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PubMed1998

[Adenosine facilitates carotid baroreflex in rats].

The effects of adenosine (Ado) on the carotid baroreflex were studied in 27 anesthetized rats with isolated carotid sinus perfusion. The results obtained were as follows: (1) By perfusing the isolated carotid sinus with adenosine (125 mumol/L), the functional curve of baroreflex was shifted to the left and downward, with the peak slope (PS) increased from 0.37 +/- 0.02 to 0.55 +/- 0.02 kPa/kPa (P < 0.001) and the reflex decrease in mean arterial pressure (RD) enhanced from 5.53 +/- 0.12 to 7.76 +/- 0.36 kPa (P < 0.001). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly decreased from 8.60 +/- 0.27 to 5.63 +/- 0.11 kPa (P < 0.001), 12.53 +/- 0.30 to 10.89 +/- 0.29 kPa (P < 0.01) and 23.69 +/- 0.15 to 20.18 +/- 0.55 kPa (P < 0.001), respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS and TP induced by Ado were dose-dependent. (2) By pretreatment with (8-cyclopentyl-1, 3-dipropylxanthine, 0.134 mmol/L), a selective adenosine A1-receptor antagonist, the above effects of Ado on carotid baroreflex were abolished. (3) The Ado-induced changes of baroreflex were also eliminated as the carotid sinus was pretreated with KATP channel blocker glibenclamide (10 mumol/L). The results strongly suggest that the carotid baroreflex could be facilitated by Ado. It is proposed that the facilitatory action of Ado on carotid baroreflex may be resulted from the opening of KATP channels mediated by Ado A1-receptors.

Adenosine↗
PubMed2001

Central and baroreflex control of heart rate during the wake-sleep cycle in rat.

UNLABELLED: Spontaneous fluctuations in Heart Period (HP) and Mean Arterial Pressure (MAP) make it possible to evaluate baroreceptor-heart rate reflex sensitivity (BRS). 30-s sequences of HP and MAP beat-to-beat values were considered in the different wake-sleep states (Wake, W; Quiet Sleep, QS; Active Sleep, AS) in rats to assess whether 1) BRS changes between states and 2) the different indexes supply consistent BRS measures. BRS indexes were calculated according to validated literature procedures as regression coefficients of HP vs. MAP 1) within all ramps of increasing or decreasing MAP of four beats or more, with HP and MAP changing in the same direction (baroreflex-mediated fluctuations, BRSp), 2) within all such ramps irrespective of the relative direction of HP and MAP changes (baroreflex + non-baroreflex, i.e. non-homeostatic centrally driven, fluctuations, BRSA). HP vs. MAP regression coefficient along the entire 30-s sequence (bHPMAP) was also calculated. RESULTS: BRSp did not change among states, BRSA decreased from QS to W to AS, bHPMAP decreased from QS to W and became negative in AS. CONCLUSIONS: 1) as indicated by BRSp, baroreflex sensitivity is state independent, 2) BRSp to BRS(A) to bHPMAP are increasingly affected by non-baroreflex fluctuations, BRSp being most apt to measure BRS, 3) non-homeostatic MAP and HP fluctuations increase from QS to W and prevail in AS. These potentially harmful fluctuations are normally buffered by baroreflexes: in the case of baroreflex impairment, circulatory risk may arise in conditions like AS, when they prevail.

Animals↗
PubMed2000

[Role of calcium in the mechanism underlying the inhibitory effect of streptomycin on carotid sinus baroreflex in rats].

