Articles: pressoreceptors-physiology.
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The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. ⋯ The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.
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A device was constructed which allowed subatomospheric pressures of up to -50 mm Hg to be applied to the neck, or to the head plus neck, of volunteer subjects riding on the USAFSAM centrifuge. Breathing pressures were always atmospheric. ⋯ Neck suction of -50 mm Hg induced less bradycardia when applied at +3 Gz than under 1-G conditions. These results were discussed in relation to intraocular tension, baroreceptor responsiveness, and jugular venous siphon effect.
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The discovery of the Bainbridge reflex 70 years ago, of a tachycardic response to a rise in central venous pressure, stimulated a lot of interest in this and other cardiovascular reflexes. The mechanoreceptors that elicit the reflex are located at the junction of the right atrium and caval veins or at the junctions of the pulmonary veins and the left atrium. The Bainbridge reflex is controversial, however, because its existence cannot always be demonstrated. ⋯ This paper reviews the history of the studies associated with the reflex. Results are reported, which demonstrate that the chronotropic response to i.v. infusions depends upon the resulting change in aortic diameter; bradycardia is evoked by infusions leading to a rise in aortic baroreceptor activity through increases in aortic diameter, volume or pressure; tachycardia follows whenever the infusion fails to trigger the baroreflex. The importance of the Bainbridge reflex as a counterbalance to the baroreceptor reflex is discussed.
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Acta Physiol. Scand. · May 1987
Reflex changes in sympathetic nerve activity during mechanical ventilation with PEEP in sino-aortic denervated rats.
The aim of this study was to evaluate the role of cardiopulmonary receptors with vagal afferents in the reflex control of sympathetic nerve activity during mechanical ventilation with positive end-expiratory pressure (PEEP). Experiments were performed on 17 chloralose-anaesthetized rats. Changes in renal sympathetic nerve activity (RSNA), heart rate and mean arterial pressure were studied at zero end-expiratory pressure (ZEEP) and at 5 and 10 cm H2O PEEP in intact animals (n = 8), after sino-aortic denervation (n = 17) and after sino-aortic denervation plus vagotomy (n = 10). ⋯ The PEEP did not induce any significant change in RSNA or heart rate after sino-aortic denervation plus vagotomy. The results indicate that cardiopulmonary receptors with vagal afferents contribute to the reflex excitation of the sympathetic nervous system during mechanical ventilation with PEEP. Under certain circumstances, PEEP may also trigger powerful depressor reflexes, mediated by vagal afferents.
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Can. J. Physiol. Pharmacol. · May 1987
Acute effects of ethanol on baroreceptor reflex control of heart rate and on pressor and depressor responsiveness in rats.
In rats anesthetized with alpha-chloralose, doses of 0.1, 0.5, and 1 g/kg of ethanol produced an upward shift of baroreflex curves constructed by plotting the heart rate response against mean arterial pressure following evoked rises in mean arterial pressures by phenylephrine or angiotensin II. Whereas the upward shift of baroreceptor curves may be related, at least in part, to a higher base-line heart rate after ethanol, the data showed that the 1 g/kg dose of ethanol significantly depressed baroreflex sensitivity, suggesting that higher doses of ethanol impair baroreflex-mediated bradycardia. The phenylephrine, but not the angiotensin II or the nitroprusside, dose-response curves were shifted to the right after ethanol, indicating a decreased pressor responsiveness and suggesting that ethanol may have alpha-adrenergic blocking activity. ⋯ That this effect was not influenced by changes in baroreflex sensitivity was supported by the finding that a similar shift of the phenylephrine pressor-response curve was obtained in bilaterally vagotomized and hexamethonium-treated rats. Whether this effect of ethanol on baroreflex control of heart rate was influenced by anesthesia was investigated in conscious rats; the 1 g/kg dose of ethanol that produced the most significant decrease in baroreflex sensitivity was used in these experiments. Ethanol was still able to significantly inhibit baroreflex sensitivity in conscious rats, but the upward shift of the baroreflex curve and the elevated base-line heart rate no longer occurred.(ABSTRACT TRUNCATED AT 250 WORDS)