The renal sympathetic baroreflex in the rabbit. Arterial and cardiac baroreceptor influences, resetting, and effect of anesthesia.

Dorward, Patricia K.; Riedel, Walter; Burke, Sandra L.; Gipps, J. H. W.; Korner, Paul I.

doi:10.1161/01.res.57.4.618

Cited by 181 publications

(165 citation statements)

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“…reflex, the baroreceptor-heart rate reflex and the renal sympathetic baroreflex (Kunze, 1981;Dorward et al 1982Dorward et al , 1985. We have now found it to occur, within 30 s, whenever there is a reversal in the direction of a slow pressure rise or fall.…”

Section: Hysteresis Shifts In Aortic Baroreceptor Unitsmentioning

confidence: 70%

“…(Salgado & Krieger, 1978; Coleridge, Coleridge, Kaufman & Dangel, 1981; Dorward, Andresen, Burke, Oliver & Korner, 1982;Munch, Andresen & Brown, 1983;Coleridge, Coleridge, Poore, Roberts & Schultz, 1984;Heesch, Thames & Abboud, 1984); once established, it is stable for at least 1-2 h (Dorward et al 1982;Munch et al 1983). Receptor resetting appears to be largely responsible for the resetting of baroreflex responses, which also occurs over a similar time span (Kunze, 1981;Forward et al 1982; Dorward, Riedel, Burke, Gipps & Korner, 1985).…”

Section: Introductionmentioning

confidence: 99%

“…min i.v. infusion) in ten rabbits (Dorward et al 1985). Anaesthesia was then lightened (Alfathesin infused at 0 1 mg/kg.…”

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confidence: 99%

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Rapid resetting of rabbit aortic baroreceptors and reflex heart rate responses by directional changes in blood pressure.

Burke¹,

Dorward²,

Korner³

1986

The Journal of Physiology

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SUMMARY1. In both anaesthetized and conscious rabbits, perivascular balloon inflations slowly raised or lowered mean arterial pressure (M.A.P.), at 1-2 mmHg/s, from resting to various plateau pressures. Deflations then returned the M.A.P. to resting. 'Steadystate' curves relating M.A.P. to (i) unitary aortic baroreceptor firing, (ii) integrated aortic nerve activity and (iii) heart rate were derived during the primary and return pressure changes and they formed typical hysteresis loops.2. In single units, return M.A.P.-frequency curves were shifted in the same direction as the primary pressure changes by an average 0 37 mmHg per mmHg change in M.A.P. Shifts were linearly related to the changes in M.A.P. between resting and plateau levels for all pressure rises and for falls less than 30 mmHg. They were established within 30 s and were quantitatively similar to the rapid resetting of baroreceptor function curves found 15 min-2 h after a change in resting M.A.P. (Dorward, Andresen, Burke, Oliver & Korner, 1982). Unit threshold pressures were shifted within 20 s to the same extent as the over-all curve shift to which they contributed.3. In the whole aortic nerve, return M.A.P.-integrated activity curves were shifted to same degree as unit function curves in both anaesthetized and conscious rabbits. Simultaneous shifts of return reflex M.A.P.-heart rate curves were also seen in conscious rabbits within 30 s. During M.A.P. falls, receptor and reflex hysteresis was similar, but during M.A.P. rises, reflex shifts were double baroreceptor shifts, suggesting the involvement of other pressure-sensitive receptors.4. We conclude that hysteresis shifts in baroreceptor function curves, which follow the reversal of slow ramp changes in blood pressure are a form of rapid resetting. They are accompanied by rapid resetting of reflex heart rate responses. We regard this as an important mechanism in blood pressure control which produces relatively high-gain reflex responses, during slow directional pressure changes, over a wider range of absolute pressure levels than would otherwise be possible.

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Section: Hysteresis Shifts In Aortic Baroreceptor Unitsmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

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Rapid resetting of rabbit aortic baroreceptors and reflex heart rate responses by directional changes in blood pressure.

Burke¹,

Dorward²,

Korner³

1986

The Journal of Physiology

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“…The sterilized guide cannula (0.71-mm O.D., 22.5-mm long) was then mounted in a stereotaxic clamp, inserted into the brain, and fixed in position with dental cement. One week before the experiments, a bipolar renal nerve electrode for recording RSNA was implanted according to the method of Dorward and colleagues (11).…”

