The sympathetic system in hypertension. State-of-the-art review.
One may postulate a genetic defect in membrane permeability, in the transport of sodium, or in the sodium pump in vascular muscle which could account for increased intracellular sodium and enhanced vascular contractility. If the electrogenic sodium pump is overactive, as in SHR, its inhibition may lead to significant depolarization and greater contraction. Sympathetic innervation may be essential for the development of membrane abnormality as well as for the development of hypertrophic vascular changes, both of which augment contraction and vascular tone. A similar membrane defect at the sensory endings of arterial stretch receptors may account for impaired arterial baroreceptor reflexes seen in very early phases of hypertension or, in some genetic models, before hypertension develops. This defect may be related to the sodium pump or sodium transport in the receptor region and cause a decrease in baroreceptor discharge and in the strain-sensitivity of the baroreceptors, resulting in exaggerated sympathetic drive. Further information is needed on the baroreflex control of various efferents in hypertension. Another membrane defect at the adrenergic nerve terminals may facilitate release of endogenous NE. Excessive salt intake may unmask or exaggerate the membrane defects. In the central nervous system a defect in glutamine, NE, or GABA receptors may contribute to a high central sympathetic drive. Greater receptor affinity to various pressor neuropeptides such as angiotensin and leucine enkephalin or greater release of these peptides may also account for the excessive CNS sympathetic activation or impairment of baroreflexes at a central level. Cardiac receptors may have a variable influence on sympathetic drive in the various stages of hypertension, depending on the degree of cardiac hypertrophy or cardiac size. Finally, increased renal afferent nerve activity may provoke an increase in sympathetic activity and provide a link between natriuretic factors and the sympathetic nervous system in hypertension.
D000818:Animals; D006321:Heart / Q000294:innervation; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007031:Hypothalamus / Q000503:physiopathology; D007668:Kidney / Q000294:innervation; D008526:Medulla Oblongata / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D009434:Neural Pathways / Q000503:physiopathology; D010275:Parasympathetic Nervous System / Q000503:physiopathology; D011311:Pressoreceptors / Q000503:physiopathology; D013116:Spinal Cord / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014630:Vagus Nerve / Q000503:physiopathology; D014655:Vascular Resistance; D014882:Water-Electrolyte Balance; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D005680:gamma-Aminobutyric Acid