Impaired Baroreflex Control Research Articles

Treatment with enalapril fails to prevent impaired cardiopulmonary baroreflex control in dogs with left ventricular dysfunction

That the cardiopulmonary baroreflex control of sympathetic nerve activity is impaired in dogs with left ventricular (LV) dysfunction has been shown previously. This study tested the hypothesis that treatment with the angiotensin-converting enzyme inhibitor enalapril prevents or delays the development of abnormalities of cardiopulmonary baroreflexes in dogs with LV dysfunction. Serial changes in LV volumes and neurohumoral profiles (plasma norepinephrine and renin activity) were assessed in conscious dogs with progressive LV dysfunction due to rapid ventricular pacing. Enalapril 5 mg orally twice daily was administered from days 4 to 12 of pacing. Cardiopulmonary baroreflexes were assessed in enalapriltreated paced dogs (n = 8) and untreated paced dogs (n = 8) by recording changes in renal nerve activity and pulmonary capillary wedge pressure during volume infusion in anesthetized sinoaortic denervated dogs on day 12 of rapid pacing. There was no difference in LV volume in the two groups. Neurohumoral factors were similar in both groups except for the expected high plasma renin activity in enalapril-treated dogs. Hemodynamic parameters also were comparable in the two groups. Cardiopulmonary baroreflex sensitivity for enalapriltreated dogs was not different from that of untreated paced dogs, and baroreflex gain in both groups was significantly lower than for the nonpaced control dogs ( P < .05). Despite adequate converting enzyme blockade, treatment with enalapril failed to prevent the development of attenuated cardiopulmonary baroreflex control of sympathetic nerve activity in dogs with developing LV dysfunction.

Dietary Na+ and cardiopulmonary baroreflex control of renal sympathetic nerve activity in SHR

In young Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with or without chronic sinoaortic denervation (SAD), we evaluated the effects of low, regular, and high dietary sodium intake (L-Na, R-Na, and H-Na, respectively) from 4 to 8 wk of age on cardiopulmonary baroreflex function, which was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) in response to acute volume expansion. In intact SHR H-Na increased blood pressure (BP), whereas L-Na decreased BP. No changes were observed in intact WKY. The gain of the cardiopulmonary baroreflex control of both HR and RSNA was significantly attenuated in SHR vs. WKY on R-Na. In both SHR and WKY, L-Na had no effects on the gain of RSNA and HR responses. In both strains, H-Na did not affect the gain of HR but attenuated the gain of the RSNA response. H-Na attenuated the gain of RSNA response more in SHR with SAD vs. intact SHR (52 vs. 69% of corresponding R-Na control) but less in WKY with SAD vs. intact WKY (80 vs. 71% of corresponding R-Na control). These data indicate that in SHR, H-Na further desensitizes the already impaired cardiopulmonary baroreflex control of RSNA. After SAD, this attenuation is more prominent in SHR but becomes less prominent in WKY. High sodium intake, therefore, modulates the interaction between the arterial and cardiopulmonary baroreflexes in the control of RSNA oppositely in WKY vs. SHR.

Cardiorespiratory reflex control in rats with left ventricular dysfunction.

Patients with heart failure exhibit a neurohumoral excitatory state and abnormal baroreflex control of the cardiovascular system. We determined whether arterial baroreflexes are impaired during left ventricular dysfunction (LVD) caused by chronic myocardial infarction in the absence of congestive heart failure and whether abnormal central mechanisms contribute to this impairment. Baroreceptors were stimulated in anesthetized rats with and without LVD by increasing arterial pressure with phenylephrine. Lumbar sympathetic nerve and phrenic nerve activity as well as heart rate were recorded. Rats were divided into different groups based on infarct size. Rats with moderate LVD showed impaired baroreflex control of sympathetic, ventilatory, and heart rate responses. Baroreflex gains were inversely related to the size of the infarct. The central gain for sympathetic nerve activity, obtained by using electrical stimulation of the aortic depressor nerve, also was impaired. Baroreflex control of the cardiorespiratory system is thus impaired in rats with moderate LVD in the absence of congestive heart failure. The attenuated baroreflexes are likely due to abnormal afferent mechanisms, although central mechanisms contribute to the impaired barosympathetic reflex.

