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PubMed2000

[K(ATP) channel opener facilitates carotid sinus baroreflex in anesthetized rats].

The effects of cromakalim (Cro), a K(ATP) channel opener, on the carotid baroreflex were studied in 32 anesthetized rats with perfused isolated carotid sinus. The results obtained are as follows. (1) By perfusing the isolated carotid sinus with Cro (10 micromol/L), the functional curve of the baroreflex was shifted to the left and downward, with a peak slope (PS) increasing from 0.36+/-0.01 to 0.48+/-0.01 kPa/kPa (P<0.001), whereas the reflex decrease in mean arterial pressure (RD) was increased from 5.78+/-0.14 to 7.87+/-0.12 kPa (P<0.001). Meanwhile, the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were all significantly decreased from 8.34+/-0.35 to 6.41+/-0.09 kPa (P<0.01), 12.71+/-0.25 to 11.78+/-0.24 kPa (P<0.01) and 24.89+/-0.25 to 22.56+/-0.16 kPa (P<0.001), respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP induced by Cro were dose-dependent. (2) By pretreatment with glibenclamide (10 micromol/L), a K(ATP) channel blocker, the above effects of Cro on the carotid baroreflex were abolished. (3) The Cro-induced change in the baroreflex was enhanced by preperfusing with adenosine (125 micromol/L). On the basis of the above results, it is concluded that Cro facilitates the carotid baroreflex, an effect attributable to the enhanced stretch of baroreceptors by dilation of sinus wall as a result of K(ATP) channel activation.

Animals↗
PubMed2003

Baroreflex resetting after successful surgical repair of tetralogy of Fallot.

BACKGROUND: Tetralogy of Fallot (TOF) and its surgical repair are associated with alterations in right ventricular systolic and diastolic functions. The cardiopulmonary baroreflex describes the peripheral vasoconstriction response to the volume-unloading deactivation of left and possibly right ventricular receptors. Alterations in cardiac geometry or distensibility and pulmonary vasculature of operated TOF may affect the mechanical stimulation of sensitive cardiopulmonary receptors leading to an impaired baroreflex function. There has to date been no report on the integrity of baroreflex function in postoperative TOF. OBJECTIVE: To characterize the combined cardiopulmonary and baroreflex response of patients successfully operated for TOF in early childhood to central volume unloading using graded lower body negative pressure (LBNP) application. METHODS: Fifteen patients operated on for TOF (mean+/-SEM) 15.7+/-1.4 years previously and 13 healthy age-matched control subjects were submitted to four consecutive 5 min LBNP applications at -10, -20, -30 and -40 mmHg. Forearm blood flow and vascular resistance, left ventricle end-diastolic diameter (LVEDD), arterial blood pressure and heart rate were obtained. RESULTS: TOF exhibited a lower LVEDD (42.7+/-1.5 mm) than control subjects (51.9+/-1.6). The forearm vascular resistance to LVEDD relationship was shifted left and upward in TOF compared with that of control subjects, but the slope of the relationship was not different between groups. LBNP -40 mmHg induced a lesser change in heart rate in TOF (+10.6+/-1.5%) than in control subjects (+14.7 +/-2.4%) and an increase (P<0.05) in diastolic blood pressure in TOF (-2.4+/-2.5%), which was not seen in control subjects (+4.3+/-2.9%). CONCLUSIONS: Young adults successfully operated on for TOF in early childhood exhibit a resetting of the cardiopulmonary baroreflex to operate at smaller LVEDD and at a higher level of forearm vascular resistance. The blunted heart rate response to LBNP -40 mmHg is consistent with previous observations pointing to disturbances in the efferent arm of the baroreflex.

Adolescent↗
PubMed2004

Capsaicin facilitates carotid sinus baroreflex in anesthetized rats.

