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PubMed1989

Baroreceptor resetting and other determinants of baroreflex properties in hypertension.

1. Rapid resetting of the arterial baroreceptor threshold in the normal circulation extends the pressure range over which baroreflexes operate at high gain. During sustained falls and rises in resting blood pressure (BP), changes in reflex threshold may be greater or less than those of the receptors, through interactions with other sources of afferent drive (e.g. cardiac baroreceptors). In chronic hypertension the magnitude of the reflex resetting again corresponds to that of the arterial baroreceptors, probably because of the resetting of the threshold of the cardiac receptors. 2. 'Baroreflexes' in intact animals are compound reflexes with input from both arterial and non-arterial baroreceptors (e.g. cardiac/pulmonary baroreceptors). The steady-state responses can be characterized by BP-autonomic output function curves, which are often sigmoidal, with a well-defined effector response range and gain. Both sets of input contribute to the high gain component close to resting, with the arterial baroreceptors the major source of reflex drive; the non-arterial baroreceptors also contribute over this part of the reflex and their role increases considerably at high and low BP. 3. In chronic mild/moderate hypertension the changes in baroreflex properties are similar to those of moderate acute rises in BP or in cardiac load; heart rate range of the vagal component of the cardiac baroreflex is depressed, gain is slightly enhanced and the Valsalva-total peripheral resistance (TPR) reflex is unaltered. In severe hypertension: (i) vagal heart rate range and gain are further depressed; and (ii) there is depression of the Valsalva-TPR reflex, much as observed in constrictor reflexes during acute hypertension in normal animals. Circulatory disturbances produce engagement of non-arterial baroreceptors more readily in hypertensives than in normotensives; depression of baroreflexes in hypertension is due partly to enhanced drive from these receptors and partly due to reduction in the gain of the arterial baroreceptors. 4. The reflex vagal depression and that of neural constrictor reflexes can be considered as important homeostatic mechanisms that limit the effects of circulatory perturbations on cardiac filling pressures and on excessive rises in vascular resistance.

Animals↗
PubMed1989

Alpha-agonist modifies baroreflex vasoconstriction by a postjunctional mechanism in dogs.

1. We examined whether or not circulating alpha-agonist modified baroreflex vasoconstriction of the hindlimb, using anaesthetized dogs in which the limb was vascularly isolated and perfused with blood from a donor dog using a pulsatile pump. 2. The open-loop gain (G) of the baroreflex was estimated from changes in mean arterial pressure following mild quick haemorrhage from the aorta of the recipient dog. 3. The hindlimb perfusion pressure increased after haemorrhage due to neurogenic vasoconstriction. 4. An overall gain (Gh) of the baroreflex hindlimb vascular bed control system was estimated from the ratio of the increase in hindlimb perfusion pressure to the change in systemic arterial pressure of the recipient dog. 5. Administration of a relatively selective alpha 1-agonist with no prejunctional beta 2 stimulating action (phenylephrine) or a selective alpha 2-agonist (clonidine) to the donor dog increased its systemic arterial pressure and augmented Gh. 6. Since both drugs were administered to the donor dog and could not enter into the recipient dog, these drugs did not affect the recipient's sympathetic nervous system, including the central nervous system and afferent limb of the baroreflex system. Therefore, these drugs could modify baroreflex vasoconstriction of the hindlimb only at the junction of the efferent sympathetic nerve and the vascular smooth muscle. 7. It was concluded that postjunctional alpha-adrenoceptor stimulation augments neurogenic vasoconstriction.

Adrenergic alpha-Agonists↗
PubMed1989

Assessment of cardiopulmonary baroreflex function in hypertensive and normotensive subjects with or without hypertensive relatives.

1. To investigate whether cardiopulmonary baroreflex control contributes to the pathogenesis and progression of hypertension, we have evaluated the function of the cardiopulmonary baroreflex in 22 patients with essential hypertension and in 17 volunteers with normotension. The normotensive group consisted of 8 subjects with a family history of hypertension and nine with no family history. 2. Forearm vascular resistance (FVR) and central venous pressure (CVP) were measured under control conditions when -10 mmHg lower body negative pressure was applied; the cardiopulmonary slope (CPS = delta FVR/delta CVP) was calculated as an index of the cardiopulmonary baroreflex function. 3. CPS was significantly higher in hypertensives (6.0 +/- 3.93 [s.d.], P less than 0.01) and also tended to be higher in normotensives with a family history of hypertension (3.9 +/- 3.53, P less than 0.05), compared with normotensives without a family history of hypertension (1.7 +/- 0.88). 4. When the hypertensives were divided into two groups, depending on whether CPS was greater or less than 6.0 units, cardiac wall thickness (20 +/- 1.6 mm vs 23 +/- 3.2 mm, P less than 0.05) and the renal vascular resistance (20.9 +/- 6.52 units vs 28.9 +/- 7.32 units, P less than 0.05) were both significantly higher in the Low CPS group. 5. These findings suggest that cardiopulmonary baroreflex function was augmented even in normotensive subjects with hypertensive relatives, as compared with those without hypertensive subjects. Furthermore, cardiopulmonary baroreflex function was augmented in the early stages of hypertension and diminished further with increasing severity.