Effect of exercise training on RSNA, baroreflex control, and blood pressure responsiveness

The effect of exercise training (ET) on renal sympathetic nerve activity (RSNA), baroreflex control of RSNA and heart rate (HR), and arterial pressure (AP) responsiveness to phenylephrine and angiotensin II (ANG II) was studied in six trained (T) and six sedentary (S) male Wistar rats. ET was performed on a motor treadmill for 13 wk. The RSNA signals of unanesthetized rats were processed by an analog-to-digital converter to quantify the nerve discharges associated with changes in AP and HR. The reflex control of RSNA and HR were evaluated during progressive injections of phenylephrine and sodium nitroprusside. Mean arterial pressure (MAP) was similar in both groups. RSNA was significantly lower in T rats (28 +/- 2 vs. 36 +/- 3%). T rats had an impairment of baroreflex control of RSNA in response to nitroprusside (4.9 +/- 0.89 vs. 12.3 +/- 1.2 bars.cycle-1.mmHg-1). ET decreased AP responsiveness for phenylephrine and ANG II. Therefore ET produces 1) no change in resting MAP but a significant decrease in RSNA and AP responsiveness and 2) partial impairment of baroreflexes, i.e., bradycardic responses and RSNA during MAP decrease.

Effects of orthostatic stress on peripheral capillary filtration in mild congestive heart failure after healing of myocardial infarction

Patients with heart failure have impaired baroreflex control of the peripheral circulation with attenuated vasoconstrictor response during orthostatic stress. The aim of this study was to test if this impaired barorefiex control not only affects the arterial, but also the capillary bed. Blood flow and capillary filtration were measured in the forearm (plethysmography) in 7 normal subjects and 7 patients with mild congestive heart failure (New York Heart Association functional class II). Measurements were done with the subjects supine and during headkup tilt at 45°. While supine, forearm vascular resistance and capillary filtration coefficient did not differ significantly between the groups. In the control subjects, tilt decreased capillary filtration coefficient by 14 ± 3% (p <0.02), and Increased forearm vascular resistance by 88 ± 37% (p <0.02); in contrast, patients with heart failure had an increase in capillary filtration coefficient of 26 ± 5% (p <0.02) and only increased the forearm vascular resistance by 10 ± 1%, (p = NS, p = 0.26). Our data provide evidence that patients with mild heart failure, in contrast to normal subjects, Increase the peripheral capillary filtration during orthostatic stress. The data indicate that impaired barorefiex mechanisms might influence the capillary filtration and it is suggested that impaired barorefiex control of the peripheral circulation can contribute to formation of edema in patients with heart failure.