The effects of capsaicin (CAP) on the carotid sinus baroreflex were studied in 30 anaesthetized rats with perfused isolated carotid sinus. The results are as follows. (1) By perfusing the isolated carotid sinus with CAP (1 micromol/L), the functional curve of the baroreflex was shifted to the left and downward, with a peak slope (PS) increasing from 0.34+/-0.01 to 0.42+/-0.01 (P<0.01), whereas the reflex decrease (RD) in mean arterial pressure was enhanced from 36.51+/-1.26 to 45.01+/-0.71 mmHg (P<0.01). Meanwhile, the threshold pressure, equilibrium pressure and saturation pressure were all significantly decreased from 70.43 +/-2.09 to 52.86 +/-2.80 mmHg (P<0.01), 95.5+/-1.71 to 87.00+/-1.58 mmHg (P<0.01) and 177.60+/-1.37 to 163.55+/-2.12 mmHg (P<0.01), respectively. Among the functional parameters of carotid baroreflex, the changes in PS and RD induced by capsaicin were dose-dependent. (2) By pretreatment with ruthenium red (RR, 100 micromol/L), an antagonist of vanilloid receptor subtype 1 (VR(1)), the above effects of CAP on carotid baroreflex were abolished. (3) The CAP-induced change in the baroreflex was also eliminated by pretreatment with glibenclamide (20 microm ol/L), a K(ATP) channel blocker. On the basis of the results, it is concluded that CAP facilitates the carotid baroreflex, an effect of which may be resulted from the opening of K(ATP) channels mediated by VR(1).

Animals↗
PubMed1997

Effects of hypovolemia on aortic baroreflex control of heart rate in humans.

INTRODUCTION: To test the hypothesis that hypovolemia can acutely increase the sensitivity of chronotropic baroreflex response, eight men (21-45 yr old) underwent measurements of heart rate response to aortic baroreceptor stimulation under normovolemic and hypovolemic conditions. METHODS: Hypovolemia was acutely induced by a bolus injection of 30 mg of furosemide. The sensitivity of the aortic-cardiac baroreflex was determined with a approximately 15 mmHg elevation in mean arterial pressure (MAP) induced by steady-state infusion of 30 to 97 micrograms.min-1 phenylephrine (PE) combined with approximately 13 mmHg lower body negative pressure (LBNP) to counteract central venous pressure elevations, and 17-19 mmHg neck pressure (NP) to offset increases in carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in MAP (delta HR/delta MAP) between baseline and aortic baroreceptor isolated conditions (i.e., PE + LBNP + NP stage). RESULTS: When compared to normovolemia (3182 +/- 163 ml), furosemide-induced hypovolemia (2812 +/- 101 ml) resulted in an average 12% reduction in plasma volume (p = 0.05). Hypovolemia increased the average gain of the aortic-cardiac baroreflex by 68% (0.71 +/- 0.26 to 1.19 +/- 0.37 beats.min-1.mmHg-1; p = 0.0349) while it had no effect on the calculated response of the carotid-cardiac baroreflex. CONCLUSIONS: These results indicate that greater aortic baroreflex sensitivity observed in individuals who are physically untrained or have been exposed to microgravity may be explained by smaller vascular volume rather than differences in autonomic function associated with adaptations to lower aerobic capacity.

Adult↗
PubMed1997

[Vasovagal syncope and increased baroreceptor activity: evidence for increased sensibility of the baroreflex and its rapid reversal with acute administration of metoprolol].

