Anterior hypothalamic disconnection attenuates the development of 1K1C but not 2K1C Goldblatt renal hypertension in rats, highlighting distinct neural mechanisms in these models.
No direct clinical implications from this animal model; leaves open differential hypothalamic involvement across renovascular hypertension variants for further research.
The role of the central nervous system, in general, and of the hypothalamus, in particular, in the genesis of various forms of experimental hypertension has been the object of increased investigation. Lesions of the anteroventral area of the third ventricle (AV3V) in rats seem to block the development of various forms of hypertension. In the present experiments, AV3V was kept intact but its connections with the caudal neuroaxis were severed by means of a curved knife (2 mm radius), stereotaxically placed at the level of the arcuate nucleus. This disconnection, per se, induces polydipsia, and a reduction of the pressor effect of i.v.-infused angiotensin II. The interactions of simultaneously performed hypothalamic disconnection (HD) and Goldblatt one-kidney, one clip, (1K1C) or two-kidney, one clip (2K1C) hypertensions was studied. It was found that HD retards and attenuates the development of 1K1C hypertension but does not materially affect the evolution of the 2K1C model. Rats with established 1K1C or 2K1C hypertensions were not affected by HD, whereas rats with chronic HD (4 weeks) showed slight and slow developing hypertension in response to clipping. The possible significance of these results with respect to the neural connections of AV3V is discussed.
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Castro et al. (1983) studied this question.
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