Effects of heart failure on baroreflex control of sympathetic neural activity

Baroreflex control of heart rate, vascular resistance and norepinephrine is impaired in patients with heart failure, but recent animal studies demonstrate preserved baroreflex control of sympathetic nerve activity in this disorder. Studies were therefore performed to compare baroreflex control of efferent sympathetic nerve activity to muscle in 10 normal subjects (age mean ± SEM 21 ± 1 years) and in 11 patients with moderate to severe heart failure (age 48 ± 5 years, New York Heart Association class II to IV, left ventricular ejection fraction 19 ± 2%, pulmonary capillary wedge pressure 27 ± 2 mm Hg, cardiac index 2.04 ± 0.22 liters/min/m 2). Baroreflex activation was produced by intravenous infusion of phenylephrine (0.5 to 2.0 μg/kg/min) and deactivation by infusion of nitroprusside (0.4 to 2.5 μg/kg/min). During phenylephrine infusion, comparable increases in mean arterial pressure were produced in normal subjects (89 ± 2 to 99 ± 3 mm Hg, p < 0.01) and in patients with heart failure (90 ± 2 to 99 ± 3 mm Hg, p < 0.01). The patients with heart failure exhibited significantly attenuated (p < 0.01 for normal vs heart failure) decreases in heart rate (93 ± 5 to 90 ± 6 beats/mm, p = not significant [NS]) compared with normal subjects (67 ± 3 to 58 ± 4 beats/min, p < 0.01) and tended to demonstrate attenuated sympathoinhibitory responses to this pressor stimulus. More strikingly, patients with heart failure demonstrated significant impairment of baroreflex responses during nitroprusside-induced baroreceptor deactivation. In normal subjects, nitroprusside produced a decrease in mean arterial (90 ± 2 to 80 ± 3 mm Hg, p < 0.001) and right atrial (4 ± 1 to 2 ± 1 mm Hg, p < 0.01) pressures with a resultant reflex increase in heart rate (68 ± 3 to 81 ± 4 beats/min, p < 0.001) and muscle sympathetic nerve activity (326 ± 74 to 746 ± 147 U/min, p < 0.01). In patients with heart failure (n = 10), nitroprusside produced comparable (p = NS for normal vs heart failure) decreases in mean arterial (89 ± 2 to 77 ± 2 mm Hg, p < 0.001) and right atrial (6 ± 1 to 1 ± 1 mm Hg, p < 0.001) pressures, but did not significantly alter heart rate (91 ± 6 to 97 ± 4 beats/ min, p = NS) or sympathetic nerve activity (936 ± 155 to 1179 ± 275 U/min, p = NS). When expressed as percent change in sympathetic nerve activity (U/min) per absolute change in moan arterial pressure (mm Hg) during nitroprusside infusion, the baroreflex sensitivity of the normal subjects (+ 14.7 ± 2.1% U/mm Hg) was significantly greater than that of patients with heart failure (+ 1.3 ± 1.7% U/mm Hg, p < 0.001). Similarly, when expressed as percent change in sympathetic neural activity (U/min) per absolute decrease in right atrial pressure during nitroprusside infusion, patients with heart failure exhibited a significantly diminished sensitivity (+ 9.7 ± 4.5%/mm Hg) than did the normal subjects (+ 59.8 ± 20.5%/mm Hg, p < 0.05). Thus, patients with moderate to severe heart failure demonstrate impaired baroreflex control of muscle sympathetic nerve activity and heart rate, which is most pronounced during conditions of baroreceptor deactivation.

Impaired baroreflex control of arterial pressure in WHHL rabbits.

The present study was designed to investigate baroreflex control capacity of arterial pressure (AP) in the conscious Watanabe heritable hyperlipidemic (WHHL) rabbit. The control capacity of the baroreflex system was assessed with overall open-loop gain (G). Seven WHHL and 14 normal Japanese white rabbits were chronically implanted two catheters in the aortic arch through the left subclavian and common carotid arteries. A small amount of blood (2 ml/kg, body weight) was rapidly extracted into a syringe via the left common carotid artery in the conscious state. Mean arterial pressure (MAP) was monitored with a catheter-transducer system through the left subclavian artery. The MAP responses to the rapid hemorrhage were averaged 8 times by a computer. G was calculated as G = delta API/delta APS-1, where delta API was an immediate MAP fall after the hemorrhage and delta APS was a steady-state error 1-2 min after the hemorrhage. The values of G in the conscious normal and WHHL rabbits were 7.35 +/- 0.24 and 1.91 +/- 0.29 (mean +/- SE, p < 0.01), respectively. To investigate effects of pentobarbital anesthesia on baroreflex system, the hemorrhage experiment was repeated several times under pentobarbital anesthesia (20 mg/kg, i.v.). The values of G in the anesthetized normal and WHHL rabbits were 6.69 +/- 0.23 and 1.68 +/- 0.34 (mean +/- SE, p < 0.01), respectively. G in the normal and WHHL rabbits did not show any significant change in the presence and absence of pentobarbital anesthesia (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between baroreflex sensitivity, renin suppression and natriuresis in salt-sensitive rabbits.

This study determined the influence of baroreflex sensitivity (BRS) on the rate of urinary sodium excretion and plasma renin activity (PRA) in response to a saline infusion in conscious male rabbits specifically bred for high (Group I; n = 7) and low (Group II; n = 10) BRS and in seven control animals. Only Group II showed significant increases in blood pressure on a chronic high-salt intake. After ensuring that each animal was in sodium balance, a (0.7-0.9%) saline infusion of 3-4 ml/kg per h for 90 min (25% daily sodium intake for each rabbit) was given and urine collected at 15-min intervals via a bladder catheter. No differences were found in control urine volumes, urinary sodium or PRA. Group I excreted over 50% of the sodium load and Group II less than 20% within 90 min. PRA fell by more than 30% within 30 min in six Group I rabbits but decreased by less than 30% or increased in Group II. In the control animals, sodium excretion rates and PRA suppression were also much greater in those with high BRS. A highly significant correlation (r = 0.808, P less than 0.01) was found between the per cent of the sodium load excreted and BRS. It is suggested that the delayed sodium excretion and blood pressure elevation in salt-sensitive subjects may be due to a genetic impairment in baroreflex control of renal sympathetic nerve activity.

