethnic groups are predisposed to develop hypertension on salt loading--that is, they are 'salt sensitive.' This genetic trait may have passed from the West Coast of Africa, with the slaves, to America and the Caribbean. Other workers have reported deficiencies in vasodilator systems in the American black, such as dopamine, kallikrein and the renal prostaglandins. These defects may lead to the nosologic entity of 'low renin' hypertension, well described in American blacks, and could open up avenues of therapy based either on DA1 activators (such as fenoldopam) or on renal prodrugs (such as gludopa).

Africa, Western↗
PubMed1990

Ethnic differences in the renal dopamine response to an oral salt load.

Dopamine is a natriuretic hormone which is synthesised within the kidney. We have previously found that some ethnic groups (e.g. British Caucasians and Thais) show strong positive correlations between 24 h urinary sodium and dopamine outputs. However no such relationship was found in Iranians and black West Africans. We have now studied the effect of oral salt loading (200 mmol) on 24 h urinary sodium and dopamine outputs in individuals from these four ethnic groups. The Caucasians showed a significant increase (35%) in urinary dopamine output after salt loading. However, there was no dopamine response to the salt load in the Ghanaians and the Iranians. The Thais were all vegetarians and fell into two distinct groups with either an increase ('positive responders') or decrease ('negative responders') in dopamine output after salt loading. The negative responders all had a very low mean control sodium output (60 +/- 21 mmol/24 h) compared to the positive responder Thais and the other three ethnic groups which all had mean sodium outputs greater than 115 mmol/24 h. We hypothesize that in some racial groups the uncoupling of the renal sodium-dopamine relationship may be an inherited mechanism to help conserve sodium (as in the Ghanaians and the Iranians) or an adaptive change to being restricted to a low salt diet for a long time (as in the Thai 'negative responders').

Asian People↗
PubMed1989

Ethnic differences in the renal sodium-dopamine relationship: a possible explanation for regional variation in the prevalence of hypertension?

Twenty-four-h urinary sodium and dopamine output by normotensive adults from 5 different ethnic groups have been measured. The groups differed substantially in the correlation between the urinary output to sodium and dopamine. Those with a traditionally salt rich diet (Thais, Caucasians, Zimbabweans) showed a strong positive correlation (p less than 0.001), whereas no such relationship was found in West Africans and Iranians, who come from traditionally salt scarce environments. It is hypothesised that in some races the lack of or uncoupling of the renal sodium-dopamine relationship, possibly as a mechanism to help conserve dietary sodium, predisposes to the development of hypertension when the individuals encounter a salt rich diet.

Adaptation, Physiological↗
PubMed1988

Further ethnic differences in the renal sodium-dopamine relationship: its uncoupling in Iranian but not in Thai normotensive subjects.

Dopamine is a natriuretic hormone and is synthesized in the kidney in response to a sodium load. This relationship results in a positive correlation between urinary sodium and dopamine outputs. Uncoupling of the renal sodium-dopamine relationship is reflected in a loss of this correlation and will result in the sluggish excretion of a sodium load. We measured 24-h urinary sodium and dopamine outputs in Thais and Iranians, who traditionally have very different dietary salt environments (salt-rich and salt-scarce, respectively). There was a highly significant positive correlation between sodium and dopamine in the Thais (r = 0.53, P less than 0.001) but no suggestion of such a correlation in the Iranians (r = 0.03). We hypothesize that in some races the uncoupling of the renal sodium-dopamine relationship, possibly as a mechanism to help conserve dietary sodium, predisposes the race to the development of hypertension when the individuals encounter a salt-rich diet.

Dopamine↗
PubMed1982

Diuresis or urinary alkalinisation for salicylate poisoning?

Forty-four adults with aspirin poisoning were treated with oral fluids only, standard forced alkaline diuresis, forced diuresis alone, or sodium bicarbonate (alkali) alone. Alkali alone was at least as effective and possibly more effective than forced alkaline diuresis in enhancing salicylate removal. Unlike the diuresis regimens it did not cause fluid retention or biochemical disturbances. The renal excretion of salicylate depends much more on urine pH than flow rate, and forced diuresis alone had little useful effect. In overdosage aspirin causes sodium and fluid retention and may impair renal function. Attempts to force a diuresis are potentially hazardous and the spurious fall in plasma salicylate concentration caused by haemodilution gives a false impression of efficacy. Further studies are required to determine the optimum treatment for salicylate poisoning.

Adolescent↗
PubMed1981

Effects of microsomal enzyme induction on paracetamol metabolism in man.

1 The metabolism of paracetamol after a single oral dose of 20 mg/kg was compared in fifteen patients with microsomal enzyme induction taking anticonvulsants or rifampicin and twelve healthy volunteers. 2 Induction was confirmed by measurement of the plasma antipyrine half-life (mean 6.4 h in the patients compared with 12.8 h in the volunteers). 3 The glucuronide conjugation of paracetamol was enhanced in the induced patients as shown by lower plasma paracetamol concentrations, a shorter paracetamol half-life, higher paracetamol glucuronide concentrations and an increased ratio of the area under the plasma concentration time curves of the glucuronide to the unchanged drug. There were no significant differences in sulphate conjugation. 4 There was a corresponding change in the pattern of urinary metabolite excretion. The induced patients excreted significantly less unchanged drug and sulphate conjugate and more glucuronide conjugate than the healthy volunteers. 5 The urinary excretion of the mercapturic acid and cysteine conjugated of paracetamol was the same in both groups. 6 Conversion of paracetamol to its potentially hepatotoxic metabolite does not seem to be increased in patients induced with anticonvulsants or rifampicin. There would seem to be no contraindication to the use of these drugs in combination.

Acetaminophen↗
PubMed1980

Failure of alkaline diuresis to enhance diflunisal elimination.

1 The effects of alkaline diuresis on the elimination of a single oral dose of 750 mg diflunisal were studied in six healthy male volunteers. 2 The plasma concentrations and half-life of diflunisal were not reduced by alkaline diuresis. 3 The 72 h urinary recovery of unchanged diflunisal was more than doubled with alkaline diuresis, but even so, only 5-7% of the administered dose was excreted unchanged. 4 With alkaline diuresis there was a significant increase in the mean renal clearance of diflunisal from 0.27 to 0.46 ml/min, but there was no significant correlation between the renal clearance of diflunisal and urine flow or pH. 5 However, there was a significant increase in the overall mean renal clearance of diflunisal from 0.22 ml/min over the period 0-24 h to 0.73 ml/min from 48-72 h. 6 Forced alkaline diuresis is unlikely to be of value in diflunisal poisoning.

Adult↗