Adult↗
PubMed1990

Influence of cardiac afferents on time-dependent changes in the renal sympathetic baroreflex of conscious rabbits.

1. The stability of the renal sympathetic baroreflex and nasopharyngeal reflex, and the role of cardiac sensory receptors, was studied in conscious rabbits over a 5 h experimental period. 2. Renal sympathetic nerve activity (SNA) was recorded during (i) slow ramp changes in mean arterial pressure (MAP) of 1-2 mmHg/s induced by inflating perivascular balloon cuffs, and (ii) the inhalation of cigarette smoke. Experiments were repeated in other rabbits after blocking cardiac afferents with 5% intrapericardial procaine. 3. Baroreflex responses to the first two caval cuff inflations of the day were significantly greater than subsequent responses. After this, triplicate sets of reflex curves were relatively stable during a 2 h period in the morning. When the experiment was repeated in the afternoon, there was a significant attenuation of baroreflex range and a small fall in resting renal SNA which were abolished by pericardial procaine. 4. Changes in baroreflex properties were minimal when the reflex was assessed only twice, at the beginning and end of a 5 h period. No change was seen in the nasopharyngeal reflex whether the rabbits had been subjected to few or to many cuff inflations. 5. We conclude that time dependent changes can occur in the renal sympathetic baroreflex of conscious rabbits which must be allowed for by appropriate protocol design. These include increasing inhibitory influences from cardiac sensory receptors in experimental situations requiring multiple reflex estimations.

Adrenergic Fibers↗
PubMed1993

Renal sympathetic baroreflex effects of angiotensin II infusions into the rostral ventrolateral medulla of the rabbit.

1. The effects of local infusion of angiotensin II (AII) into the rostral ventrolateral medulla (RVLM) pressor area on the renal sympathetic baroreflex were compared with the excitatory amino acid glutamate in urethane anaesthetized rabbits with chronically implanted renal nerve electrodes. Baroreflex blood pressure-renal nerve activity curves were obtained by intravenous infusion of phenylephrine and nitroprusside before and after treatments. 2. Infusion of 4 pmol/min of AII into the RVLM increased blood pressure by 12 +/- 2 mmHg and transiently increased resting sympathetic nerve activity. The renal sympathetic baroreflex curves were shifted to the right. The upper plateau of the sympathetic reflex increased by 29 +/- 8% (n = 6, P < 0.025). 3. Infusions of glutamate into the RVLM, at a dose which was equipressor to that of AII, also increased resting renal sympathetic nerve activity. In contrast to AII, this increase was maintained throughout the infusion. Glutamate shifted the reflex curve to the right and increased the upper plateau of the sympathetic reflex by 44 +/- 5% without affecting the lower plateau. 4. These results support the suggestion that AII can act at the level of the RVLM pressor area to facilitate baroreflex control of renal sympathetic activity in a similar fashion to that produced by fourth ventricular administration. 5. Thus the RVLM is a likely candidate site for modulation of the renal sympathetic baroreflex. The similarity of the actions of AII to those of glutamate suggest that it may directly excite sympathetic vasomotor cells in this region.

Angiotensin II↗
PubMed1992

Testing arterial baroreflex function in acutely unwell patients.

Cardiovascular function is deranged in acute illnesses but specific details of this pathophysiological phenomenon are poorly understood. With advances in intensive care it is now necessary to define these changes. Existing tests of cardiovascular reflex function are ill-suited to the study of acutely unwell patients. The arterial baroreflex is the principal cardiovascular homeostatic reflex. We have modified the neck suction test of baroreflex function such that it can be performed in 30 min using portable equipment. The protocol was validated on control subjects. Testing of injured patients showed that this test and protocol could be used sequentially, beginning within 2 h of injury, to demonstrate acute changes in baroreflex function and to follow these changes through the disease process. Patient tolerance of the test was excellent. Subsequently, further modification developed an even shorter protocol whereby similar information could be obtained within 15 min. The cardiac response to deep respiration can be measured with minimal patient upset or compliance and is ideal for repetitive testing in critically ill patients. This is not a specific test of baroreflex function but responses to it show interesting parallels with changes in baroreflex function which merit further study.

