Why the study?
Does electrical stimulation of the central amygdaloid nucleus elicit exaggerated cardiovascular responses in spontaneously hypertensive rats compared to normotensive rats?
Does electrical stimulation of the central amygdaloid nucleus elicit exaggerated cardiovascular responses in spontaneously hypertensive rats compared to normotensive rats?
Stimulation of the central amygdaloid nucleus does not elicit exaggerated cardiovascular responses in spontaneously hypertensive rats, challenging previous evidence of its role in spontaneous hypertension development.
Challenges prior evidence for amygdaloid involvement in SHR hypertension; leaves open central mechanisms in experimental models.
Our studies were done to determine 1) the regional hemodynamic effects of stimulating the central amygdaloid nucleus in conscious and anesthetized rats and 2) whether these effects differ between normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Flow was recorded with miniaturized pulsed Doppler probes placed on the renal and superior mesenteric arteries and the lower abdominal aorta. In rats anesthetized with Dialurethane, electrical stimulation elicited a depressor response accompanied by a decrease in hindquarter vascular resistance, with little or no change in heart rate or renal or mesenteric resistance in both SHR and WKY. By contrast, in conscious rats, stimulation was accompanied by a pressor response, tachycardia, and renal and mesenteric vasoconstriction in both groups. Hindquarter vascular resistance was unchanged in WKY and decreased at higher frequencies in SHR. There were no significant differences between SHR and WKY, whether anesthetized or awake, in hemodynamic responses to amygdaloid stimulation. Despite previous evidence indicating that the central amygdaloid nucleus contributes to the development of spontaneous hypertension, our results show that stimulation of this region does not elicit exaggerated cardiovascular responses in SHR.
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Galeno et al. (1983) studied this question.
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