Abnormal baroreflex control of heart rate in decompensated congestive heart failure and reversal after compensation

Congestive heart failure (CHF) causes impairment of baroreflex control of heart rate (HR). To determine if this derangement is reversible, the cardiac chronotropic control was assessed in 10 patients with class IV chronic CHF of various etiologies before and after compensation achieved by bed rest, salt restriction, diuretics and vasodilators. Mean time between the 2 studies was 15 ± 3 days. The management was modified 3 days before the second autonomic evaluation, so as to reestablish the same diet and pharmacologic conditions of the previous study. Compensation led to significant reduction in symptom-based class, body weight, and pulmonary and systemic congestion. Mean ± standard error of the mean HR responses (beats/min) before and after compensation were, respectively: (1) to atropine (0.04 mg/kg): 10 ± 2 and 27 ± 2 (p < 0.01); (2) to handgrip (30% maximum capacity, 1 minute): 9 ± 2 and 19 ± 3 (p < 0.005); (3) to headup tilt (5 minutes): 4 ± 3 and 20 ± 4 (p < 0.005). Mean ± standard error of the mean baroreflex sensitivity (ms/mm Hg) of RR responses to phenylephrine and amyl nitrate-induced changes in systolic pressure was, respectively, in each condition: phenylephrine, 0.9 ± 0.2 and 8 ± 2.3 (p < 0.05); amyl nitrate, 0.3 ± 0.2 and 4.1 ± 1.1 (p < 0.05). A significant correlation between improvement in HR responses to atropine and tilt and changes in body weight was obtained. These findings show a reversible component of impaired baroreflex control of HR in severe CHF, possibly due to its congestive effects.

Parasympathetic impairment of baroreflex control of heart rate in Dahl S rats

To test the hypothesis that impaired baroreflex control of heart rate in Dahl salt-sensitive (S) rats is due to an impairment of the parasympathetic limb of the bradycardic response, baroreflex sensitivity was evaluated in conscious, chronically instrumented Dahl S and salt-resistant (R) animals. Sensitivity was impaired in Dahl S rats when bolus doses of phenylephrine were administered (0.863 +/- 0.042 vs. 1.43 +/- 0.055 ms/mmHg), but it was not different than in R rats when tested with sodium nitroprusside. When the sensitivities before and after blocking the parasympathetic nervous system with atropine were compared, it was revealed that 82% of the reflex bradycardia resulting from bolus doses of phenylephrine was due to the parasympathetic nervous system, whereas the majority (73%) of the bradycardia induced by 5-min infusions of phenylephrine was due to withdrawal of sympathetic tone. Neither baroreflex sensitivity to infusions of phenylephrine (73% sympathetic) or to infusions after atropine (100% sympathetic) were significantly different between S and R rats. Therefore, the impairment of the heart rate reflex in Dahl S rats is due to an impairment of the parasympathetic limb of the response. In addition, a high-salt diet before the development of hypertension did not alter baroreflex sensitivity in either Dahl S or R rats.

Effects of oxygen inhalation on tissue oxygenation in patients with cirrhosis: Evidence for an impaired arterial baroreflex control

In patients with cirrhosis, O 2 uptake, i.e., O 2 consumption, is abnormally decreased. We administered 50% O 2 for 30 min in eight patients with alcoholic cirrhosis to determine whether the subsequent increase in arterial O 2 content may correct the low O 2 consumption. In addition, we studied in these patients the reflex control of cardiac output and blood pressure by arterial baroreceptors, as O 2 inhalation induces a systemic vasoconstriction. Arterial O 2 tension, oxyhaemoglobin saturation and arterial O 2 content significantly increased as well as systemic vascular resistance and arterial pressure. In contrast, O 2 consumption (which was below normal values) under basal conditions, O 2 transport, O 2 extraction ratio, heart rate, right atrial and pulmonary wedged pressures, cardiac output, hepatic venous pressures, hepatic and azygos blood flows were unaffected by O 2 administration. In three patients receiving air, no significant change was observed. Our results show that, in patients with cirrhosis, inhalation of 50% O 2 does not correct O 2 consumption. We may conclude that reflex control of cardiac output and arterial pressure by arterial baroreceptors is impaired in these patients.

