The nucleus tractus solitarius and experimental neurogenic hypertension: evidence for a central neural imbalance hypothesis of hypertensive disease.
1. Interference with neuronal transmission through the NTS can result, depending upon species and mode of perturbation, in a panoply of abnormalities of blood pressure control simulating many of the features of the human disease. These are summarized in Table 1. 2. The abnormalities of pressure control resulting from abnormal transmission in NTS met most of the criteria of an animal model of central neurogenic hypertension. The only criterion yet to be met is that of pathology, a deficiency which may soon be overcome when animals, such as dogs, are maintained for prolonged periods of time. 3. The studies establish the possibility that subtle abnormalities involving neurochemical balances with NTS, resulting either from abnormal neurochemical transmission or variations of the organization of the nucleus with preponderance of one transmitter or deficiencies in others, can result in hypertension. 4. Impaired NTS function can produce an amplification of the action of the environmental stresses on blood pressure. Thus environmental stimuli or the expression of behaviors which normally result in trivial elevations of blood pressure will, after the NTS is perturbed, result in marked elevations. 5. A neural or neurochemical imbalance in brain can produce hypertension.
D000320:Adrenergic Fibers / Q000502:physiology; D000818:Animals; D005971:Glutamates / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008526:Medulla Oblongata / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology*
D005971:Glutamates