Acute Disease↗
PubMed1989

The influence of oral glucose loading on baroreflex function in the elderly.

Blood pressure in the elderly may decrease after a meal or after oral glucose loading. It has been suggested that eating may affect blood pressure homeostasis through an insulin-induced blunting of baroreflex sensitivity. We investigated the effects of oral glucose loading on baroreflex sensitivity in young normotensives and in elderly normo-and hypertensive subjects. Blood pressure was measured by a new noninvasive device, Finapres, which measures blood pressure continuously in the finger. Baroreflex sensitivity was estimated with the phenylephrine and nitroglycerin method. In both elderly groups mean arterial pressure fell significantly after the glucose load (11 +/- 1 mm Hg, P less than .001 in the hypertensives, and 8 +/- 2 mm Hg, P less than .01 in the normotensive subjects), whereas no change in blood pressure was found in the young group. Baroreflex sensitivity was lower in both elderly groups than in young normotensives. Glucose loading had no influence on baroreflex sensitivity in the three groups. Therefore, we conclude that other factors are involved in the phenomenon of postprandial hypotension in the elderly.

Administration, Oral↗
PubMed1983

Impaired baroreflex control of vascular resistance in prehypertensive Dahl S rats.

The purpose of this study was to examine baroreflex control of vascular resistance and heart rate in prehypertensive Dahl salt-sensitive (DS) and salt-resistant (DR) rats. Urethan-anesthetized normotensive DS rats demonstrated significantly impaired baroreflex control of both hindlimb vascular resistance and heart rate. This impairment was not secondary to elevated arterial pressure since blood pressure did not differ between DR and DS rats fed a low sodium diet. Vascular baroreflex responses were shown to depend on the integrity of efferent sympathetic innervation and to be mediated by the sinoaortic afferent arterial baroreceptors. No strain difference was observed for hindlimb vasodilation produced by papaverine or graded doses of nitroprusside, indicating that differences in resistance vessel vasodilator capacity or responsiveness could not account for differences in baroreflex responses. Since impaired baroreflex control was evident in DS rats prior to any elevation in arterial pressure, this abnormality may contribute to the DS rat's genetic propensity to develop hypertension.

Animals↗
PubMed1984

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity.

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

Angiotensin II↗
PubMed1984

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.

Anesthesia, General↗
PubMed1985

Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits.

The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.

Animals↗
PubMed1987

Acute resetting of arterial baroreflexes in hypertensive rats.

Acute baroreflex resetting was studied in one-kidney, one-clip renal hypertensive (HT) and normotensive (NT) control male Wistar-Kyoto rats. Systolic blood pressure (SBP) was monitored weekly in conscious rats by the indirect tail-cuff occlusion method. At the time of experimentation (4-6 wk after placement of the clip), SBP in the HT rats (238 +/- 9 mmHg) was elevated compared with NT rats (117 +/- 5 mmHg). Baroreflex control of lumbar sympathetic nerve activity (LSNA) was assessed in alpha-chloralose (120 mg/kg)-urethan (600 mg/kg)-anesthetized rats by raising and lowering mean arterial pressure (MAP) between 50 and 200 mmHg (phenylephrine and nitroprusside infusions). The baroreflexes of the hypertensive rats were less sensitive to increments in pressure compared with normotensive rats as evidenced by a decreased slope of the baroreflex curve (-0.396 +/- 0.064 HT vs. -0.637 +/- 0.042 NT). In both groups, curves were obtained before (control) and after (reset) base-line MAP was increased by 30-55 mmHg for 15 min. The MAP for 50% maximum inhibition of LSNA (EP50) was increased in both groups of rats after exposure to the elevated pressure (NT, control = 109 +/- 5.2, reset = 120 +/- 5.0 mmHg; HT, control = 114 +/- 6.5, reset = 131 +/- 10.0 mmHg) with no significant change in slope. There was no significant difference in degree of upward resetting between the two groups (NT, 21 +/- 4%; HT, 30 +/- 7%). Thus, although hypertensive rats exhibited the depressed baroreflex function associated with chronic resetting, the ability to reset acutely was maintained.

Animals↗
PubMed1988

Exercise training attenuates baroreflex regulation of nerve activity in rabbits.

Baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) during changes in arterial pressure were examined in conscious rabbits before and after 8 wk of treadmill endurance exercise training. Exercise-induced bradycardia (decreased HR at rest and at identical workloads) was used to document a cardiovascular training effect. At 29.4 m/min, 20% grade, posttraining HR was significantly lower than pretraining values (295 +/- 6 beats/min vs. 361 +/- 8 beats/min, P less than 0.05). Rabbits were instrumented with an occluder around the inferior vena cava (IVCO), arterial and venous catheters, and recording electrodes around renal sympathetic nerves. Baroreflex-mediated changes in HR and RSNA to a 25-mmHg decrease and increase in mean arterial pressure (MAP) were obtained by inflating the IVCO or progressive infusion of phenylephrine, respectively. After training, the range (maximum response minus minimum response) of baroreflex control of RSNA and HR was significantly attenuated (209 +/- 12 vs. 413 +/- 14% and 123 +/- 16 vs. 162 +/- 8 beats/min). In addition, the slope of baroreflex control of HR and RSNA was significantly attenuated after training (4.17 +/- 0.35 vs. 8.32 +/- 0.23%/mmHg and 2.57 +/- 0.4 vs. 4.14 +/- 0.4 beats.min-1.mmHg-1). These data demonstrate that endurance exercise training significantly attenuated baroreflex control of HR and RSNA in conscious rabbits.

Animals↗
PubMed1991

Increase in sympathetic activity with age. II. Role of impairment of cardiopulmonary baroreflexes.

We have previously shown that arterial baroreflex function is significantly impaired in a group of old beagles [G. Hajduczok, M. W. Chapleau, S. L. Johnson, and F. M. Abboud. Am. J. Physiol. 260 (Heart Circ. Physiol. 29): H1113-H1120, 1991]. In the present study, we determined whether the neural limb of the cardiopulmonary baroreflex control of renal sympathetic nerve activity (RSNA) and the interaction between the arterial and cardiopulmonary reflexes is also impaired with senescence. In the anesthetized state, the aortic nerves were sectioned and carotid sinuses were isolated bilaterally with carotid sinus pressures held at 50 mmHg in both young (1 yr) and old animals (11 yr). In response to graded volume expansion (VE) with 3% dextran (0 to 30 ml/kg iv), the gain of cardiopulmonary baroreflex control of RSNA was significantly lower in the old (5.1 +/- 3%/mmHg) compared with the young (13.4 +/- 3%/mmHg) animals. There were no significant differences in systemic vascular compliance or left ventricular mass index between the two groups. The gain of the carotid sinus baroreflex inhibition of RSNA was significantly attenuated by VE in the young group but was not affected in the old group. Bilateral vagotomy (VX) resulted in a 182 +/- 74% increase in RSNA in the young (P less than 0.05), but VX did not significantly increase RSNA in the old (12 +/- 17%). After VX, the carotid sinus baroreflex gain markedly increased by nearly eightfold in the young group (P less than 0.05) but was not altered in the old dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1993

Carotid baroreflex responsiveness to lower body positive pressure-induced increases in central venous pressure.

Lower body positive pressure (LBPP) was applied at 4 and 30 Torr to increase central venous pressure (CVP). CVP increased with LBPP (r = 0.55, P < 0.01), and the increases were significant at 4 and 30 Torr (7.4 and 7.8 mmHg) from the control (6.0 mmHg). During LBPP cardiac output increased, which was significantly related to the increase in CVP (r = 0.63, P < 0.01). The carotid baroreflex was elicited by trains of neck pressure and suction from 40 to -65 Torr. The carotid-cardiac and carotid-vasomotor baroreflex responses were assessed by determining the maximal gains of heart rate (HR) interval and intraradial mean arterial pressure (MAP) to changes in carotid sinus pressure using a logistic model. The carotid-cardiac and carotid-vasomotor baroreflex gains were negatively related to LBPP, and at 30 Torr, both gains (5.6 ms/mmHg and -0.14 mmHg/mmHg) were significantly smaller than the control (12.4 ms/mmHg and -0.24 mmHg/mmHg). The decreases in carotid-cardiac and carotid-vasomotor baroreflex sensitivity during LBPP were primarily associated with the increases in CVP (r = -0.52, P < 0.01, and r = -0.74, P < 0.01, respectively). These data suggest that the increases in CVP and/or central blood volume diminish the sensitivity of the carotid baroreflex control of HR and MAP by enhancing the tonic inhibitory influence from the cardiopulmonary baroreceptors.

Adult↗
PubMed1993

Pressure-independent baroreflex resetting produced by chronic infusion of angiotensin II in rabbits.