In 17 patients suffering from recurrent episodes of vasovagal syncope as well as in 21 healthy subjects without clinical episodes of presyncope or syncope, we evaluated the reflex decrease in heart rate evoked by the phenilephrine test. In the syncopal patients, the measurements were taken 4-12 hours after the clinical appearance of syncope. We divided the syncopal patients as follows: 9 patients, undergoing pharmacological treatment, and 8 untreated patients (drug free arm). In the pharmacological arm of the study, an alternate, randomized administration of metoprolol (150 mg twice daily for 2 days) and verapamil (80 mg every 6 hours for 2 days) was provided. Therefore, in the pharmacological arm as well as in drug free patients, we tested again the baroreflex sensitivity, by means of iv phenilephrine bolus, 3 and 7 days after the clinical appearance of the syncopal event. The baroreflex sensitivity values were significantly higher in the syncopal group compared to the control group (21 +/- 5 vs 13 +/- 4.5 ms/mm Hg; p < 0.01). Of the two tested drugs, only the metoprolol produced a fast (day 3) decrease in baroreflex sensitivity. On the basis of measurements taken after 7 days, we noted a pattern of widespread reduction in baroreflex sensitivity values, found in both treated and untreated patients. In conclusion, patients with vasovagal syncope exhibited a more pronounced maximal parasympathetic activation compared to the control group. The high baroreflex sensitivity values were soon (day 3) reduced by metoprolol, but not by verapamil therapy; a spontaneous normalization in baroreflex sensitivity values was found 7 days after the clinical episode, regardless of therapy.

Adult↗
PubMed1983

Baroreflex dysfunction in patients with adult-onset diabetes and hypertension.

Ten patients with adult-onset diabetes in whom diabetes antedated the appearance of hypertension were evaluated. These patients had evidence of diabetic autonomic neuropathy, including significant orthostatic hypotension (four patients), impotence (three patients), and evidence of diabetic peripheral sensorimotor neuropathy (nine patients) in clinical testing and nerve conduction study results. Baroreflex function was evaluated by multiple hemodynamic tests, including inhalation of amyl nitrite and intravenous administration of phenylephrine, before and after parasympathetic blockade with atropine, and the cold pressor test; results were compared with results in normal control subjects, patients with essential hypertension, and two subgroups of uremic patients undergoing maintenance hemodialysis. Baroreflex function was significantly abnormal in the diabetic patients and was consistent with combined parasympathetic and sympathetic motor nerve (efferent) dysfunction in the baroreflex arc. There was a significant inverse correlation between the degree of orthostatic hypotension in the diabetic patients and their baroreflex response to phenylephrine (r = -0.680, p less than 0.05). There was no significant correlation between supine hypertension in the patients with diabetes and any of the hemodynamic or biochemical parameters examined. The results suggest that orthostatic hypotension in these patients is related to baroreflex dysfunction. However, baroreflex dysfunction does not appear to be a factor in the development of hypertension in these patients, although more studies with normotensive diabetic patients are needed to confirm this point.

Aged↗
PubMed1993

Effects of cocaine on baroreflex control of heart rate in conscious rats.

Cocaine administration elicits a pressor response reportedly dependent upon central and peripheral actions. The present study was designed specifically to determine whether cocaine affects baroreflex sensitivity and whether this is mediated by an action in the CNS. Baroreflex control of heart rate was assessed by noting the change in the duration of the arterial pulse pressure or in the heart rate elicited by administration of pressor and depressor agents. The effects of intracerebroventricular and intravenous cocaine administration were compared. Cocaine (0.1-0.15 mg/kg/min, i.v.) produced a decrease in baroreflex sensitivity that was greater than that produced by an approximately equipressor infusion of phenylephrine (0.5-1.3 micrograms/kg/min, i.v.). Intracerebroventricular (i.c.v.) administration of cocaine (1.5-150 micrograms) or procaine (100 micrograms) had no effect on arterial pressure, heart rate or baroreflex control of heart rate. Furthermore, central administration of yohimbine (3 and 10 micrograms, i.c.v.) was capable of preventing the suppression of the heart rate responses induced by cocaine administration. Propranolol (15 micrograms, i.c.v.) was not able to attenuate the suppression of baroreflex sensitivity elicited by intravenous cocaine administration but higher doses (50-150 micrograms, i.c.v.) could mimic this effect. These data suggest that cocaine suppresses baroreflex control of heart rate by a central alpha 2-adrenergic mechanism. In contrast, the pressor response to intravenous cocaine is not likely to be dependent upon a forebrain periventricular site.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Impairment of central mediation of the arterial baroreflex by acute ethanol administration.

