Role Of Arterial Baroreceptors Research Articles

Role of arterial baroreceptors on commissural NTS (cNTS) neurons involved in hemodynamic (Hd) control

Role of arterial baroreceptors on commissural NTS (cNTS) neurons involved in hemodynamic (Hd) control

Dynamic interactions between arterial pressure and sympathetic nerve activity: role of arterial baroreceptors.

The role of arterial baroreceptors in controlling arterial pressure (AP) variability through changes in sympathetic nerve activity was examined in conscious rats. AP and renal sympathetic nerve activity (RSNA) were measured continuously during 1-h periods in freely behaving rats that had been subjected to sinoaortic baroreceptor denervation (SAD) or a sham operation 2 wk before study (n = 10 in each group). Fast Fourier transform analysis revealed that chronic SAD did not alter high-frequency (0.75-5 Hz) respiratory-related oscillations of mean AP (MAP) and RSNA, decreased by approximately 50% spectral power of both variables in the midfrequency band (MF, 0.27-0.74 Hz) containing the so-called Mayer waves, and induced an eightfold increase in MAP power without altering RSNA power in the low-frequency band (0.005-0.27 Hz). In both groups of rats, coherence between RSNA and MAP was maximal in the MF band and was usually weak at lower frequencies. In SAD rats, the transfer function from RSNA to MAP showed the characteristics of a second-order low-pass filter containing a fixed time delay ( approximately 0.5 s). These results indicate that arterial baroreceptors are not involved in production of respiratory-related oscillations of RSNA but play a major role in the genesis of synchronous oscillations of MAP and RSNA at the frequency of Mayer waves. The weak coupling between slow fluctuations of RSNA and MAP in sham-operated and SAD rats points to the interference of noise sources unrelated to RSNA affecting MAP and of noise sources unrelated to MAP affecting RSNA.

Arterial baroreceptors control blood pressure and vasopressin responses to hemorrhage in conscious dogs

The goal of this study was to determine the role of arterial baroreceptors in the reflex control of arginine vasopressin (AVP), renin, and cortisol secretion in response to a 30-ml/kg hemorrhage in conscious dogs. The hormonal responses were measured in six dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD + CD. In the intact condition, mean arterial pressure (MAP) was maintained at control levels until blood loss reached 20 ml/kg and the absolute magnitude of the fall at 30 ml/kg was 35 +/- 10 mmHg. Similar responses were obtained during acute CD. In contrast, MAP fell earlier (at 5 ml/kg, P < 0.05) and to much lower levels in both the SAD and SAD + CD conditions. The individual slopes relating systolic pressure to plasma AVP, renin activity (PRA), and cortisol were used to compare the treatment effects using a 2 x 2 factorial analysis. There was a significant (P < 0.01) effect of SAD on the slope relating AVP to systolic pressure but no effect of CD and no SAD x CD interaction. In contrast, there was no effect of either SAD or CD on the relationship between PRA or plasma cortisol and systolic pressure. These results indicate that maintenance of blood pressure and the normal pattern of AVP secretion during hemorrhage depend on intact arterial baroreceptor reflexes.

The Role of Arterial Baroreceptors in the Undivided Circulation of Anuran Amphibians

Baroreceptors with afferent fibers in branches of the glossopharyngeal nerve or the vagus have been identified in all three arterial arches in anuran amphibians. Baroreceptors in the pulmocutaneous arch (PCA) appear to provide the principal feedback of arterial blood pressure to the cardiovascular centers of the medulla. An additional contribution arises from receptors within the aortic arch. The receptors are slowly adapting mechanoreceptors and, at least in the case of the PCA baroreceptors, transmit baroreceptive information via nonmyelinated afferents. Pressure thresholds coincide with the range of systolic arterial pressures associated with undisturbed toads. Therefore, increases in systolic pressure above resting result in both increases in firing frequency and the recruitment of previously inactive receptors. Denervation experiments demonstrate that feedback from PCA baroreceptors tonically inhibits the cardiovascular system even at rest. Experimental elevation of PCA pressure above resting values causes bradycardia and reduces systemic vascular resistance, resulting in a compensatory reduction in systemic arterialpressure. In addition, PCA resistance increases, which probably reflects a constriction of the extrinsic pulmonary artery. This response opposes the negative feedback regulation of arterial pressure but may protect the pulmonary microvasculature by increasing upstream resistance, thereby reducing intravascular pressures in pulmonary vessels. This is consistent with the view that the primary role of anuran PCA baroreceptors is to protect the delicate vasculature of the gas-exchange organ against high central driving pressures transmitted by the incompletely divided anuran circulation. Future studies should be directed toward an investigation of the central pathways involved in the PCA baroreflex.

Baroreflex control of arterial blood pressure during involuntary diving in ducks (Anas platyrhynchos var.).

The dynamic role of arterial baroreceptors in control of mean arterial blood pressure (MAP), heart rate (HR), cardiac output (CO), hindlimb vascular (HLVR) and total peripheral (TPR) resistance responses to forced dives was investigated in acutely and chronically barodenervated ducks. To activate the baroreflex, the proximal end of one aortic nerve was stimulated electrically with bipolar electrodes that had been implanted under pentobarbital sodium anesthesia. Predive nerve stimulation caused CO to fall (by reducing HR; stroke volume remained constant), producing a decrease in MAP to half the prestimulation level. During diving (for 2.5-min periods) nerve stimulation did not affect HR and MAP after the first minute of submersion. Neither HLVR nor TPR contributed to the fall in MAP during aortic nerve stimulation before or during diving. The effects of nerve stimulation on HR and MAP were maintained to the end of dives in animals given 100% O2 to breathe before diving. In separate experiments, increasing arterial chemoreceptor input by perfusing one vascularly isolated carotid body with venous blood caused a reduction in the effects of aortic nerve stimulation on MAP. Arterial baroreceptors may thus act on HR to alter MAP early in the dive, but as the dive progresses the baroreflex is attenuated by an increase in peripheral chemoreceptor drive.

