Abstract

A possible reason for inconsistent results in attempts to produce NTS lesion-dependent hypertension in larger animals such as the dog may be incomplete destruction of baroreceptor afferents. Neuroanatomical studies in the dog revealed that the 8 mm length of the distribution of baroreceptor afferents within the nucleus tractus solitarius makes interruption of the baroreflex pathway by lesioning this nucleus unfeasible. However, the discovery that the baroreceptor afferents are bundled together in the solitary tract between 5 mm and 7 mm anterior to the obex suggested that bilateral destruction of the tracts would produce central baroreflex interruption. Pharmacological evaluations in dogs following rostral solitary tract lesions revealed both successful baroreflex interruption and an acute hypertension which was primarily dependent on increased circulating vasopressin. However, the similar decrease in arterial pressure following ganglionic blockade in both solitary tract lesioned and sham lesioned animals leaves the importance of augmented sympathetic outflow in solitary tract lesion hypertension in doubt.Although the intermediate portion of the nucleus tractus solitarii (NTS) has long been known as the site of the first relay for the baroreceptor afferents (1) in the central nervous system (CNS), a number of investigators have encountered difficulty in producing hypertension that is sustained for weeks or months after central interruption of this CNS input. Doba and Reis (2) first showed that bilateral NTS lesions in the rat produced severe hypertension leading to acute cardiac failure and pulmonary edema. In contrast, Buchholz and Nathan (3) found that somewhat more restricted NTS lesions which abolished the reflex bradycardia to the rise in blood pressure following phenylephrine injections produced only lability of arterial pressure without altering its average level in rats studied between one week and 7 months after operation. Similarly, the hypertension which followed NTS lesions in the cat was reported to be moderate and associated with lability (4). Previous studies in the dog have yielded conflicting results. Carey et al. (5) reported mild hypertension during ten days of observation, Laubie and Schmitt (6) described severe hypertension sustained for several months after NTS lesions, whereas we found mild hypertension with lability during one to two months of post-lesion study (7). Although these inconsistencies in NTS lesion dependent hypertension may be attributed to differences in lesioning and/or recording techniques, the controversy is far from settled. It is possible that hypertension of neurogenic origin is associated with only intermittent bouts of blood pressure elevation. In the final analysis either labile or sustained hypertension may both have the same deleterious consequences upon the cardiovascular system if they occur over a period of time measured in years rather than weeks or months.KeywordsMean Arterial PressureCarotid SinusNucleus Tractus SolitariiSolitary TractDorsal Motor NucleusThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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