We investigated the possibility that the impairment of baroreflex control of heart rate was due to an action of ethanol on the central component of the baroreflex arc. Baroreceptors and baroreceptor afferents were removed from the arc by sino-aortic denervation and the central end of the left aortic depressor nerve was stimulated. Stimulation frequency response curves relating the decreases in blood pressure, heart rate and sympathetic efferent nerve discharge to the frequency of stimulation were constructed before and after the administration of 0.33, 0.66 and 1 g/kg of ethanol administered systemically. Except for a small decrease in blood pressure following the 1 g/kg dose, ethanol administration did not produce any change in baseline heart rate or blood pressure but the frequency response curve of heart rate was reset by the two lower doses of ethanol whereas the dose of 1 g/kg produced frank impairment of baroreflex control. Similarly the dose of 1 g/kg also impaired the depressor response to aortic nerve stimulation whereas it did not impair the baroreflex control of sympathetic efferent discharge. These data suggest a differential effect of ethanol on central pathways that control baroreflex responses. To ensure that the effect of ethanol was not due to an action of ethanol on an end organ, the heart, a separate group of rats were prepared with sino-aortic denervation and the peripheral end of the cut right vagus nerve was stimulated with increasing frequency. Ethanol did not affect the response to stimulation of the vagus nerve showing that the impairment of baroreflex control of cardiovascular variables was primarily of central origin.

Animals↗
PubMed1984

Baroreflex setting and sensitivity after acute and chronic nicardipine therapy.

Intra-arterial pressure, baroreflex sensitivity and the baroreflex set point were measured in eight patients with essential hypertension during a control period and then after acute treatment (2 h after a 30 mg oral dose) and after chronic treatment (at least 2 months) with nicardipine hydrochloride, a calcium channel antagonist. Mean intra-arterial blood pressure fell after the acute treatment from 130 +/- 14 (SD) control to 118 +/- 11 mmHg, P less than 0.05, and after chronic treatment to 112 +/- 19 mmHg, P less than 0.05. Heart rate increased from 72 +/- 11 control to 81 +/- 16 beats/min, P less than 0.05, during acute treatment indicating activation of the baroreflex control mechanism, but returned to control values with chronic treatment (72 +/- 11 control vs 69 +/- 9 beats/min chronic), indicating a significant shift to the left of the baroreflex set point. There was no change in baroreflex sensitivity after either acute or chronic treatment (control 4.7, acute 4.3, chronic 5.1 ms/mmHg, P not significant for all values). Nicardipine significantly reduces mean intra-arterial pressure both acutely and chronically; the latter is associated with a return of the heart rate to control values due to resetting of the baroreflex control mechanism.

Adult↗
PubMed1986

Effects of fentanyl-diazepam-nitrous oxide anaesthesia on arterial baroreflex control of heart rate in man.

The effects of fentanyl 7.5 micrograms kg-1 (group I), 10.0 micrograms kg-1 (group II) and 12.5 micrograms kg-1 (group III) with diazepam 0.25 mg kg-1 and 70% nitrous oxide on baroreflex control of heart rate in humans were investigated. Phenylephrine (the pressor test), sodium nitroprusside (the depressor test) and graded neck suction provoked baroreflex responses. In group I the pressor, depressor and neck suction baroreflex slopes decreased during anaesthesia. In groups II and III the depressor test slopes were also decreased during anaesthesia. However, the slopes derived from the pressor and neck suction tests did not decrease. These data suggest that baroreflex control of heart rate is attenuated during low doses of fentanyl (7.5 micrograms kg-1). Baroreflex mediated tachycardia is decreased by higher doses of fentanyl (10.0 and 12.5 micrograms kg-1). However, baroreflex-mediated bradycardia is maintained during the higher doses of fentanyl. We suggest this effect is the result of enhanced vagal efferent activity mediated by fentanyl.