The effect of streptomycin (SM) on carotid baroreflex was examined in 23 anesthetized rats with isolated carotid sinus perfusion. The results obtained are as follows. (1) In response to perfusion with SM (200 micromol/L), the functional curve of carotid baroreflex was shifted to the right and upward with a decrease of peak slope (PS) and a reflex decrease in mean arterial pressure (RD)(P<0.01), indicating an inhibitory effect of SM on carotid sinus baroreflex. (2) By perfusing the isolated carotid sinus with high Ca(2+) solution (4 mmol/L), the inhibitory effect of SM on carotid baroreflex was partially eliminated. The functional curve of SM was shifted to the left and downward with PS increasing from 0.27+/-0.04 kPa to 0.37+/-0.02 kPa (P<0.01) and RD was enhanced from 4.32+/-0.14 kPa to 6.18+/-0.17 kPa (P<0.01). On the other hand, the threshold pressure (TP) and saturation pressure (SP) were significantly decreased from 10.29+/-0.29 kPa to 9.98+/-0.33 kPa (P<0.05) and from 27.26+/-0.42 kPa to 25.22+/-0.38 kPa (P<0.05), respectively. (3) By pretreatment with Bay K 8644 (500 nmol/L), an agonist of calcium channels, the effect of SM on carotid baroreflex was completely abolished. (4) Exposure of the carotid sinus to SM following pretreatment with charybdotoxin (ChTX,100 nmol/L), a blocker of the Ca(2+)-activated K(+) channel (KCa), still inhibited the baroreflex. These results suggest that the inhibitory action of SM on carotid baroreflex may be mediated by suppressing Ca(2+) influx.

Animals↗
PubMed2003

Baroreflex control of heart rate during heating in subjects with low orthostatic tolerance.

BACKGROUND: Heat stress induces a reduction of orthostatic tolerance. The cardiovascular responses, including the cardiac baroreflex response to heat stress, were examined to test the hypothesis that subjects with orthostatically low tolerance demonstrate an impaired baroreflex control of heart rate (HR) during heat stress. METHODS: There were 44 healthy young volunteers who underwent whole body heat stress produced by a hot-water-perfused suit during supine rest for 45 min and 75 degrees head-up tilt (HUT) for 6 min. Esophageal temperature, HR, arterial pressure, and skin blood flow in the forearm and palm were measured continuously throughout the experiment. The sensitivity of the arterial baroreflex control of HR was calculated from the spontaneous changes in beat-to-beat arterial pressure and HR. RESULTS: The HUT was uneventful for 22 volunteers (higher tolerance group), but 22 volunteers (lower tolerance group) reached presyncope after 195 +/- 19 s. Esophageal temperature, HR, arterial pressure, and skin blood flow changed similarly in the two groups during heating. In the preheating condition, the sensitivity of the baroreflex control of HR did not differ significantly between the two groups. Heating did not alter the sensitivity of baroreflex control of HR in the higher tolerance group, but decreased it significantly in the lower tolerance group. Heating increased the number of heartbeats used for analysis of the baroreflex sensitivity in the higher tolerance group, but did not change it in the lower tolerance group. CONCLUSIONS: These results suggest that the impairment of vagal baroreflex control of HR during heat exposure aggravates the orthostatic intolerance in heat-stressed humans.

Adult↗
PubMedDate not supplied

Acute baroreflex resetting and its control of blood pressure in an open loop model.

Acute baroreflex resetting has been quantitatively studied in anesthetized dogs. Carotid sinuses were isolated bilaterally and carotid sinus conditioning pressure (CPcsp) was set at nine different levels for 20 min over a range of from 40 to 200 mm Hg. Over this range of 160 mm Hg in CPcsp, the magnitude of baroreflex resetting of set point pressure (Psp), threshold pressure (Pth) and BP50 was 32.0 +/- 5, 43.3 +/- 6 and 39.6 +/- 6 mm Hg, respectively. The extent of resetting was a non-linear function of the level of CPcsp. There is less resetting at high CPcsp. The average extent of resetting is only about 25%. In contrast to this small degree of resetting, a profound inverse relationship between the baseline pressure and the conditioning pressure was observed at the end of the conditioning period for each CPcsp. In addition, we also observed an attenuation in the buffering capacity of the baroreflex at very high or very low CPcsp. Vagotomy and aortic section did not alter baroreflex resetting. This data indicates that the baroreflex is capable of monitoring the absolute level of blood pressure during acute resetting in addition to buffering transient disturbances in arterial pressure. Based upon the results of the present experiments, the concept that acute baroreflex resetting results in an inability of the baroreflex to monitor the absolute level of arterial pressure does not appear to be valid.

Animals↗
PubMed1988

Brainstem mechanisms in the modulation of the sympathetic baroreflex by piperoxan.