The purpose of this study was to test the hypothesis that chronic infusion of angiotensin II (ANG II) in rabbits shifts or resets baroreflex control of heart rate to a higher pressure level via a mechanism that is independent of the hypertension that is produced. The baroreflex relationship between arterial pressure and heart rate was assessed by first infusing progressively increasing doses of nitroprusside (3, 6, 12, 24, and 48 micrograms.kg-1 x min-1) to lower pressure and then increasing doses of phenylephrine (0.5, 1, 2, 4, and 8 micrograms.kg-1 x min-1) to raise pressure. Two weeks of intravenous ANG II infusion (20 ng.kg-1 x min-1) increased plasma ANG II levels from 9 +/- 1 to 146 +/- 24 pg/ml (P < 0.05), increased arterial pressure from 62 +/- 2 to 95 +/- 2 mmHg (P < 0.05), and transiently increased heart rate. The baroreflex was shifted to a higher pressure level after 30 min and 1, 3, 7, 9, and 14 days of ANG II infusion. Thirty minutes after the ANG II infusion on days 1, 7, and 14 was stopped, arterial pressure decreased, and the baroreflex shifted back to control, indicating that ANG II was required for the resetting that was produced. However, when the ANG II infusion was continued and arterial pressure was instead reduced for 30 min by infusing nitroprusside on days 3 and 9, the baroreflex relationship between arterial pressure and heart rate remained positioned at a higher pressure level.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

Increased left ventricular pressure attenuates the baroreflex in unanesthetized dogs.

To determine whether stimulation of left ventricular mechanoreceptors alters the baroreflex control of heart rate (HR), dogs were instrumented with a vascular occluder around the ascending aorta and appropriate instrumentation for the recording of left ventricular pressure (LVP), aortic pressure, left atrial pressure, HR, and left ventricular dP/dt. Baroreflex sensitivity (pulse interval or HR vs. aortic systolic pressure linear-regression slopes to infusions of phenylephrine or nitroprusside) was determined in the conscious state a minimum of 7 days postoperatively. After control responses were determined with both phenylephrine and nitroprusside, the experiment was repeated during inflation of the ascending aortic occluder so as to significantly raise left ventricle systolic pressure from 127.9 +/- 8.4 to 178.5 +/- 11.3 mmHg (P less than 0.01) and left ventricle end-diastolic pressure from 3.5 +/- 0.7 to 8.9 +/- 1.0 mmHg (P less than 0.01). There were no changes in mean arterial blood pressure, pulse pressure, or HR during elevation of LVP. The baroreflex sensitivity was reduced only during the infusion of nitroprusside from a control of 11.03 +/- 1.9 to 4.80 +/- 1.2 ms/mmHg (P less than 0.01) for the pulse interval relationship and from -2.51 +/- 0.53 to -1.14 +/- 0.32 beats . min-1 . mmHg-1 (P less than 0.05) for the HR relationship. Cholinergic blockade with atropine abolished the depression in the baroreflex sensitivity during nitroprusside infusion when LVP was increased. beta 1-Adrenergic blockade with metoprolol did not significantly reduce the baroreflex sensitivity during increased LVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Augmentation of baroreflex-mediated bradycardia in conscious pregnant rats.

The goal of the present study was to examine baroreflex control of heart rate during pregnancy in chronically instrumented unrestrained rats. The same rats (n = 6) were studied before conception, again on gestational days 5, 12, and 19, and last on postpartum day 6; thus each rat served as its own control. Time control experiments were also conducted in a separate group of virgin rats (n = 7). Resting mean arterial pressure decreased by 10 mmHg on gestational day 19 (P less than 0.01 vs. prepregnant), and heart rate significantly increased by approximately 10% relative to time control rats. Dose-response curves were constructed for methoxamine and sodium nitroprusside comparing the various dosages with systemic pressor and depressor responses, respectively. The dose-response relationship for methoxamine was shifted to the right in gravid rats of 19 gestational days (P less than 0.03 vs. prepregnant), indicating an attenuation of alpha-adrenergic receptor-mediated pressor responsiveness. In contrast, depressor responses to sodium nitroprusside were not significantly altered in pregnancy. Baroreflex-mediated bradycardia was unchanged until gestational day 19, when enhanced bradycardia responses to methoxamine were observed. Baroreflex-mediated tachycardic responses elicited by sodium nitroprusside were not affected at any stage of pregnancy. Baroreflex control of heart rate did not change significantly with either increases or decreases of blood pressure in time control experiments. We conclude that during late pregnancy in conscious rats 1) resting blood pressure decreases and heart rate increases, 2) systemic pressor responses to methoxamine are diminished, and 3) baroreflex-mediated bradycardia is enhanced.

Analysis of Variance↗