Cryoblockade of the ventromedial frontal cortex reverses hypertension in the rat.
The anteroventral part of the hypothalamus adjacent to the third ventricle (AV3V) has been implicated in electrolytic lesion studies as a site crucial to the development and maintenance of hypertension. Cryoblockade is known to alter synaptic and axonal transmission differently at different temperatures. In this study, cooling of the hypothalamus, including the AV3V area, to the temperature known to block only synaptic function did not alter blood pressure in two different models of experimental hypertension in the rat. Cooling sufficient to block both synaptic and axonal transmission, however, reduced blood pressure elevations to near normotensive levels. Synaptic cryoblockade in the ventromedial portion of the frontal cortex lowered experimental hypertension by 21 +/- 3 mm Hg (p less than 0.05). In normotensive controls, blood pressure was not altered by cryoblockade in either the frontal cortex or hypothalamus. Anatomical evidence provided by others shows that cells in the ventromedial frontal cortex project, in part, through the AV3V region to the brainstem cardioregulatory structures. These results indicate that neural activity arising in frontal cortex is axonally projected through the hypothalamus to maintain elevated blood pressure in experimental hypertension.
D000818:Animals; D007025:Anterior Hypothalamic Nucleus / Q000503:physiopathology*; D001794:Blood Pressure; D003900:Desoxycorticosterone; D006339:Heart Rate; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007036:Hypothermia, Induced; D051381:Rats; D013569:Synapses; D013696:Temperature
D003900:Desoxycorticosterone