Piperoxan (50-100 micrograms/kg) injected into the cisterna magna of anaesthetized dogs increased blood pressure, heart rate and resting rate of sympathetic nerve discharge. The baroreflex curve was shifted to the right with an elevation of the upper plateau (when blood pressure was lowered below resting values, renal sympathetic nerve activity rose to an upper plateau) and with no change in baroreflex sensitivity. Catecholamine depletion, produced by reserpine and alpha-methyl-p-tyrosine, did not change the effects of piperoxan on resting sympathetic nerve activity and on the baroreflex curve. Piperoxan (50 micrograms/kg i.c.) enhanced the rate of renal sympathetic nerve discharge in baroreceptor-denervated dogs. Piperoxan (5 micrograms) injected bilaterally into the nucleus tractus solitarii (NTS) increased blood pressure and resting sympathetic nerve activity with a shift of the sympathetic baroreflex curve to the right and no change in baroreflex sensitivity. Piperoxan (5 micrograms) injected bilaterally into the ventrolateral pressor area did not change blood pressure or the rate of sympathetic discharge. However, the baroreflex curve was shifted to the right with an elevation of the upper plateau level and the baroreflex sensitivity was increased. The present findings suggest that tonically active alpha 2-adrenergic mechanisms located within the NTS regulate resting and reflex sympathetic activity. An alpha 2-adrenergic mechanism in the rostral ventrolateral medulla modulates reflex sympathetic activity but has no influence on resting activity.

Animals↗
PubMed1985

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.

Animals↗
PubMed1986

Differences in age-independent effects of blood pressure on baroreflex sensitivity between normal and hypertensive subjects.

Inter-relationship between age, systolic blood pressure and baroreflex sensitivity index derived from the Valsalva manoeuvre was investigated in either combined or separated groups of normal and hypertensive subjects. Both in the total population as a whole and in each blood pressure subgroup, the baroreflex sensitivity index was significantly inversely related to age and to systolic blood pressure. Furthermore, age was significantly related to systolic blood pressure except in the hypertensive group. Partial correlation analysis showed that, in the total and hypertensive population, the baroreflex sensitivity index was significantly related to age and systolic blood pressure independently of each other variable. In the normal group, however, the baroreflex sensitivity index was not related to systolic blood pressure after adjusting for the effect of age, but remained significantly related to age independently of systolic blood pressure. The estimates of relative effects of the two variables on baroreflex sensitivity by multiple regression analysis were consistent with these results. Thus a prevailing concept of the inhibitory effect of blood pressure on baroreflex function may be accurate exclusively in hypertensive patients, and baroreflex function appears to be more sensitive to age-related changes in this system than to those related to blood pressure level, particularly in non-hypertensive normal subjects.

Adult↗
PubMedDate not supplied

Endogenous vasopressin modulates the baroreflex sensitivity in rats.

The effect of endogenous vasopressin on the baroreceptor reflex has been examined by comparing baroreflex function in Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI rat) with that in Long-Evans rats (LE rat). Baroreflex function was assessed in conscious unrestrained rats during increases in blood pressure with phenylephrine. The slope of the baroreflex function line in LE rats [(19.0, s.e.m. = 1.4) X 10(-4), n = 34] was significantly steeper than that in DI rats [(6.9, s.e.m. = 0.6) X 10(-4), n = 44, P less than 0.0001]. A subpressor infusion of arginine8-vasopressin (2 ng/kg per min for 2 h i.v.) and an equidose of DDAVP caused bradycardia and increased the baroreflex function slope significantly. Acute volume expansion in DI rat did not change the baroreflex sensitivity. A specific vasopressin vascular receptor antagonist, d(Ch2)5Tyr(Me)AVP, did not alter the baroreflex sensitivity in LE rats. These results suggest that endogenous vasopressin is an important physiological regulator of the baroreflex sensitivity in normal rats.

Animals↗
PubMed1984

Reduced effectiveness of the carotid baroreflex during arterial hypoxia in dogs.