Area postrema and cardiovascular regulation in rats.

The area postrema (AP) of the dog mediates pressor responses to angiotensin II and plays a role in the maintenance of normal arterial pressure. Ablation of the AP (APX) in the rat has been reported to have little or no effect on cardiovascular regulation. In the present study, computer data acquisition techniques were used to investigate this question. APX in the rat significantly lowered resting mean arterial pressure within 1 h (P less than 0.005) and lowered heart rate within 1 day (P less than 0.05) following the lesion. Increases in heart rate following atropine injections were significantly greater (P less than 0.05) in AP relative to sham lesion rats, suggesting higher vagal tone in the AP lesion rats. In addition, APX significantly enhanced the baroreflex control of heart rate in response to intravenous phenylephrine (P less than 0.05). Lability of pressure was not affected by the lesion. The hypotension and bradycardia produced by APX were still present 1 wk after APX. These AP lesions apparently did not produce significant damage to the function of the nearby NTS, since 1) histological analysis revealed minimal NTS damage, 2) arterial pressure lability was not increased, and 3) APX enhanced rather than impaired baroreflex control of heart rate. We conclude that the AP may have a role in the maintenance of resting arterial pressure and heart rate in the rat.

Impaired cardiopulmonary baroreflex control of renal nerves in renal hypertension.

We recently reported that arterial baroreflex control of renal nerve traffic is impaired in renal hypertensive rabbits. The purpose of this study was to determine if vagal cardiopulmonary baroreflex control of renal nerve traffic is also impaired. Experiments were performed in 10 hypertensive (mean arterial pressure +/- SE in conscious state, 110 +/- 3 mm Hg) and 10 normotensive (79 +/- 1 mm Hg) chloralose-anesthetized rabbits. Responses to graded blood volume expansion (+5, +10, +15 ml/kg) with dextran in saline were recorded with all baroreflexes intact, after sinoaortic baroreceptor denervation, and after vagotomy. With arterial and cardiopulmonary baroreflexes intact, volume expansion resulted in decreases in renal nerve traffic of -12 +/- 2%/mm Hg increase in left atrial pressure in normotensive rabbits, but of only -5 +/- 2%/mm Hg in the hypertensive rabbits (P less than 0.05). This difference is particularly striking in view of the larger maximum increases in arterial (25 +/- 7 vs. 12 +/- 3 mm Hg) and left atrial pressure (9 +/- 1 vs. 6 +/- 1 mm Hg) during volume expansion in hypertensive vs. normotensive rabbits. After sinoaortic baroreceptor denervation, the responses of normotensive rabbits were preserved (-11 +/- 3%/mm Hg), while those of hypertensive rabbits were impaired further (-2 +/- 1%/mm Hg). Vagotomy abolished responses of renal nerves to volume expansion in both groups. These data demonstrate striking impairment of vagal cardiopulmonary baroreflex control of renal nerve traffic in renal hypertension. Even though arterial baroreflexes have been shown to be abnormal in renal hypertension, they still may partially compensate for markedly impaired cardiopulmonary baroreflex control of the renal nerves.

Impaired baroreflex sensitivity in the aetiology of salt hypertension in the rabbit.

