Abstract
Patients with tension-type headache (TTH) have an increased risk of developing arterial hypertension (AH), while hypertensive subjects do seem to have an increased risk of TTH. We searched for full-text English publications in databases using keywords and combined word searches over the past 15 years. In addition, earlier publications of historical interest were included in the review. In our review, we summed up the single nucleotide variants (SNVs) of Nitric Oxide Synthases (NOSs) genes involved in the development of essential AH and TTH. The results of studies we discussed in this review are contradictory. This might be due to different designs of the studies, small sample sizes in some of them, as well as different social and geographical characteristics. However, the contribution of genetic and environmental factors remains understudied. This makes the issue interesting for researchers, as understanding these mechanisms can contribute to a search for new approaches to pathogenetic and disease-modifying treatment of the AH and TTH phenotype. New drugs against AH and TTH can be based on inhibition of nitric oxide (NO) production, blockade of steps in the NO-cGMP pathway, or NO scavenging. Indeed, selective neuronal NOS (n-NOS) and inducible NOS (i-NOS) inhibitors are already in early clinical development.
Highlights
Arterial hypertension (AH) is a prevalent condition worldwide and is the key risk factor for non-fatal and fatal cardiovascular complications [1]
The Nitric Oxide Synthases (NOSs) family proteins are encoded by the genes NOS1, NOS2, and
Experimental evidence suggests that nNOS (NOS1), inducible NOS (iNOS) (NOS2), and eNOS (NOS3) have important effects on cardiovascular function and pain, but their cumulative effect on the AH and Tension-type headache (TTH) phenotype in humans is unknown
Summary
Arterial hypertension (AH) is a prevalent condition worldwide and is the key risk factor for non-fatal and fatal cardiovascular complications [1]. The relationship between AH and TTH is potentially of great pathophysiological and clinical interest, but it is poorly understood [3]. This allows us to hypothesize the presence of the AH and TTH phenotype. The connection between acute or chronic pain and cardiovascular changes is supported observationally [4], but some of this indirect evidence is confirmed by experimental animal models and human studies. AH and TTH may share common mechanisms like endothelial dysfunction, deficiency of autonomic cardiovascular regulation, and renin angiotensin system involvement. AH and TTH may share common m2eocfh anisms like endothelial dysfunction, deficiency of autonomic cardiovascular regulation, and renin angiotensin system involvement. Heivgehrl,ythfuenfuctnioctniaoln,alol wactfiuvnitcytioofneanl,zaynmdensoonftfhuenNctOioSnaflamsinilgylednepuecnledostiodne tvhaericaanrtrsia(SgNe oVfs)woifldN, OhiSg1h,lNy OfuSn2c,taionndaNl, OloSw3 gfuenncetsioennaclo,dainndg nthone-efnuznycmtioeniaslofsoinrmglse. nucleotide variants (SNVs) of NOS1, NOS2, and NOS3 genes encodinTghteheaiemnzoyfmtheeisroefvoiremws.is to study the role of SNVs of the NOS1, NOS2, and NOS3 geneTshine tahime coofmtohrebridevitiyewof iasrtteorisatluhdyyptehreternoslieonofaSnNd Vtesnosifotnh-etyNpeOhSe1a, dNaOchSe2., and NOS3 genes in the comorbidity of arterial hypertension and tension-type headache
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