A hypothesis linking intracellular sodium, membrane receptors, and hypertension.
Studies in clinical and experimental hypertension have identified alterations both in intracellular [Na+] and in response to hormones and neurotransmitters. We propose a hypothesis that links these two alterations. Based on recent data showing that changes in intracellular [Na+] can alter the affinity and function of platelet alpha2-adrenergic receptors, we hypothesize that elevated intracellular [Na+] in hypertension leads to enhanced response at membrane receptors. This enhancement in response to hormones and/or neurotransmitters could then contribute to the development and maintenance of the hypertensive state. Because a variety of membrane receptors are Na+-sensitive (e.g., adrenergic, muscarinic cholinergic, opiate, angiotensin, dopamine, histamine H1), this mechanism may be operative at one or more receptor types located in tissues critical to the pathophysiology of hypertension.
D000818:Animals; D001794:Blood Pressure; D002462:Cell Membrane / Q000378:metabolism / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D011941:Receptors, Adrenergic / Q000502:physiology; D011956:Receptors, Cell Surface / Q000378:metabolism / Q000502:physiology*; D017981:Receptors, Neurotransmitter / Q000378:metabolism / Q000502:physiology; D012964:Sodium / Q000378:metabolism / Q000502:physiology*
D011941:Receptors, Adrenergic; D011956:Receptors, Cell Surface; D017981:Receptors, Neurotransmitter; D012964:Sodium