Central Nervous System Control of Baroreceptor Reflexes in the Rabbit

Korner, Paul I.; Shaw, John H.; West, MJ; Oliver, James M.

doi:10.1161/01.res.31.5.637

Cited by 151 publications

(87 citation statements)

References 31 publications

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“…24 ' " • " It is well known that angiotensin can increase BP and heart rate by a central action involving the sympathetic nervous system 2 *-M~M and CEI could interfere with these actions of All. The observed parallel shift of the whole baroreflex function curve, which might be expected to involve both sympathetic and parasympathetic components in a similar manner, suggests that a more fundamental action of CEI exists on a controlling mechanism that equally affects both systems at some common point.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

Hatton¹,

Clough²,

Faulkner³

et al. 1981

Hypertension

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SUMMARYThe present experiments investigate whether the absence of tachycardia during lowering of blood pressure (BP) with an angiotensin-converting enzyme Inhibitor (CO) in salt-depleted dogs Is due to an alteration in the activity of the baroreflex. Baroreflex activity was measured after pharmacological manipulation of BP using intravenous nitroglycerine or phenylephrine, and the heart period (R-R interval) relative to the arterial pressure pulse was recorded. The slope of the relationship between BP and R-R interval is a measure of the sensitivity of the baroreceptor reflex and displacement of the line indicates a change in the setpoint of BP. On normal sodium diet, the sensitivity and setpoint of the baroreflex were unaltered by the nonapeptide CEI given both intravenously and into a lateral cerebral ventricle. During salt depletion, however, intravenously but not centrally administered CEI altered the setpoint of the baroreflex without modifying the sensitivity. (BP) is maintained by the autonomic nervous system and by angiotensin, and it has been shown in isolated preparations that the two systems interact.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

Hatton¹,

Clough²,

Faulkner³

et al. 1981

Hypertension

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“…Baroreceptor reflex sensitivity was assessed as the gain in baroreceptor reflex function according to the method of Korner et al 25 Graded increments in mean arterial pressure were produced by bolus injections of phenylephrine (0.5-8.0 ^ig/kg). Phenylephrine was dissolved in saline, and the injection volume was held constant at 0.05 ml/100 g body wt with a flush volume of approximately 0.1 ml.…”

Section: Measurement Of Baroreceptor Reflex Sensitivitymentioning

confidence: 99%

Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

Abdel‐Rahman

1989

Hypertension

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We studied the acute effect of ethanol on the hypotensive response to clonidine in conscious spontaneously hypertensive rats. When administered during the hypotensive response to clonidine, ethanol not only reversed the response but also caused a slight but significant short-lived pressor effect. The maximal hypotensive effect of graded doses of clonidine was significantly (p<0.05) attenuated by a dose of 1 g/kg ethanol, which resulted in a peak blood ethanol concentration of 54.2 ±6.3 mg/dl. The data strongly suggest the adverse effect of ethanol on the hypotensive response to clonidine is ethanol mediated and that their antagonistic interaction is both reversible and reproducible because: 1) an equal volume of saline had no effect on the hemodynamic responses to clonidine and 2) crossing over ethanol and saline treatments on days 2 and 3, which allowed longitudinal comparisons, showed that the effect of ethanol was similar both in naive rats (day 1) and in rats that were pre-exposed to ethanol (day 3). Whether this negative effect of ethanol also involves other antihypertensive agents that do not act primarily by a central nervous system mechanism was investigated. The same dose of ethanol had little or no effect on the hypotensive response to hydralazine, suggesting the negative effect of ethanol is selective to centrally acting antihypertensive agents. Although the mechanism by which ethanol reverses the hypotensive effect of clonidine is not known, it is possible that it involves an ethanol-evoked increase in plasma catecholamine levels, which are known to be decreased by clonidine. That ethanol did not reverse the hypotensive effect of hydralazine, which is also known to be associated with increased plasma catecholamine levels, supports this notion. The findings of the present study may explain, at least in part, why regular use of alcohol is associated with an inadequate control of blood pressure in treated hypertensive patients who are regular consumers of alcohol. (Hypertension 1989;14:531-541)

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“…With aortic balloon inflation, the average shift in the reflex curves was double that observed in the aortic baroreceptors. Balloon inflation alters the discharge of other pressure-sensitive receptors including those in the heart, which may explain this result (Korner et al 1972;Paintal, 1973;Thoren, 1979;Ludbrook, 1984).…”

Section: Hysteresis Shifts In Aortic Baroreceptor Unitsmentioning

confidence: 99%

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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Central Nervous System Control of Baroreceptor Reflexes in the Rabbit

Cited by 151 publications

References 31 publications

Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

Reversal by ethanol of the hypotensive effect of clonidine in conscious spontaneously hypertensive rats.

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

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