Adult↗
PubMed1987

Effects of droperidol on sympathetic activity and baroreflex control of heart rate in humans.

The effects of intravenous droperidol, 0.2 mg . kg-1, on baroreflex control of heart rate and on plasma catecholamine levels were determined in 10 ASA physical status I unpremedicated patients. Baroreflex control of heart rate was assessed by a pressor test using phenylephrine. Plasma concentrations of norepinephrine and epinephrine were determined by high pressure liquid chromatography, and plasma droperidol concentrations were measured by radioimmunoassay, from blood samples withdrawn before baroreflex evaluation. All data were obtained before and 5, 10, and 15 min following droperidol administration. Baroreflex response was significantly decreased after droperidol at each time of the study with the maximal decrease (-47% from control) observed at 5 min. No resetting of baroreflex was present since the pulse interval at the reference pressure was unchanged. Plasma norepinephrine concentrations were moderately but significantly increased only at 5 min, while no significant change in epinephrine concentrations was observed. It is concluded that droperidol induces a moderate but sustained alteration of baroreflex function and a transient increase in plasma norepinephrine concentrations.

Adult↗
PubMed1996

Evaluation of reproducibility of spontaneous baroreflex sensitivity at rest and during laboratory tests.

OBJECTIVE: The aim of the present study was to examine the reproducibility of arterial baroreflex sensitivity (BRS) provided by the spontaneous baroreflex method at rest and during laboratory tests. METHODS: Twenty healthy volunteers were studied 24 h apart, in the same laboratory and under the same environmental conditions, at rest, during active standing, while performing mental arithmetics and during static hand-gripping. Systolic blood pressure, mean arterial pressure and pulse interval were continuously and non-invasively measured by using a Finapres device. BRS was evaluated by analysing the slopes of spontaneously occurring sequences of three or more consecutive beats in which systolic blood pressure and pulse interval of the following beat both increased or decreased, in the same direction, in a linear fashion. Individual BRS were obtained by averaging all slopes computed within a given test. RESULTS: Under each test condition BRS did not differ significantly between the two consecutive days, showing strikingly similar values. The mean group coefficients of variation (CVAR), obtained by averaging individual CVAR, between the two experimental days were 15.0, 13.9 and 19.7% for resting, standing, static hand-gripping and mental arithmetic, respectively. No relationships were found between individual CVAR and individual mean arterial pressure, pulse interval and number of baroreflex sequences under any tested condition, on both experimental days. CONCLUSIONS: These results show that the spontaneous baroreflex method provides good BRS reproducibility under various stimuli that affect the neural control of circulation differently. They also suggest that BRS variability is dependent neither on haemodynamic modifications nor on the degree of baroreflex engagement, but it seems to reflect an inherent feature of the way in which arterial baroreflex modulate the heart period.

Adult↗
PubMed1989

Sensitivity of arterial baroreflex changes during daily activity.

1. Continuous ambulatory arterial pressure monitoring was performed by telemetry in 34 hypertensive and four normotensive subjects and arterial baroreflex sensitivity was evaluated by computer analysis of pulse wave. Three consecutive pulses were selected, on two criteria, from the 24 h recording: (i) progressive and linear increase or decrease in systolic arterial pressure and heart period, (ii) change of systolic arterial pressure in three pulses exceeds a threshold value. The systolic arterial pressure and heart period of three pulses were averaged and the slopes of systolic arterial pressure and heart period were calculated as baroreflex sensitivity. 2. When the threshold value was set to 5 mmHg, baroreflex sensitivity measured by the present method correlated with baroreflex sensitivity as measured by the phenylephrine method (r = 0.667, P less than 0.001). 3. The baroreflex sensitivity from the pressor-bradycardia and the depressor-tachycardia reflex decreased as threshold value was increased from 3 to 4 mmHg to over 20 mmHg. With the pressor-bradycardia reflex, the initial systolic arterial pressure of three pulses did not change, but the initial heart period shortened progressively as the threshold increased. With the depressor-tachycardia reflex, the initial systolic arterial pressure increased and the initial heart period shortened progressively. This suggests that the sensitivity of arterial baroreflex changes dynamically according to input of reflex are during daily activity.

