Enhancement of hypothalamic pressor responses in spontaneously hypertensive rats.
The cardiovascular effects of stimulating  the posterior hypothalamus electrically were recorded in awake rats to permit in situ evaluation of central neural mechanisms without previous depression by anesthesia. Weak currents ineffective in normotensive or Doca-hypertensive rats elicited measurable pressor responses in spontaneously hypertensive rats, and when currents above threshold strength were used the responses were always larger in spontaneously hypertensive rats than in others. Reduction in reflex bradycardia probably contributed, at least in part, to the increased pressor responsiveness of spontaneously hypertensive rats to hypothalamic stimulation. Since pressor responses to injected norepinephrine or angiotensin were the same as or less than those in normotensive rats, it was concluded that some mechanism other than enhancement of cardiovascular reactivity is involved. Hypersensitivity of hypothalamic pressor areas was considered an attractive explanation but on the basis of the evidence available a possible hypersensitivity of other sites in the efferent neural pathway cannot be excluded.
D000768:Anesthesia, General; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D005260:Female; D006339:Heart Rate; D006973:Hypertension / Q000503:physiopathology*; D007031:Hypothalamus / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D014520:Urethane / Q000494:pharmacology
D000804:Angiotensin II; D014520:Urethane; D009638:Norepinephrine