Immediate hypotensive after-effects of posterior hypothalamic lesions in awake rats with spontaneous, renal, or Doca hypertension.

If the posterior hypothalamus contributes to elevate blood pressure in hypertension by increasing sympathetic vasomotor activity, then lesions of the posterior hypothalamus should lower blood pressure more in hypertensive than in normotensive rats. To test this hypothesis without complications caused by anaesthesia, aortic pressures were recorded from indwelling catheters in awake rats before and after selective hypothalamic destruction. In normotensive rats rats, bilateral lesions of the medial areas of the posterior hypothalamus always lowered blood pressure while those in the anterior hypothalamus slightly increased it. Heart rate responses varied widely and did not seem to contribute to the blood pressure changes. Posterior hypothalamic lesions of approximately the same size had significantly greater hypotensive after-effects in renal and spontaneously hypentensive rats than in normotensive or Doca hypentensive ones. These results imply that sympathetic overactivity emanating from posterior hypothalamic centres contributes to the blood pressure elevation in spontaneous or chronic renal hypentension but not in Doca hypertension. However, because of inherent weaknesses in the 'lesion method' and the complexity of blood pressure regulation in awake animals, other explanations are possible.