Adult↗
PubMed1989

Acute changes in the properties of baroreflexes in man after beta-blockade.

1. To clarify whether acute changes in the properties of baroreflexes can occur in man, we evaluated the time course of baroreflex control of heart rate and cardiopulmonary baroreflex control of forearm vascular resistance (FVR) over 240 min after intravenous administration of propranolol (0.2 mg/kg) in 13 healthy young men. 2. Systolic and diastolic blood pressure remained unchanged after propranolol. Propranolol significantly decreased cardiac index and heart rate, and significantly increased total peripheral resistance. These effects remained unchanged for 240 min after propranolol. 3. Baroreflex control of heart rate was significantly augmented immediately after, and at 30, 60 min after propranolol, but partly reverted to the initial level afterwards. Cardiopulmonary baroreflex control of FVR was reduced immediately after, and at 30, 60 min after propranolol, but partly reverted to the initial level afterwards. Pressor responses to phenylephrine was reduced immediately after propranolol, but no significant differences were observed after 30 min. 4. These results suggest that acute changes in the properties of baroreflexes occur in man after propranolol.

Adrenergic beta-Antagonists↗
PubMed1977

Baroreflex inhibition of the human sinus node: importance of stimulus intensity, duration, and rate of pressure change.

1. Carotid baroreceptors were stimulated with electronically controlled neck suction in five healthy young men and pulse interval prolongation was measured. Timing of the onset of stimuli in relation to cardiac activity was held constant, and stimulus intensity, duration, and dP/dt were varied independently. 2. In the subjects studied, sinus node responses to neck suction were proportional to dP/dt. However, variations of stimulus dP/dt within or above the normal range for arterial dP/dt did not influence the magnitude of integrated baroreflex responses, or the earliest portion of baroreflex sinus node inhibition. 3. Carotid baroreflex responses were linear over a wide range which extended beyond the normal range for human systolic arterial pressures. 4. Saturation of the carotid baroreceptor-cardiac reflex occurred at distending pressures of about 160 mmHg. 5. The average baroreflex responses of the group studied were highly reproducible over time. 6. Baroreflex gain correlated very strongly with base line pulse interval. 7. The magnitude of baroreflex responses increased linearly with the duration of carotid sinus distension and reached a maximum level with stimuli lasting 0-5 sec or more. 8. The results demonstrate that carotid sinus transfer characteristics can be measured in normal man, and that human response patterns are strikingly similar to those observed earlier in experimental animals.

Adult↗
PubMed1989

Acute carotid baroreflex resetting in conscious dogs.

1. Acute baroreflex resetting in the control of arterial pressure was studied in six chronically instrumented, conscious dogs. Following aortic baroreceptor denervation, the carotid sinuses were surgically prepared for reversible vascular isolation. 2. During the experiments both carotid sinuses were temporarily isolated from the systemic circulation and conditioned with a pulsatile pressure. The carotid sinus conditioning pressure (CPCSP) was at a level of 100, 140 or 60 mmHg for 20 min each. Carotid sinus pressure (CSP) versus mean arterial pressure (MAP) baroreflex curves were constructed after each conditioning period. 3. The baroreflex curves were shifted downward and to the left at low CPCSP and upward and to the right at high CPCSP. 4. We used four parameters to quantify baroreflex resetting. These were: (1) the set point pressure (PSP), (2) the threshold pressure (PTh), (3) BP50 or mid-point pressure and (4) the CSP at maximum gain (PGmax). At high CPCSP, these four parameters were increased by 18.5 +/- 4.0, 23.4 +/- 4.3, 21.7 +/- 5.0 and 22.0 +/- 5.1 mmHg, respectively (P less than 0.05). 5. Resetting was not complete in these studies. The extent of resetting was approximately 50% for upward and 35% for downward baroreflex conditioning. 6. Analysis of the present experimental data indicates that when the cardiovascular system is exposed to a short-term hyper- or hypotension, the baroreflex is capable of correcting the baseline arterial pressure while preserving its ability to buffer transient disturbances as a result of partial resetting.

