Intravenous labetalol in hypertensive emergency.
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Biomedical subjects
Publications and source records attributed to A M Cumming.
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The smoking habits of 82 patients with malignant-phase hypertension were compared with those of subjects in three control groups matched for age and sex. Sixty-seven (82%) of the patients with malignant-phase hypertension were smokers compared with 41 (50%) and 71 (43%) of the patients in two control groups with non-malignant hypertension, and 43 people (52%) in a general population survey. The excess of smokers in the malignant-phase group was significant for men and women, together and separately, for cigarette smoking alone, and for all forms of smoking. There were no significant differences between the control groups. The chance of a hypertensive patient who smoked having the malignant phase was five times that of a hypertensive patient who did not. Twelve patients in the malignant-phase group had never smoked. All were alive three and a half years on average after presentation (range 11 months to seven years). Twenty-four (36%) of the smokers with malignant-phase hypertension died during the same period. The mortality rate was significantly higher among patients with renal failure, as was the prevalence of smoking. Eighteen patients with malignant-phase hypertension had a serum creatinine concentration higher than 250 mumol/l (2.8 mg/100 ml); 17 were smokers and one an ex-smoker. Eleven of these 18 patients died.It is concluded that hypertensive patients who smoke are much more likely to develop the malignant phase than those who do not, and that once the condition has developed it follows a particularly lethal course in smokers.
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1. Arterial pressure and exchangeable sodium (NaE) were measured in patients with Conn's syndrome, essential hypertension, renal artery stenosis and chronic renal failure. Comparison was made with a control group. Urine sodium excretion was measured separately from the two kidneys in patients with renal artery stenosis. 2. Compared with control, mean NaE was significantly increased in Conn's syndrome, and was normal in essential hypertension, renal artery stenosis and chronic renal failure. 3. The correlation of arterial pressure with NaE was positive and significant in Conn's syndrome, essential hypertension and chronic renal failure. 4. In contrast the correlation was significantly negative in unilateral renal artery stenosis. Patients with lowest NaE had hyponatraemia, hypokalaemia and secondary hyperaldosteronism. 5. Urinary sodium excretion from the unaffected kidney in unilateral renal artery stenosis correlated positively with arterial pressure, possibly reflecting the phenomenon of pressure-natriuresis. Patients subsequently responding least well to surgery excreted least sodium from the untouched kidney for a given arterial pressure. 6. The findings suggest important roles for arterial pressure in the regulation of sodium balance (predominant in renal artery stenosis), and for sodium balance in the regulation of arterial pressure (predominant in Conn's syndrome). The observations in essential hypertension are compatible either with an exact balance between these mechanisms or with the existence of some other mechanism raising blood pressure.
The rare opportunity arose to assess in detail the renin-angiotensin system before and after the development of a renal artery stenosis with severe hypertension. Peripheral plasma concentrations of renin, angiotensin II, and aldosterone were known to be normal before the development of renal artery stenosis, and there were no lateralising features on renal vein sampling. Acute hypertension associated with very high peripheral plasma concentrations of renin and angiotensin II, and with pronounced lateralisation on renal vein sampling followed the development of acute unilateral renal artery stenosis. These measurements all returned to normal after nephrectomy, conforming with the pattern of changes previously established only in experimental animals.
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Serum concentrations for the cholesterol and triglyceride content of very low density lipoprotein (VLDL) and the cholesterol content of intermediate density lipoprotein (IDL), low density lipoprotein (LDL), and the high density lipoprotein fractions (HDL2), HDL3) were measured in 337 men and women with the apo E phenotype who were born in the Grampian Region of North East Scotland. The subjects' ages ranged from 45 to 60 years (mean, 53 years). Cigarette smoking and alcohol consumption were recorded and were shown to have minor, but suggestive, effects on serum lipoprotein concentrations. The LDL concentration of E-3/2 subjects was compared with the commonest category, E-3/3, and was found to be about 20% lower in men and about 12% lower in women, in whom the VLDL and IDL concentrations were substantially elevated. In E-4/3 women, the serum LDL concentration was about 10% higher than in E-3/3 women, and the other differences were minor. The effect of allelic substitutions differed between the sexes. The relations between C-peptide ratios and serum lipoprotein concentration differed by gender and phenotype. A comparison with earlier estimates of LDL heritability suggests that in this population, a substantial fraction of the genetic variance of LDL is due to segregation at the apo E locus. The implications of this significant finding are discussed.
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Dose-response curves relating plasma angiotensin II (AII) concentration during AII infusion to blood pressure (BP), to plasma aldosterone, and to plasma 18-hydroxycorticosterone were compared in normal subjects and in patients with essential hypertension, Conn's syndrome, and nontumorous hyperaldosteronism. The BP response was steeper than normal in patients with Conn's syndrome and essential hypertension. Before infusion, mean plasma aldosterone concentration was approximately four-fold higher in Conn's syndrome than in the normal group, while that of 18-hydroxycorticosterone was ninefold higher. Neither increased significantly during AII infusion. In essential hypertension, both corticosteroids were within the normal range, but their responses to AII infusion were greater than normal. In the three subjects with non-tumorous hyperaldosteronism, plasma aldosterone and 18-hydroxycorticosterone concentrations were raised, and their responses to AII infusion resembled those found in essential hypertension and were different from those found in Conn's syndrome. This suggests that nontumorous hyperaldosteronism is not a variant of Conn's syndrome. In the response to AII and in other ways, it is indistinguishable from essential hypertension.