ABSTRACT
Background: blood pressure [BP] levels appear to have strong familial tendencies. An estimated 30-60% of the variation of the BP between individuals, after adjustment of age and sex, is attributed to gene factors. Recent reports suggest occurrence of endothelial dysfunction in development of essential hypertension. The defective nitric oxide production resulting in reduced vasodilator capacity of the peripheral blood vessels, with consequent increase in the peripheral resistance and BP
Aim of work: is to address the genetic familial factor in hypertension through the evaluation of vasodilator capacity in normotensive offsprings of hypertensive patients
Patients and methods: 53 Subjects age from 15 to 35 years old were included: Group I: 20 subjects with normal BP but one or both of their parents is hypertensive, 12 subjects having only one of their parents is hypertensive [Group 1A], while 8 subjects of this group [40%] having both parents are hypertensives [Group 1B]. Group 2: 20 subjects with normal BP and their parents are of normal BP too, as a control group and 13 subjects were excluded as they were discovered to be hypertensives [By APBM]. Subjects were divided into two groups according to family history of hypertension: Both groups were subjected to: History taking, Clinical Examination, FBS and PPBS, lipogram, Ambulatory blood pressure monitoring, Coloiured duplex ultrasound to test the vasodilator capacity before and after reactive hyperaemia and GTN
Results: there is significant difference between both groups for mean post FMD [p=0.014], mean FMD% [p<0.001] and mean Dil.ratio [p<0.001]. While there is no statistical significance between both groups as regard mean pre FMD, mean pre and post GTN-MD and GTN-MD%. There is significant difference between group 1A and group 1B for mean post FMD [p=0.033], mean FMD% [p<0.001] and Dil.ratio [p=0.001].While there is no statistical significance between both groups as regard mean pre FMD, mean pre and post GTN-MD, and GTN-MD%
Conclusion: there is an obvious endothelial dysfunction in offsprings of hypertensive parents, preceding their development of hypertension. Those traits are inherited to them from their hypertensive parents, and being more if they are inherited from both parents. This endothelial dysfunction may be due to a genetic defect in nitric oxide [NO] synthesis pathway either in production of NO synthase enzyme [NOS] isoforms, co-factors for NOS induction and inhibition andlor L-arginine which is the. NO substrate or its analogues. Also the autonomic disturbance is due to a genetic defect, which makes them more susceptible to environmental stresses resulting in a high sympathetic tone in those subjects. Finally, the inherited impaired baroreceptors sensitivity and autonomic dysfunction together with the endothelial dysfunction and defective nitric oxide may represent mechanisms through which subjects with familial predisposition for hypertension may develop hypertension later on in their life