Pressor response buffering by beta-adrenergic and cholinergic vasodilation in tranquilized dogs

Abstract

Buffering of alpha-receptor-mediated pressor responses by beta-adrenergic or cholinergic vasodilation in tranquilized, chronically instrumented gos was investigated. Increases in aortic pressure were produced in the same animal by intravenous injections of phenylephrine in the control state and in three successive experimental states by 1) pacing the heart to remove the reflex capability to lower heart rate, 2) pacing the heart and beta-blockade to remove beta-adrenergic vascular buffering, and 3) beta-blockade plus atropine to also remove cholinergic vascular buffering. The pressor response in each experimental state was greater than that in the state preceding it. With the combined beta-adrenergic and cholinergic blockade, the pressor response to an alpha-receptor stimulation was three times greater than that of the control state. From an analysis of the components of the pressor response, cardiac output, and peripheral resistance, it is suggested that normal buffering of an alpha-mediated pressor response may include beta-adrenergic and cholinergic vascular dilation in addition to a decrease in heart rate.

Vagal cardiac function and arterial blood pressure stability

“…Although species and protocol differences must be considered when interpreting these results, we believe that these previous studies and our current data suggest a minimal physiological contribution from the ␤-adrenoceptor or cholinergic fiber elicited vasodilation at rest. Furthermore, neither the previous study (8) nor the current data support the theory of a sensitized ␣-adrenoceptor mechanism in the augmented pressor response to phenylephrine. If the ␣-adrenoceptor sensitivity were enhanced by MC blockade, a hypotension or depressor response after bilateral thigh cuff inflation/deflation would be diminished after atropine or glycopyrrolate.…”

“…indicated that an augmented pressor response to phenylephrine was present after MC blockade alone with either atropine or glycopyrrolate ( Table 2), suggesting that the ␤-adrenoceptor mechanism of peripheral vasodilation described by Evans et al (8) had little effect on ABP changes elicited by phenylephrine. Sanders et al (18) reported a significant increase in forearm blood flow during contralateral arm exercise, which was attenuated after atropine.…”

“…A previous study (8) reported that the pressor response to phenylephrine injection in tranquilized dogs was substantially augmented after atropine treatment combined with the ␤-adrenoceptor antagonist propranolol. These authors postulated that the augmented pressor response to phenylephrine after propranolol and atropine was related to the blockade of a peripheral vasodilation mechanism modulated by the ␤-adrenoceptor and the cholinergic fiber (8). Our data and after (closed symbols) parasympathetic blockade using atropine (circles) and glycopyrrolate (squares).…”

Effect of haemodynamic changes during rapid atrial pacing on determination of sinus node recovery time.

“…An increase in pressure amplitude, such as we regularly observed during the counter-regulatory rise in blood pressure (Table 2), elicits a depressor response.26-28 This depressor response in turn attenuates a pressor response, which is simultaneously modulated by concomitant beta adrenergic and cholinergic mechanisms. 29 Although the pacing rate at which a certain blood pressure amplitude influences the carotid sinus may also be responsible for the pronounced fall in arterial blood pressure after an initial rise, at rates between 70 and 100 beats/min, it probably plays a minor role at higher rates. 26 28 30 All catheterisations were performed between 0800 and 1200 hours to eliminate any effect of circadian variations in baroreflex sensitivity.…”