1502

patient is now being treated with warfarin. Pain has not recurred onthe left side 40 weeks after the second autotransplantation.

In human kidney transplants early regeneration of autonomicaxons has been seen 4 weeks after grafting. This regenerationprogresses with graft survival such that axon-bearing nerves extendto the interlobular arteries by 8 months after transplantation.7Functional reinnervation may account for the recurrence of pain inour patient. Until further experience has accumulated we suggestthat autotransplantation should be reserved for patients whosesymptoms are incapacitating and uncontrollable by conventionalmeans.

Edinburgh Royal Infirmary,Edinburgh EH3 9YW

STEPHEN M. W. HUTCHISONANDREW DOIGANDREW McL. JENKINS

1. Burden RP, Booth LJ, Ockenden BG, Boyd WN, Higgins P McR, Aber GM.Intrarenal vascular changes in adult patients with recurrent haematuria and loinpain: a clinical, histological and angiographic study. Quart J Med 1975, 44: 433-47.

2. Burden RP, Dathan JR, Etherington MD, Guyer PB, MacIver AG. The loinpain/haematuria syndrome. Lancet 1979; i: 897-900.

3. Bell GM, Williams P, Thomson D. Is the loin pain and haematuria syndrome a renalmanifestation of hypersensitivity? Lancet 1984; i: 340.

4. Sheil AGR, Ibels LS, Thomas MAB, Graham JC. Renal autotransplantation forsevere loin pain/haematuria syndrome. Lancet 1985; ii: 1216-17.

5. Aber GM, Higgins PM. The natural history and management of the loin

pain-haematuria syndrome. Br J Urol 1982; 54: 613-15.6. Fairley KF, Birch DF. Haematuria: a simple method for identifying glomerular

bleeding. Kidney Int 1982; 21: 105-08.7. Gazdar AF, Dammin GJ. Neural degeneration and regeneration in human renal

transplants. N Engl J Med 1970; 283: 222-24.

EICOSAPENTAENOIC AND DIHOMO-&ggr;-LINOLENICACIDS

SIR,-In confirming Dr Wood and colleagues’ paper (Jan 24,p 177), C.H. Rapley and colleagues (May 23, p 1202) findsignificantly less linoleic acid in erythrocyte fatty acids from patientswith myocardial infarction than from controls. However, dihomo-y-linolenic acid levels were similar in the two groups. These

findings are somewhat at variance with an earlier paper fromWood’s group’ in which low levels of dihomo-y-linolenic acid inadipose tissue were reported to be strong predictors of high risk inScottish men.

Linoleic acid’s beneficial activity depends on its conversion bydesaturation enzymes (D6D) through dihomo-y-linoleic acid toPGE1. Whereas linoleic acid levels may be a diagnostic test

forewarning of myocardial infarction, linoleic acid does not

necessarily provide a treatment.With regard to eicosapentaenoic acid (EPA), Dr Akos (May 9,

p 1083) explains just how small the EPA/arachidonic acid:plateletmembrane ratio is in Europe, and in Scotland in particular. Thissignifies the extreme lack of EPA in the Scottish diet and thedoubtful relevance of the work of Dr Wood and colleagues in tryingto use that statistic to show that EPA in platelets does notsignificantly help in cases of myocardial infarction. I have evidencethat the Scottish diet lacks EPA and also that EPA is beneficial in

angina and with exercise tolerance.These two essential fatty acids, EPA and dihomo-y-linolenic

acid, may be the missing links in the coronary heart disease

epidemic. Although, as suggested by Dr Sinclair and Dr Gale (May23, P 1202), the desaturation process tends to be slow, this may bedue to such rogue elements of hydrogenation as trans fatty acids.Certainly, linolenic acid, unless desaturated, has no prostaglandinactivity and the same applies to the ill3 vegetable essential fatty acid,a-linolenic acid, which is desaturated by the same enzyme D6D toEPA. It is thus important to pursue Sinclair and Gale’s suggestionthat "we need to know more about the factors that affect the

composition of adipose tissue". The essential fatty acids may actthrough their cell membrane effects, where prostaglandins are lessat issue, or by reducing cholesterol levels.