The ability of the carotid baroreflex to produce cardiac slowing during arterial hypoxia was investigated in dogs anesthetized with morphine-chloralose. The heart rate response to baroreflex stimulation decreased by about 20% at an arterial O2 tension (PaO2) of 65-70 Torr and by over 60% at a PaO2 of 15-20 Torr. After the aortic nerves were cut bilaterally, baroreflex stimulation produced greater cardiac slowing (P less than 0.001) during arterial hypoxia (PaO2 20 Torr) than at the same PaO2 with intact aortic nerves. The systemic depressor response to baroreflex stimulation was reduced in a qualitatively similar manner but with greater variability. After atropine (0.2 mg/kg iv) or vagal transection the heart rate response to baroreflex stimulation during hypoxia was not suppressed from its control. Perfusion of the head with hypoxic blood in carotid-denervated animals also reduced the baroreflex bradycardia. The results suggest that the vagal component of the baroreflex bradycardia is suppressed during arterial hypoxia both by a reflex mediated by the aortic chemoreceptors and by a direct effect of hypoxia on the central nervous system.

Animals↗
PubMed1996

Baroreflex gain: characterization using autoregressive moving average analysis.

To study heart rate baroreflex gain, autoregressive moving average (ARMA) analysis, a multivariate method that allows evaluation of the dynamic ("beat-to-beat") interactions between changes in biological signals, was used to evaluate the relationships between R-R interval and arterial blood pressure (BP) during random-interval breathing. Parameters obtained by ARMA analysis of spontaneous fluctuations in BP and R-R interval in 17 volunteers were used to model the response of R-R interval to a transient 1-mmHg increase in BP; the resulting impulse-response and step-response curves were compared with baroreflex gain measured using bolus injections of phenylephrine (PE) and sodium nitroprusside (SNP). Impulse-response curves for the systolic BP-R-R relationship showed an early (0-1 s) sharp maximum of 5.5 +/- 4.2 ms/mmHg, which was smaller in magnitude but linearly correlated with baroreflex gain derived from SNP (14.5 +/- 9.7 ms/mmHg; r = 0.80, P < 0.002) and PE (31.6 +/- 26.7 ms/mmHg; r = 0.53, P < 0.05) injections. A similar relationship was also found between the one-beat ARMA step response and SNP injection (r = 0.70, P = 0.01). The integrated step response of the BP-R-R relationship over 6 s was 6.4 +/- 4.1 ms/mmHg, with no correlation to baroreflex gain determined by SNP (r = 0.33, P = 0.20) or PE (r = -0.15, P = 0.57). In conclusion, quantification of baroreflex gain consistent with other techniques may be achieved by ARMA analysis without perturbing mean BP. Correlation of baroreflex gain obtained by bolus injection to early measures of baroreflex gain obtained from the ARMA maximum impulse and early step responses, but not the late step response, suggests that the ARMA method may provide additional information regarding the frequency dependent effects of BP on R-R-interval.

Adolescent↗
PubMed1988

Baroreflex unimpaired by operant avoidance or classical aversive conditioning in dogs.

Previous studies showed that baroreflex control of heart rate is impaired during operant shock avoidance conditioning and classical aversive conditioning. However, the effects of such "emotionally stressful" paradigms on the ability of the baroreflex to control arterial pressure have not been directly assessed. We prepared the carotid sinus regions of dogs for reversible isolation from the systemic circulation, and we derived complete stimulus-response relations for the effects of carotid sinus pressure on both heart rate and arterial pressure. For any given carotid sinus pressure, arterial pressure and heart rate were higher during operant shock-avoidance conditioning and during classical aversive conditioning than in a neutral environment, which indicates an upward resetting of the baroreflex. However, threshold and saturation carotid sinus pressures were unaffected by operant conditioning or classical conditioning, which indicates that the baroreceptors themselves were not reset. The ranges over which the carotid baroreflex could vary arterial pressure and heart rate were significantly increased during both operant conditioning and classical conditioning. Baroreflex gain was unchanged during operant conditioning and was significantly increased during classical conditioning. We conclude that the baroreflex is not impaired during operant shock-avoidance conditioning or classical aversive conditioning in dogs. However, the baroreflex is reset and regulates blood pressure at an elevated level.

Animals↗
PubMed1990

Baroreflex control of sympathetic outflow in pregnant rats: effects of captopril.

