Hypertension induced changes in cerebral capillary permeability to water are mediated by afferent neuronal connections from the carotid sinus to the brain.
Mild acute hypertension was induced in rats pharmacologically and non-pharmacologically with metaraminol, angiotensin II or bilateral vagotomy. The extraction fraction of water (Ew) was measured in both hypertensive and normotensive animals. It was demonstrated that cerebral blood flow did not change during hypertensive states. Under constant flow conditions Ew becomes a direct index of the cerebral capillary permeability to water. Ew was significantly decreased (P less than 0.001) in all brain regions examined in the hypertensive animals as compared to normotensive controls. However, the decrease Ew induced by hypertension was not observed if the animal had previously received bilateral carotid sinus denervation. This observation indicated that the capillary permeability response induced by hypertension is mediated by a neurogenic mechanism involving information transfer from the peripheral baroreceptors in the carotid sinus along afferent connections into the central nervous system.
D000344:Afferent Pathways / Q000033:anatomy & histology*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001834:Body Water / Q000502:physiology*; D001921:Brain / Q000033:anatomy & histology* / Q000503:physiopathology; D002199:Capillary Permeability / Q000187:drug effects; D002346:Carotid Sinus / Q000033:anatomy & histology* / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005260:Female; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008680:Metaraminol / Q000494:pharmacology; D009474:Neurons / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D014628:Vagotomy
D000804:Angiotensin II; D008680:Metaraminol