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This preclinical study demonstrates that left ventricular receptor stimulation in cats produces distinct reflex bradycardia and vasodilatation patterns compared to arterial baroreceptor activation.
Left ventricular receptors, firing in non‐medullated vagal afferents, were stimulated in chloralose‐anesthetized cats by brief aortic occlusions or by intrapericardial injections of nicotine. The induced reflex effects on heart rate, renal and skeletal muscle resistance vessels and muscle capacitance vessels were followed and compared with the reflex effects of arterial baroreceptor stimulation. Stimulation of the ventricular receptors induced a considerable reduction in heart rate, almost entirely due to vagal activation, and to a reflex dilatation of renal and muscle resistance vessels and of the muscle capacitance vessels. For a given reflex reduction of skeletal muscle flow resistance with the two reflex mechanisms, the concomitant reflex bradycardia and renal vasodilatation was more pronounced when the ventricular receptors were stimulated than upon activation of the arterial baroreceptors. The capacitance vessels seemed, however, to be engaged to the same extent from the two receptor groups. The reflex muscle dilatation, following ventricular receptor activation, was solely due to inhibition of adrenergic vasoconstrictor fibre activity with no evidence of any cholinergic vasodilator fibre activation.
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ÖBerg et al. (1973) studied this question.
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