Arterial baroreflex control of renal sympathetic nerve activity (RSNA) was compared in nonpregnant (NP) and near-term pregnant (P) chloralose-anesthetized rats. Baroreflex curves were obtained by recording reflex changes in RSNA (expressed as a percent of base line) due to increases and decreases in mean arterial pressure (MAP) [intravenous phenylephrine and nitroprusside (NTP)]. The slope, midpoint (EP50), and threshold pressures of the baroreflex curves were compared. Base-line MAP was significantly lower in the pregnant animals (P = 96 +/- 3 vs. NP = 113 +/- 5 mmHg). The baroreflex curves of pregnant animals also had significantly lower threshold (P = 95 +/- 3 vs. NP = 110 +/- 5 mmHg) and midpoint values (P = 105 +/- 4 vs. NP = 119 +/- 5 mmHg). The response to unloading the baroreceptors was attenuated in the pregnant animals as indicated by a decrease in slope of the NTP portion of the baroreflex curve (P = 0.95 +/- 0.17 vs. NP = 1.61 +/- 0.29% nerve activity/mmHg). Responses to blockade of angiotensin-converting enzyme with captopril (2 mg/kg iv) were also examined. There were no differences in EP50 or slope among the control, captopril, and recovery baroreflex curves within either the nonpregnant or pregnant animals. However, after captopril, MAP decreased to a greater extent in the pregnant rats, yet RSNA increased to the same level for the two groups. Thus pregnancy results in a leftward shift of the baroreflex function curve toward a lower operating pressure range. In addition, pregnant rats demonstrated an impaired ability to increase sympathetic outflow above base-line values in response to a hypotensive challenge.

Animals↗
PubMed1990

Baroreflex responses to acute changes in blood volume in humans.

To test the hypothesis that acute changes in plasma volume affect the stimulus-response relations of high- and low-pressure baroreflexes, eight men (27-44 yr old) underwent measurements for carotid-cardiac and cardiopulmonary baroreflex responses under the following three volemic conditions: hypovolemic, normovolemic, and hypervolemic. The stimulus-response relation of the carotid-cardiac response curve was generated using a neck cuff device, which delivered pressure changes between +40 and -65 mmHg in continuous steps of 15 mmHg. The stimulus-response relationships of the cardiopulmonary baroreflex were studied by measurements of forearm vascular resistance (FVR) and peripheral venous pressure (PVP) during low levels of lower body negative pressure (0 to -20 mmHg). Altered vascular volume had no effect on response relations of the carotid-cardiac baroreflex but did alter the gain of the cardiopulmonary baroreflex (-7.93 +/- 1.73, -4.36 +/- 1.38, and -2.56 +/- 1.59 peripheral resistance units/mmHg for hypovolemic, normovolemic, and hypervolemic, respectively) independent of shifts in baseline FVR and PVP. These results indicate greater demand for vasoconstriction for equal reductions in venous pressure during progressive hypovolemia; this condition may compromise the capacity to provide adequate peripheral resistance during severe orthostatic stress. Fluid loading before reentry after spaceflight may act to restore vasoconstrictive capacity of the cardiopulmonary baroreflex but may not be an effective countermeasure against potential post-flight impairment of the carotid-cardiac baroreflex.

Adult↗
PubMed1989

Opiate receptor inhibition improves the blunted baroreflex function in conscious dogs with right-sided congestive heart failure.

The endogenous opiate system is activated in congestive heart failure. because endogenous opioids are known to depress the baroreflex function, we conducted studies to determine whether the increased endogenous opioids play a role in causing the reduced baroreflex function that occurs in heart failure. Right-sided congestive heart failure was produced in 16 dogs by tricuspid avulsion and progressive pulmonary artery constriction. Seven sham-operated dogs were included for comparison. Baroreflex function was measured in the conscious dogs after pretreatment with either normal saline or an opiate-receptor antagonist by bolus administration of phenylephrine. The slope of the regression line relating systolic blood pressure to cardiac cycle (R-R) interval was taken as an index of baroreflex sensitivity. Plasma beta-endorphin was elevated in the dogs with heart failure (15.3 +/- 2.5 pmol/l) compared with the sham-operated dogs (4.2 +/- 0.4 pmol/l, p less than 0.001). The dogs with heart failure also exhibited a reduced baroreflex sensitivity (3.84 +/- 0.19 msec/mm Hg) after saline pretreatment when compared with the sham-operated dogs (10.86 +/- 1.20 msec/mm Hg, p less than 0.001). Administration of naloxone hydrochloride increased the baroreflex sensitivity of dogs with heart failure to 5.16 +/- 0.26 msec/mm Hg (p less than 0.01) but produced no significant effects in sham-operated dogs (11.36 +/- 1.42 msec/mm Hg). To further study the site of action for the effect of naloxone, we measured baroreflex sensitivity in the dogs with heart failure after pretreatment with naloxonazine, a selective mu-receptor antagonist, with ICI 154,129, a selective delta-receptor antagonist, or with naloxone methobromide, a quaternary analogue of naloxone that does not penetrate the blood-brain barrier.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Age-related changes of baroreflex function, plasma norepinephrine, and blood pressure.