Animals↗
PubMed2000

Chronic blockade of brain "ouabain" prevents sympathetic hyper-reactivity and impairment of acute baroreflex resetting in rats with congestive heart failure.

In rats with congestive heart failure (CHF) post myocardial infarction (MI) acute blockade of brain "ouabain" reverses sympathetic hyperactivity and chronic blockade prevents the desensitization of baroreflex function. This study was conducted to determine: i) if chronic blockade of brain "ouabain" maintains normal sympathetic reactivity; and ii) if acute baroreflex resetting (another parameter of baroreflex function) also becomes impaired, and if so, does brain "ouabain" contribute to impairment in acute baroreflex resetting. CHF post MI was induced by acute coronary artery ligation in Wistar rats. Animals were treated with 200 microg x day(-1) i.c.v. or i.v. Fab fragments (which bind brain "ouabain" with high affinity), or treated with 200 microg x day(-1) i.c.v. gamma-globulins (control group). The length of treatment was 0.5-8 weeks or 4-8 weeks post MI. At 8 weeks mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded in concious rats at rest and in response to: i) air-jet stress, ii) i.c.v. guanabenz (an alpha2-adrenoceptor agonist), and iii) a 30 min i.v. infusion of nitroprusside (NP). Excitatory responses to air stress and inhibitory responses to guanabenz of MAP, HR, and RSNA were significantly enhanced in rats with CHF versus the sham-operated treated group. This enhancement was prevented in the CHF group treated with i.c.v., but not i.v., Fab. Nitroprusside induced a sustained decrease in MAP (approximately 25 mmHg) and a transient decrease in CVP. Heart rate and RSNA increased significantly within 1 min of beginning the infusion. The peak increases as well as the product of changes in MAP-HR and RSNA-HR were significantly smaller in rats with CHF treated with gamma-globulins versus sham rats and versus CHF rats treated with i.c.v. Fab. In sham-operated rats and CHF rats treated with i.c.v. Fab, RSNA and HR began to decrease within 3-4 min of beginning the NP infusion and had returned to baseline by 20 min. In contrast, RSNA and HR remained increased throughout the infusion in the CHF rats treated with gamma-globulins. These data indicate that in rats with CHF acute resetting of the arterial baroreflex in response to a lower BP becomes impaired, and chronic blockade of brain "ouabain" prevents both this change in baroreflex resetting as well as sympathetic hyperactivity.

Animals↗
PubMed1982

Pressor response to vasopressin and impaired baroreflex function in DOC-salt hypertension.

Baroreflexes and pressor responses to intravenous arginine vasopressin (AVP) and phenylephrine (PE) were evaluated in conscious, less severely hypertensive desoxycorticosterone (DOC)-salt-treated rats, hypertensive DOC-salt-treated rats, and control rats (n = 6, each group). Pressor responses were retested after ganglionic blockade. In control rats pressor responses to AVP were augmented more than those to PE after ganglion blockade; thus AVP appeared uniquely to augment baroreflex buffering. In hypertensive DOC-salt-treated rats baroreflexes were impaired (P less than 0.05); pressor responsiveness to AVP was augmented compared with control rats (P less than 0.05). After ganglion blockade augumentation of pressor responses was similar for AVP and PE. In less severely hypertensive rats baroreflexes were normal; pressor responses to AVP and PE were like those in control rats before and after ganglion blockade. These results suggest that AVP augments baroreflex buffering, which imposes a restraint on pressor effects of AVP that is not evident with PE. In hypertensive DOC-salt-treated rats a defect in baroreflex buffering during infusion of AVP may contribute to augmented pressor effects of AVP.

Animals↗