26 Gorse Road,Blackburn, Lancs. G.P. WALSH

1. Wood, DA, Butler S, Riemersma RA, Thomson M, Oliver MF. Adipose tissue andplatelet fatty acids and coronary heat disease m Scottish men. Lancet 1984; ii:

117-21.

THE Na+-H+ ANTIPORT IN ESSENTIALHYPERTENSION

SIR,—Professor Livne and colleagues report increased plateletNa+-H+ exchange rates in essential hypertension (March 7,p 533). The key question is do their findings indicate a generalisedcell-membrane transport disorder which could relate to the

pathogenesis of hypertension?We have found that erythrocyte Na influx rates in men with

newly-detected hypertension were higher than in male controlsfrom the same screening clinic.1 This difference was not accountedfor by between-group differences in race, age, adiposity, or ethanolconsumption. The increased values in the hypertensive patientswere mainly attributable to an increase in the ouabain-resistant,frusemide-resistant (ORFR) component of the total Na+ influx(table). This component has been generally ascribed to the sum ofcarrier-mediated Na + -Na countertransport and passive inward"Na leak".

ERYTHROCYTE CATION FLUXES*

*Unidirectional sodium influx was measured in packed cells, which were tnple-washed at4&deg;C in artificial medium contaming 145 mmol/I Na’, 5 mmol/I K’, and 20 mmol/Iittiidazole chloride (pH 74), then incubated for 20 min at 37&deg;C in same medium withNa ,01 1 mmol/I ouabain, and 10 mmol/I glucose, with or without 1 mmol/I frusemide.tp < 0 01tp<000t.

Using the inhibition of 22Na influx into erythrocytes by 0.1mmol/f phloretin to measure countertransport, we have confirmed aprevious observation2 that this process accounts for only one-eighthof the ORFR Na influx, and thus could explain no more than asmall part of the flux increase in our hypertensive group. Indeed,the increase in countertransport in essential hypertension has beencalculated to be only one-third of the increase in "Na leak".2

Evidence for an amiloride-sensitive, Na + -H + exchange systemin human erythrocytes has now been presented.3 This system isapparently separate from the phloretin-sensitive countertransporterthat mediates Na+-Na- or Na--Li+ exchange. At present,the extent to which Na+-H+ exchange is responsible for Na+

+

influx into erythrocytes under physiological conditions is uncertain.However, in rat vascular smooth muscle, Na + -H exchangeaccounts for about 80% of the basal Na influx rate.4We speculate that increased Na+ -H+ exchange occurs in the

erythrocytes of hypertensive patients as well as in their platelets, thatthis increased exchange constitutes part of what has been regardedas the "Na+ leak", and that it contributes to the increase in

erythrocyte Na+ influx in essential hypertension found byourselves1 and several other groups .2,5-7

Hypertension Unit,Department of Clinical Pharmacology,Royal North Shore Hospital,St Leonards, NSW 2065, Australia

GORDON S. STOKES

JUDITH C. MONAGHANJOHN F. MARWOOD

1. Stokes GS, Monaghan JC, Willcocks D, Jones MP, Marwood JF. Erythrocyte cationfluxes m the normotensive and hypertensive clients of a health screening clinic. JHypertension (in press).

2. Wessels F, Zumkley H. New aspects concerning the 22sodium influx into red cells inessential hypertension. Klin Wochenschr 1985; 63 (suppl III): 38-41.

3. Escobales N, Canessa M. Amiloride-sensitive Na+ transport m human red cells:Evidence for a Na/H exchange system. J Membr Biol 1986; 90: 21-28.

4. Little PJ, Cragoe EJ, Bobik A. Na-H exchange is a major pathway for Na influx in ratvascular smooth muscle. Am J Physiol 1986; 251: C707-12.

5. Birks RI, Langlois S. Ouabain-insensitive net sodium influx in erythrocytes ofnormotensive and essential hypertensive humans. Proc R Soc Lond B 1982; 216:53-69.

6. Mahoney JR, Etkin NL, McSwigan JD, Eaton JW. Assessment of red cell sodiumtransport in essential hypertension. Blood 1982; 59: 439-42.

7. Shalev O, Eaton JW, Ben-Ishay D. Erythorocyte 22Na+ influx in hypertension. ClinExp Hypertens 1984; 6: 1367-77.