Interrelationships between age, baroreflex sensitivity, plasma norepinephrine levels, and systolic blood pressure were assessed in a group of 54 normal subjects ranging in age from 14 to 77 years. Baroreflex sensitivity was measured by the change in R-R intervals per unit change in systolic blood pressure during phase 4 of the Valsalva maneuver. All correlations among these four variables were statistically significant (p less than 0.05 or 0.01). To investigate possible causal relationships between age-related changes of baroreflex sensitivity, plasma norepinephrine levels, and blood pressure, partial correlative analysis was then performed. After the effect of age was eliminated, plasma norepinephrine levels were found to be related positively to blood pressure (r = 0.29, p less than 0.05) and negatively to baroreflex sensitivity (r = -0.34, p less than 0.05). The increase in plasma norepinephrine levels could be causally related to the elevation of blood pressure, as plasma norepinephrine levels could provide an index of sympathetic activity. Furthermore, baroreflex sensitivity was found to be negatively related to age (r = -0.44, p less than 0.01) independent of plasma norepinephrine levels, whereas plasma norepinephrine levels were no longer related to age (r = 0.10) after adjusting for the effect of baroreflex sensitivity. This finding suggests that an increase in plasma norepinephrine levels with age could be mediated by the age-related change of baroreflex sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

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.

Animals↗
PubMed1989

Effects of calcium channel antagonists on carotid sinus baroreflex control of arterial pressure and heart rate in anesthetized dogs.

Our study was designed to determine whether the calcium channel antagonists verapamil, diltiazem, and nifedipine and the nitrate vasodilator sodium nitroprusside modulate carotid sinus (CS) baroreflex control of mean arterial pressure (MAP) and heart rate (HR). Pentobarbital-anesthetized, vagotomized dogs were surgically prepared for reversible vascular isolation of the CS regions. Open-loop performance of the CS baroreflex was determined under control conditions and after intravenous infusion of each agent for 20 minutes at four rates (nitroprusside: 0.3-10 micrograms/kg/min; verapamil and diltiazem: 1-30 micrograms/kg/min; nifedipine: 0.1-3 micrograms/kg/min). With the CS baroreflex loop closed, each vasodilator decreased MAP from control (nitroprusside: 127 +/- 3 to 69 +/- 5 mm Hg; verapamil: 137 +/- 7 to 86 +/- 5 mm Hg; diltiazem: 137 +/- 9 to 100 +/- 5 mm Hg; nifedipine: 140 +/- 6 to 109 +/- 7 mm Hg). Each compound also caused a dose-dependent downward shift in the open-loop CSP-MAP relations. The higher doses of each vasodilator also depressed the total range of control of MAP (i.e., maximum MAP minus minimum MAP) by the baroreflex and significantly attenuated the peak open-loop MAP/CSP gains (nitroprusside: 1.21 +/- 0.19 to 0.56 +/- 0.12; verapamil: 1.36 +/- 0.16 to 0.64 +/- 0.10; diltiazem: 1.52 +/- 0.34 to 0.89 +/- 0.11; nifedipine: 1.35 +/- 0.20 to 0.83 +/- 0.14) but did not alter the CSP at which the peak gain was manifest. Only verapamil and diltiazem significantly shifted downward the CSP-HR relations, whereas none of the drugs affected the total range of baroreflex control of HR (i.e., maximum HR minus minimum HR) or the peak open-loop HR/CSP gains. Our results suggest that 1) it is unlikely that calcium channel antagonists act directly on the baroreceptors or the neural components of the baroreflex loop (i.e., afferent, central and efferent nerves) because they impair CS baroreflex control of MAP but not HR and 2) the impairment of MAP control is predominantly due to a nonspecific blunting of adrenergic vasoconstriction.

Animals↗