title: Altered venous responses to vasoconstrictor agonists and nerve stimulation in human primary hypertension.
abstract: The reactivity of human veins, biopsied from the forearms of 15 patients with untreated primary hypertension and 14 normotensive subjects, was studied in vitro. Veins of hypertensive patients were less distensible since the slope of their wall tension-circumference relationships was steeper than in normotensive subjects. There was no difference between the groups with regard to their sensitivity (location of the concentration corresponding to 50% of the maximum response) or their normalized maximum contractile force (Fmax/unit radius) in response to potassium or serotonin. However, veins from hypertensive subjects were less sensitive to noradrenaline and the selective alpha 2-adrenoceptor agonist UK14304, and showed a fall in normalized Fmax with all alpha-adrenoceptor agonists. In contrast, in veins from hypertensive subjects, normalized Fmax was 3.7 times higher in response to angiotensin II than in veins from normotensive subjects. Despite the reduced responses to exogenous alpha-adrenoceptor agonists, contractile responses to transmural field stimulation were enhanced in veins from hypertensive patients. There was no evidence of medial hypertrophy in the veins of hypertensive subjects. The effect of selective alpha 2-adrenoceptor blockade suggested a decrease in prejunctional autoinhibition, while the effect of desipramine on field stimulation and tritiated noradrenaline efflux suggested a decreased neuronal amine uptake in veins of hypertensive subjects. We conclude that veins in hypertension are stiffer, have reduced alpha-adrenoceptor responsiveness, and generate a greater Fmax in response to angiotensin II and nerve stimulation when compared with veins from normotensive subjects.
authors.affiliation: Baker Medical Research Institute, Prahran, Victoria, Australia.
authors.forename: K
authors.initials: K
authors.lastname: Sudhir
authors.forename: J A
authors.initials: JA
authors.lastname: Angus
authors.forename: M D
authors.initials: MD
authors.lastname: Esler
authors.forename: G L
authors.initials: GL
authors.lastname: Jennings
authors.forename: G W
authors.initials: GW
authors.lastname: Lambert
authors.forename: P I
authors.initials: PI
authors.lastname: Korner
mesh_terms: D000328:Adult; D004558:Electric Stimulation; D005542:Forearm / Q000098:blood supply; D006801:Humans; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D066298:In Vitro Techniques; D008875:Middle Aged; D009638:Norepinephrine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014680:Veins / Q000187:drug effects* / Q000502:physiology
chemical_list: D011942:Receptors, Adrenergic, alpha; D014662:Vasoconstrictor Agents; D009638:Norepinephrine