This study was designed to see whether normotensive rabbits with an impairment in baroreflex control of heart rate due to genetic factors are more susceptible to high salt or deoxycorticosterone acetate (DOCA)-salt hypertension. The baroreflex sensitivity of 27 conscious rabbits was assessed by both the 'steady-state' and 'ramp' methods in response to injections of phenylephrine (2.5-30 micrograms/kg). Animals with differing baroreflex sensitivities were then given 4 weeks treatment with 8% NaCl and 1.3% KCl in food (treatment A), or DOCA (25 mg pellet, subcutaneously) with 0.5% NaCl and 0.13% KCl in drinking water (treatment B). A third group were maintained on a regular diet of food and water (controls). A highly significant negative correlation (r = 0.91, P less than 0.01) was found between the increase in mean arterial pressure (MAP) produced either by treatment A or treatment B and the baroreflex sensitivity before treatment. There was no significant correlation between the increase in MAP and initial MAP; increase in body weight; serum K+ after treatment; baroreflex sensitivity before treatment, when assessed by the 'ramp' method. It is concluded that animals with low baroreflex sensitivity due to a reduced ability to suppress cardiac sympathetic activity in response to a pressor stimulus, are more likely to develop hypertension as a result of salt loading. It remains to be determined whether the susceptibility to salt of rabbits with lower baroreflex sensitivity is also associated with a difference in the renal excretion of Na+ ions.

Impaired baroreflex control of vascular resistance and heart rate in acute myocardial infarction.

The baroreflex control of vascular resistance and heart rate was studied in 11 patients to determine whether it is impaired in patients with acute myocardial infarction. Reflex forearm vasoconstriction in response to lower body negative pressure at 40 mm Hg was less in the early convalescent phase (mean seven days) than in the late convalescent phase (mean 41 days). Pressor as well as vasoconstricting responses to the cold pressor test did not differ between the early and late convalescent phases. The slope of the regression line relating systolic blood pressure and the RR interval during a transient rise in blood pressure produced by intravenous phenylephrine was appreciably reduced in the early convalescent phase of myocardial infarction. These results suggest that baroreflex control of vascular resistance and heart rate is impaired in patients with acute myocardial infarction.

Occlusive summation of carotid and aortic baroreflexes in control of renal nerve activity.

We recently reported that denervation of aortic or carotid baroreceptors impaired baroreflex control of heart rate but not of hindlimb vascular resistance or lumbar sympathetic nerve activity. Since baroreflex control of sympathetic outflow to different vascular beds is nonuniform, we determined whether carotid or aortic baroreceptor denervation would impair baroreflex control of renal nerve activity. Experiments were performed in 23 alpha-chloralose-anesthetized rabbits. Phenylephrine and nitroglycerin were infused to raise or lower arterial pressure. Pressure elevation inhibited and pressure reduction increased renal nerve activity. The linear regression relationships between changes in arterial pressure and percent change in renal nerve activity were determined with baroreflexes intact and after aortic or carotid denervation. Neither carotid nor aortic denervation alone impaired baroreflex control of renal nerve activity. In nine experiments responses were determined first with vagi sectioned. The results were comparable to those obtained without prior vagotomy. Our data indicate that one group of baroreceptors (aortic or carotid) exerts full control of renal nerve activity and that aortic and carotid baroreflex influences on renal nerve activity add by occlusive or mutual inhibitory summation.

Impaired central mediation of the arterial baroreflex in chronic renal hypertension.

After 6 wk of renal hypertension in rabbits, the arterial baroreflex control of heart rate (HR) is impaired but the baroreflex control of lumbar sympathetic nerve activity ( LSNA ) is preserved. This selective impairment may reflect a predominant abnormality in the baroreceptors. In this study, we tested the hypothesis that renal hypertension of longer duration may impair baroreflex control of LSNA through a defect in the central nervous system mediation of the reflex. Four months after induction of renal hypertension, baroreflex responses were determined during increases in arterial pressure with intravenous phenylephrine or decreases in pressure with vena caval occlusion under chloralose-urethan anesthesia. Reflex control of LSNA and HR was impaired markedly in hypertensive rabbits. Reflex inhibition of LSNA and HR in response to afferent electrical stimulation of the left aortic depressor nerve (all arterial baroreceptor afferents cut) was attenuated in hypertensive in contrast to normotensive rabbits. This attenuation was noted when the medullated fibers only were stimulated or when both medullated and nonmedullated fibers were stimulated. We conclude that baroreflex control of LSNA that is preserved after 6 wk of hypertension is impaired after 4 mo of hypertension. The impairment reflects an abnormality in the central nervous system mediation of the reflex.

Mechanism of impaired baroreflex control in prehypertensive Dahl salt-sensitive rats.

