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Selective central alpha-2 adrenoceptor control of regional haemodynamic responses to air jet stress in conscious spontaneously hypertensive rats
Authors:D R Kapusta  S Knardahl  J P Koepke  A K Johnson  G F DiBona
Affiliation:Department of Internal Medicine, University of Iowa, Iowa City 52246.
Abstract:The role of central nervous system alpha 2-adrenoceptors in the regulation of peripheral sympathetic outflow to regional vascular resistance beds during environmental stress was examined in conscious chronically instrumented spontaneously hypertensive rats (SHR). SHR were instrumented with pulsed Doppler flow probes on the renal and mesenteric arteries and the lower abdominal aorta. The mean arterial pressure (MAP), heart rate and regional vascular resistance responses to air jet stress were determined before and after cumulative administration of the alpha 2-adrenoceptor agonist, guanabenz, into the lateral cerebral ventricle in doses of 5 and 25 micrograms. Compared with intracerebroventricular (i.c.v.) administration of isotonic saline vehicle which did not affect baseline systemic and regional haemodynamic measurements, guanabenz produced significant decreases in baseline MAP and heart rate but did not affect regional vascular resistances. During air jet stress, the characteristic pattern of the classic defense reaction with an increase in MAP, heart rate, renal and mesenteric vascular resistances and a decrease in hindquarters vascular resistance was observed and was not affected by i.c.v. administration of isotonic saline vehicle. Guanabenz did not affect the MAP, heart rate or renal vascular resistance responses to air jet stress. The air jet stress-induced increase in mesenteric vascular resistance was reduced by 25 micrograms guanabenz. The air jet stress-induced decrease in hindquarters vascular resistance was converted to an increase by 25 micrograms guanabenz. These results demonstrate that the regulation of environmental stress-stimulated sympathetic neural outflow to different vascular beds may be independently controlled by central nervous system alpha 2-adrenoceptors.
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