Sodium-potassium cotransport activity as genetic marker in essential hypertension.

Abstract

539hypertensive action of ketanserin is thus characterised by a favourable haemodynamic profile. The observation that ketanserin lowered not only systemic arterial pressure but also cardiac filling pressures suggests that this balanced vasodilatation may be of particular interest for the treatment of congestive heart failure. Indeed, a favourable response to ketanserin in this condition has been reported recently."' 5-HT not only acts as a direct vasoconstrictor, but it also amplifies the vasoconstrictor responses to agents such as noradrenaline and angiotensin II.2 5-HT is released by aggregating platelets in atherosclerotic arteries, which are abnormally responsive to this amine.'2 Ketanserin antagonises not only the direct vasoconstrictor effect of 5-HT but also its amplifying effects on other vasoactive substances.5 These mechanisms may all be implicated in the haemodynamic effects of 5-HT2 receptor blockade by ketanserin. This compound is thus a new therapeutic tool for investigating the role of 5-HT in the pathogenesis of various forms of hypertension. Experience so far warrants further assessment of its place in the management of hypertension.We thank Dr J Symocns of Janssen Pharmaceutica for generous supplies of ketanserin. Sodium-potassium cotransport activity is thought to be defective in essential hypertension and could be a useful genetic marker for susceptibility to essential hypertension. In this study cotransport activity in subjects with hypertension was compared with that in normotensive controls. The effects of ethnic differences, environment, and antihypertensive drugs were also studied. Mean cotransport activity was lower in hypertensive subjects than in controls of the same ethnic groups. There was, however, a large overlap between controls and hypertensive subjects. No ethnic or environmental influences were found. The large overlap found suggests that sodium-potassium cotransport activity is not a useful genetic marker in essential hypertension. References

Race and sex differences in erythrocyte Na+, K+, and Na+-K+-adenosine triphosphatase.

“…At present, a lack of agreement exists in regard to this possibility (38)(39)(40). Therefore, it seems reasonable to conclude that the difference in erythrocyte Na+ concentration between blacks and whites is at least partially a result of a variation in the Na+-K+-ATPase activity, while a contribution of the Na+,K+-cotransport system to this difference may also exist.…”

Racial differences in erythrocyte cation transport.

“…17 Davidson et al 18 did not confirm these observations in the South African population, noting no differences for blacks and whites, although within each race, hypertensives tended to be lower than normotensives. Canessa et al 19 have suggested in a preliminary report that hypertension is associated with lower cotransport activity in American blacks but not in whites.…”

Erythrocyte Na+,K+ cotransport and Na+,K+ pump in black and caucasian hypertensive patients.

“…Cotransport values were virtually absent to very low in all hypertensive subjects sampled from this population, which has a very high incidence of hypertension. In a study from Capetown, South Africa, Davidson et al 12 reported lower levels of RBC cotransport expressed as the mean value of Na + plus K + efflux in black, Caucasian, and racially mixed hypertensive patients compared to normotensive subjects. They did note a large overlap of values among study groups and could not detect an environmental influence on RBC cotransport activity.…”

“…One other study noted no differences in RBC cotransport between untreated and hypertensive patients treated with various antihypertensive agents. 12 It is uncertain whether that study examined prospectively in the same patients the effects of blood pressure reduction on RBC cotransport before and during therapy. Erythrocyte Na+,K+ cotransport and Na+,K+ pump in black and caucasian…”