Dahl salt-sensitive rats fed a low salt diet demonstrate functional impairment in baroreflex control of cardiovascular function prior to the development of hypertension. The purpose of this study was to identify the mechanism(s) responsible for impaired baroreflex control in prehypertensive Dahl salt-sensitive rats. To examine the central and efferent portions of the baroreflex arc, we electrically stimulated the aortic depressor nerve of urethane anesthetized Dahl salt-sensitive and Dahl salt-resistant rats while recording arterial pressure, heart rate, and sympathetic nerve activity. Aortic nerve stimulation produced equivalent responses in both groups, indicating that central and efferent mechanisms could not account for functional baroreflex impairment. In separate groups of Dahl rats, multifiber afferent aortic baroreceptor discharge was recorded while arterial pressure was increased with phenylephrine. Prehypertensive Dahl salt-sensitive rats demonstrated significantly less baroreceptor activation than Dahl salt-resistant rats, indicating that impaired baroreceptor discharge is the mechanism responsible for baroreflex abnormalities. Aortic arch distensibility was not different between Dahl strains, suggesting that impaired baroreceptor discharge in Dahl salt-sensitive rats is probably not due to abnormalities in vessel wall distensibility. Since arterial pressure of both Dahl strains was in the normotensive range and did not differ significantly between Dahl salt-sensitive and salt-resistant rats, baroreceptor impairment appears to be a primary defect in Dahl salt-sensitive rats, rather than being secondary to hypertension. We speculate that this impairment in baroreceptor function in Dahl salt-sensitive rats prior to any elevation in arterial pressure may contribute to the Dahl salt-sensitive rat's genetic propensity to develop hypertension.

Impairment of baroreflex control of the sinoatrial node after cardiac operations with extracorporeal circulation in man

The sensitivity of the baroreceptor reflex to transient hypertension was determined in 13 patients before (control) and after (72 hours) open cardiac operations with extracorporeal circulation (ECC). In all patients early postoperative values were appreciably decreased (p less than 0.01) as compared to the preoperative values. This decrease suggested severe impairment of baroreflex control of the sinoatrial node. These changes were not correlated with concurrent alterations in heart rate or systemic arterial, left atrial, or right atrial pressures. In addition, respiratory sinus node arrhythmia was absent in all subjects. In four patients, subsequent studies 4, 8, 10, and 12 months, respectively, after the operation revealed good recovery of baroreflex sensitivity and respiratory influences on beat-to-beat variation. No similar effects were observed in two patients studied before and after cardiac operations without ECC. It is possible that direct trauma to the nervous supply of the sinoatrial node is a major factor in that reversible dysfunction; in fact, in three patients evidence was obtained that while sinoatrial node responses were impaired, the reflex control of the atrioventricular region remained unaltered. These findings point to further impairment of the fine control of heart rate imposed by the conditions of cardiac operations with ECC in patients with previously curtailed cardiac reserve.

Abnormal baroreflex control in renal hypertension is due to abnormal baroreceptors.

We determined if baroreflex control (BC) of lumbar sympathetic nerve activity (LSNA) is preserved despite impaired control of heart rate (HR) in rabbits with 6 wk of renal hypertension (HT). Baroreflex responses were determined during transient or steady-state increases (phenylephrine, PE) or decreases (nitroglycerin or caval occlusion) in arterial pressure. Impaired BC of HR was confirmed in conscious and anesthetized HT rabbits with all baroreflexes intact. In contrast, BC of LSNA was preserved in anesthetized HT rabbits. We further determined whether this selective impairment of BC of HR but not of LSNA could be due to an abnormality in the central nervous system (CNS) or in the afferent limb of the baroreflex. With only the left aortic depressor nerve (ADN) intact (other arterial baroreceptor afferents cut), BC of both HR and LSNA in HT was significantly impaired during infusion of PE. However, responses of HR and LSNA to afferent electrical stimulation of the left ADN (all arterial baroreceptor afferents cut) were similar in HT and normotensive controls. We conclude that 1) BC of LSNA is preserved in renal HT even though control of HR is impaired; 2) selective impairment of BC of HR in HT results from an abnormality in the afferent limb of baroreflex and not in CNS; 3) this abnormality in the afferent limb is not sufficient to impair BC of LSNA when all baroreflexes are intact but is sufficient after partial arterial baroreceptor denervation.