Neurohumoral mechanisms and the role of arterial baroreceptors in the reno-vascular response to haemorrhage in rabbits.

1. Conscious rabbits, with implanted renal artery Doppler flow probes were bled at a constant rate (4 ml min-1). We assessed the contribution of autonomic, hormonal and local factors to the renal vasoconstrictor response to 20% loss of blood volume (BV) and the role of the sinoaortic baroreceptors in the neurohumoral response. 2. With intact autonomic effectors, 20% BV loss was associated with a small fall in vascular conductance, which was completely unaffected by inhibition or blockade of the combined effects of the two major pressor hormones angiotensin II (AII) and arginine vasopressin (AVP). Combined blockade of the autonomic effects plus those of the two pressor hormones resulted in marked elevation of vascular conductance, considered to be due to the local effects of haemorrhage. This response provided the baseline for assessing the constrictor response in the intact animal which, during 20% BV loss, was entirely due to reflex activity through the sympatho-adrenal system. 3. In contrast to the early phase of haemorrhage (less than 20% BV removal) both hormones played a role in the maintenance of mean arterial pressure immediately after haemorrhage and in the maintenance of renal vascular tone. This suggested that the contribution by hormones occurs only after more pronounced blood loss and hypotension. 4. In the presence of autonomic blockade with mecamylamine plus methscopolamine (plus a constant infusion of noradrenaline to maintain resting blood pressure) the renal vasoconstrictor response was similar to that of the intact animal. We have previously found that this regime is associated with greatly enhanced release of AVP and plasma renin activity. Sinoaortic denervation had no effect on this hormonally mediated vasoconstriction. 5. When the autonomic nervous system was intact but the effects of AII and AVP were blocked to prevent the accentuated hormonally mediated vasoconstriction, sinoaortic denervation completely abolished the normal autonomic renal constrictor response, which is thus largely under control of the arterial baroreceptors.

Cardiopulmonary receptors and coronary circulation

Coronary blood flow has long been regarded as being regulated primarily by the metabolic demand of the myocardium [1,2]. Experimental and clinical reports [3-9], however, indicate that such coronary regulation can be overridden by the adrenergic drive to the heart. In particular, previous studies in dogs [7,10] demonstrated that carotid sinus hypotension results in a reflex sympathetic a-receptor coronary vasoconstriction, independent of changes in myocardial oxygen metabolism or aortic pressure. Other investigators [4] observed in dogs that stimulation of the carotid sinus nerve can produce a profound coronary vasodilatation mediated by reflex suppression of tonic a-vasoconstrictor tone. Finally, we described in humans a reflex increase of coronary vascular resistance induced by reduction in carotid transmural pressure [11]. While a modulatory role of arterial baroreceptors has been demonstrated, the possible influence exerted by cardiopulmonary receptors on the coronary vascular tone is still debated. It is well known that these receptors affect peripheral vascular tone [12,13]; in addition, Thames [14] has shown reflex withdrawal of renal sympathetic dis-

Aortic baroreceptor deafferentation diminishes saline-induced drinking in rats

The effect of bilateral surgical deafferentation of the baroreceptors in the aortic arch and carotid sinus on experimentally induced water intake was investigated in rats. Drinking was induced by subcutaneous administration of one of the following agents: hypertonic saline, polyethylene glycol, isoproterenol and angiotensin II, or by 18 h of water deprivation. Hypertonic saline-induced drinking was significantly attenuated after bilateral denervation of either the aortic arch plus the carotid sinus or the aortic arch alone. However, this diminished response disappeared when hypertonic saline was given in subsequent tests. The initial drinking deficit following hypertonic saline was independent of the time elapsed since the animals had undergone surgery. All other thirst challenges tested resulted in water intake that was not statistically different from sham-operated control groups. It is concluded that aortic baroreceptor deafferentation initially results in a diminished drinking response following hypertonic saline, possibly due to interruption of afferent information originating in osmosensitive areas in the aortic arch. A role of arterial baroreceptors in the regulation of non-osmotically induced water intake is not supported by the present data.

Nutrient control of cardiac rate in infant rats: role of arterial baroreceptors

A surgical procedure is described for the deafferentation of carotid sinus (CS) and aortic depressor (AD) baroreceptors in 2-wk suckling rats. Baroreflex testing in unanesthetized pups showed that cardiac rate responses to acute elevations of blood pressure were reduced to less than 9% of controls after combined denervation (CSAD), 28% after AD and 47% after CS denervation at 4 h. After 24 h of nutrient deprivation, resting cardiac rates of sham operated controls fell a mean of -148 beat/min, significantly more than CS, AD, or CSAD groups (P less than 0.01). Baroreflex test responses in individuals correlated significantly with their later responses to nutrient deprivation (r = 0.67, P less than 0.01). There were no significant differences in base-line cardiac rate, systolic blood pressure, or cardiac rate during 24 h intragastric milk infusion between deafferented and control pups. These experiments suggest that arterial baroreceptors are important in the cardiovascular adjustments after nutrient deprivation in suckling rats.

Role of arterial baroreceptors in mediating cardiovascular response to exercise.

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.