Section: Methodsmentioning

confidence: 99%

Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits

Mayorov

Head

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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In this study, we examined the effect of excitatory amino acid (EAA) receptor blockade in the rostral ventrolateral medulla (RVLM) on the renal sympathetic baroreflex in conscious rabbits. Rabbits were implanted with guide cannulas for bilateral microinjections into the RVLM (ϩ2 to ϩ3 mm from the obex, n ϭ 8) or into the intermediate ventrolateral medulla (IVLM; 0 to ϩ1 mm from the obex, n ϭ 5) and with an electrode for measuring renal sympathetic nerve activity (RSNA). After 7 days of recovery, microinjection of the EAA receptor antagonist kynurenate (10 nmol) into the RVLM did not affect resting RSNA or arterial pressure. Kynurenate decreased the gain of the RSNA baroreflex by 53% but did not change the reflex range. By contrast, injection of kynurenate into the IVLM increased resting arterial pressure and RSNA by 27 mmHg and 88%, respectively, but did not alter the RSNA baroreflex gain or range. Pentobarbital sodium anesthesia attenuated the gain and range of the RSNA baroreflex by 78 and 40%, respectively. Under these conditions, microinjection of kynurenate into the RVLM did not cause any further change in the gain of this reflex. These results suggest that endogenous EAA neurotransmitters in the RVLM are important in modulating the sympathetic baroreflex in conscious rabbits. Anesthesia can mask the functional significance of EAAs in the RVLM in modulating the baroreflexes, which may explain why previous studies in anesthetized animals found no effect of blocking EAA receptors in the RVLM on sympathetic baroreflexes. excitatory amino acids; kynurenate; arterial pressure; anesthesia; heart rate THE PRESSOR REGION of the rostral ventrolateral medulla (RVLM) is critical in the generation and maintenance of sympathetic activity and is also an essential part of the central baroreflex pathways (8,9,15). The GABAergic synapse is believed to be a principal relay in the RVLM in transmission of baroreceptor information, because blockade of GABA receptors in this area abolished the vasomotor component of the reflex (8,15). By contrast, the excitatory amino acids (EAAs) in the RVLM are thought to play a little role in mediating cardiovascular responses to baroreceptor stimulation. This assumption is supported by numerous findings that the blockade of ionotropic EAA receptors in the region with local administration of kynurenate did not affect sympathetic baroreflexes in rats (27, 40), rabbits (41), or cats (12). This contrasts with the essential role of EAAs in the RVLM in mediating many other cardiovascular reflexes. In particular, administration of kynurenate into the RVLM has been shown to attenuate the pressor and sympathoexcitatory reflex responses to hypothalamic stimulation (40), muscular contraction (4), noxious stimulation (34), and renal and vagal afferent stimulation (6, 41) in anesthetized animals. Furthermore, this also contrasts with the ability of glutamate, given into the RVLM, to enhance the sympathetic baroreflex, indicating that local glutamate-sensitive inputs may also play a role in modulating bar...

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“…There is some circumstantial evidence from studies in anaesthetized animals which lend further support to this idea. It has been observed that anaesthesia augments the renin response to ACE-inhibition (Bing & Poulsen, 1975), and anaesthesia is known to depress the function of some central synapses, distorting the autonomic nervous response to various cardiovascular stimuli, in favour of sympathetic outflow (Korner et al, 1968;Zimpfer et al, 1974;Dorward et al, 1985). It would therefore seem that the renal sympathetic innervation is conveniently placed to mediate the release of renin following ACE-inhibition.…”

Section: Discussionmentioning

confidence: 99%

The effects of combined angiotensin converting enzyme inhibition and β‐adrenoceptor blockade on plasma renin activity in anaesthetized dogs

Cambridge

Whiting

Butterfield

et al. 1992

British J Pharmacology

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1 The effects of P-adrenoceptor blockade on the changes in plasma renin activity (PRA) following angiotensin enzyme (ACE) inhibition were investigated in pentobarbitone-chloralose anaesthetized dogs. 2 ACE-inhibition, with enalapril (2 mg kg-'), caused a significant reduction in systemic arterial blood pressure (BP) with little or no effect on cardiac function, and a significant elevation of plasma renin activity (PRA). By contrast P-adrenoceptor blockade with atenolol (1 mg kg-'), caused a similar reduction in BP but in addition, significantly reduced cardiac function and PRA. 3 A combination of enalapril with atenolol, caused a significant reduction in BP, cardiac function and PRA, hence there was no elevation of PRA, as was seen following ACE-inhibition with enalapril alone. 4 The observations with P-adrenoceptor blockade alone, show that there is an important homeostatic role for the renal sympathetic innervation, mediated by P-adrenoceptors, in controlling basal renin levels. Furthermore, the renal sympathetic innervation appears to be an important contributor to the renin release caused by an ACE-inhibitor as the additional presence of a P-adrenoceptor blocking agent will prevent this release.5 BW B385C (2 mg kg-'), which combines both ACE-inhibition and P-adrenoceptor blocking properties, also produced reductions in BP and cardiac function similar to those seen with the enalapril/ atenolol combination. In addition, for an equivalent degree of ACE-inhibition by BW 385C, to that seen with enalapril alone, the elevation of PRA was attenuated.6 A combination of ACE-inhibition and P-adrenoceptor blocking activity in a single entity, such as BW B385C, therefore also produces a reduced renin release when compared with an ACE-inhibitor, such as enalapril. This provides further confirmation of the importance of the renal sympathetic innervation in the renin response to ACE-inhibition, and supports the concept of combining ACEinhibition with P-adrenoceptor blockade.

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The renal sympathetic baroreflex in the rabbit. Arterial and cardiac baroreceptor influences, resetting, and effect of anesthesia.

Cited by 181 publications

References 57 publications

Rapid resetting of rabbit aortic baroreceptors and reflex heart rate responses by directional changes in blood pressure.

Rapid resetting of rabbit aortic baroreceptors and reflex heart rate responses by directional changes in blood pressure.

Glutamate receptors in RVLM modulate sympathetic baroreflex in conscious rabbits

The effects of combined angiotensin converting enzyme inhibition and β‐adrenoceptor blockade on plasma renin activity in anaesthetized dogs

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