Cardiac afferents attenuate renal sympathetic baroreceptor reflexes during acute hypertension.

Abstract

We have studied the effect of acute hypertensive episodes on the renal sympathetic baroreceptor reflex in conscious rabbits and the role played by cardiac afferents and endogenous opiate mechanisms. Renal sympathetic nerve activity was recorded during brief perivascular ballooninduced ramp changes in mean arterial pressure before and during 40-minute elevations in resting pressure. Methoxamine infusion was adjusted to increase pressure by +30 and +45 mm Hg in the presence of autonomic blockade of the heart with atenolol and methscopolamine. Experiments were repeated in other rabbits after blocking cardiac afferents with 5% intrapericardial procaine or during intravenous naloxone (4-6 mg/kg, then 0.12 mg/kg/min). We found a progressively severe attenuation of the renal sympathetic baroreceptor reflex during increasing elevations in resting pressure. The upper plateau and range of the reflex curve were both reduced by one third and two thirds during moderate and severe hypertension, respectively. The average gain fell by 64% and 87%, and the range-independent gain and hypotensive reversal response were also reduced. There was no resetting of the reflex to higher pressures as would be expected. One third of the reflex inhibition was prevented by blocking cardiac afferents; none of it was affected by intravenous naloxone, which had previously been shown to reverse the renal baroreceptor reflex depression elicited by hemorrhagic hypotension. Factors possibly responsible for the remaining two thirds of the hypertension-induced sympathoinhibition are suggested to be either central depression of sympathetic tone after elevation of arterial baroreceptor discharge during the hypertensive episode or additional inhibitory afferent input arising from the pulmonary circulation. {Hypertension 1990;16:131-139) C hanges in resting blood pressure lasting longer than a few minutes cause shifts in the thresholds of arterial baroreceptors and baroreceptor reflex curves that occur in the same direction as the changes in pressure.1 " 6 This rapid resetting of baroreceptor reflexes can largely be explained by the resetting of the arterial baroreceptors themselves. However, during moderate falls and rises in resting pressure, resetting of the renal sympathetic and cardiac baroreceptor reflexes is greater than baroreceptor resetting, and during somewhat larger increases in resting pressure of approximately 20 mm Hg, resetting of the renal baroreceptor reflex is suppressed in the face of continued baroreceptor

Renal sympathetic activation from long-term low-dose angiotensin II infusion in rabbits

“…The surprising aspect is the very long-lasting nature of the baroreflex inhibition of RSNA, which was still evident after 3 months, but only if the increase in BP was marked (approximately >20 mmHg). Dorward et al [39] described inhibition of the upper plateau of the RSNA curve (closely similar to that observed in these animals) after 40 min of elevated pressure and provided evidence, using naloxone and intapericardial procaine, that this effect is mediated by activation of cardiopulmonary afferents. Barrett et al [40] provided evidence that the sympatho-inhibition persisting for 1 week during high-dose AngII infusion in conscious rabbits is mediated by the baroreflex.…”

Excitatory Inputs to the RVLM in the Context of the Baroreceptor Reflex

“…Arterial baroreceptors influence the control of a variety of processes relevant to the control of the circulation, including autonomic regulation of the heart and vasculature,1,2 renal function,3 water drinking,4 and the activity of vasopressin‐secreting cells 5. Of these, baroreceptor control of the heart and vasculature has received the most attention because of its prominence in the control of arterial blood pressure (AP).…”

Respiratory Alterations With Intrapericardial Procaine in the Conscious Rabbit

“…Selective blockade of cardiac nerves with intrapericardial administration of local anaesthetics has been used in anaesthetized animals for nearly 100 years (Heitler 1898). However, only recently have intrapericardial anaesthetics been used in conscious animals to produce cardiac nerve blockade (Dorward et al 1983;Bell et al 1990;Dorward et al 1990;Evans et al 1990Evans et al ,1991Shen et al 1990;O'Donnell et al 1991;Shen et al 1991). The advantage of using intrapericardial local anaesthetics is that they produce a short-lived (-30 min), localized, reversible 'denervation' of the heart (Samodelov et al 1982;Dorward Correspondence: Dr Leonard B.…”

“…In most cases, a 'loading dose' of procaine is used, followed by periodic supplements or continuous infusion. In rabbits, complete cardiac nerve blockade has been achieved using concentrations of either 2% (Dorward et al 1983;Trenchard et al 1984) or 5% procaine (w/v; Bell et al 1990;Dorward et a/. 1990;Evans et al 1990, 199 1) with loading doses of 20 mg and 20-40 mg, respectively.…”

“…Several studies have shown that intrapericardial procaine is effective in blocking cardiovascular reflexes mediated by cardiac afferents (Sleight 1964;Ledsome & Linden 1968;Arndt et al 1981;Dorward et al 1983;Dorward et al 1990;Evans et al 1990Evans et al , 1991 and efferents (Samodelov et al 1982;Dorward et al 1983;Dorward et al 1990;Evans et al 1990Evans et al , 1991. However, Ledsome and Linden (1968) anecdotally reported that respiration was also affected in one anaesthetized dog following intrapericardial infusion of 2% procaine.…”