COMPARISON OF THE REFLEX EFFECTS OF ARTERIAL BARORECEPTORS AND CARDIAC RECEPTORS ON THE HEART RATE OF CONSCIOUS RABBITS

1. The reflex effects on heart rate (HR) of presumptive cardiac receptors have been differentiated from those of the arterial baroreceptors in conscious rabbits by inflating cuffs on the ascending aorta, descending aorta, inferior vena cava and pulmonary artery. 2. When the outflow from the right ventricle was progressively impeded the accompanying increase in HR was entirely explicable by unloading of the arterial baroreceptors. 3. As the outflow from the left ventricle was progressively impeded there was an initial increase in HR due to unloading of the arterial baroreceptors, followed by a progressive decline. This decline was attributed to a reflex arising from vagallyinnervated receptors in the left side of the heart. The threshold of this cardiac receptor-HR reflex occurred at a higher level of mean aortic pressure than that at which the effects of the arterial baroreceptors on HR were maximal. Cholinergic (vagal) efferent nerves were responsible for two-thirds of the decline in HR caused by the reflex. 4. The properties of the cardiac receptor-HR reflex were altered by drugs that affect myocardial contractility. Isoprenaline raised the mean aortic pressure at which the threshold occurred, but lowered the corresponding level of left ventricular end-diastolic pressure. Propranolol virtually abolished the reflex, even though left ventricular end-diastolic pressure reached a high level. 5. It is concluded that in the conscious rabbit the arterial baroreceptor reflexes normally prevent the threshold of the cardiac receptor-HR reflex from being attained.     

EFFECTS OF NEUROPEPTIDE Y ON BAROREFLEX CONTROL OF HEART RATE AND MYOCARDIAL CONTRACTILITY IN CONSCIOUS RABBITS

1. The effects of intravenous (i.v.) neuropeptide Y (NPY, 10 micrograms/kg bolus) on the stimulus-response curves relating changes in heart period (HP) and in peak left ventricular (LV) dP/dt to acute changes in mean arterial pressure (MAP) were determined in conscious, normotensive rabbits. 2. The relationship between increases and decreases in MAP and the subsequent changes in HP were represented by a sigmoid-shaped curve described by a logistic function. Following NPY administration there was a baroreflex-dependent increase in the maximum slope (sensitivity) at the midpoint of this MAP-HP curve from 7.0 +/- 0.5 to 10.6 +/- 1.3 ms/mmHg (P less than 0.05). NPY caused an upward shift in the whole curve which reflected the NPY-induced bradycardia and was independent of baroreflexes. 3. The relationship between increases in MAP and decreases in peak LV dP/dt was determined during fixed-rate atrial pacing to prevent the effects of the accompanying bradycardia. Increases in MAP and the corresponding reductions in peak LV dP/dt were represented by an exponential function. The slope of the curve, measured at its origin 5-15 min after NPY administration, was reduced from -0.9 +/- 0.2 to -0.4 +/- 0.1 units (P less than 0.05). 4. The effects of NPY are consistent with an action on efferent connections of the arterial baroreceptor reflex, mediated through a reduction in cardiac beta-adrenergic tone. They would also be explained through actions on the afferent or central neural connections of the baroreflex.     

ARTERIAL PRESSURE AND HEART PERIOD IN THE CONSCIOUS RABBIT: DIURNAL RHYTHM AND INFLUENCE OF ACTIVITY

Mean-arterial pressure (MAP), heart period (HP) and the level of physical activity were measured in conscious rabbits and averaged over one-hour periods during 14 consecutive days. Serial autocorrelation coefficients and serial crosscorrelation coefficients were computed, to analyse periodicity. Measurements were started immediately after implantation of the cannula (group A, n = 11) or 10-46 days after implantation of the cannula (group B, n = 6). In the course of 14 days, in group A, MAP decreased 9 mmHg and HP increased 21 ms (P less than 0.05). In group B, MAP decreased and HP increased in a similar way. Percentage activity did not show a trend. Significant diurnal rhythms were found. MAP and percentage activity reached the lowest values at noon, and the highest late in the evening. HP reached the highest values at noon and the lowest late in the evening. MAP and HP fluctuated exactly in antiphase. This suggests a common origin for both rhythms. During physical activity MAP was 10-15 mmHg higher and HP was 35-40 ms shorter than during rest. These differences did not show a trend or a diurnal variation. In individual animals MAP and HP varied greatly from hour to hour. These biological variations in MAP and HP as well as the influence of activity should be taken into account when conclusions are drawn from short-term measurements.     

EFFECTS OF ENDOTHELIN-1 ON ARTERIAL PRESSURE: A COMPARISON OF INTRAVENOUS AND INTRA-ARTERIAL ADMINISTRATION IN CONSCIOUS RABBITS

1. Intravenous endothelin-1 releases endothelium-derived relaxing factor (EDRF) and prostacyclin from the lungs, and substantial pulmonary clearance is claimed. Since these vaso-active substances could alter the haemodynamic effects of endothelin-1, the effects of boluses of endothelin-1 injected intravenously and into the left ventricle (intra-arterial) were compared, measuring arterial pressure and heart rate in conscious male New Zealand rabbits. The pulmonary clearance of endothelin-1-like immunoreactivity (Et-1LI) and initial plasma half-life were measured in anaesthetized rabbits during and after intravenous infusion of endothelin-1. 2. The effects of intravenous and intra-arterial routes of administration were not significantly different. Arterial pressure decreased (intravenous: 21.6, intra-arterial: 24.2 mmHg, P= 0.12, n= 10, t-test, 9 d.f.), then increased (intravenous: 21.2, intra-arterial: 16.4 mmHg, P= 0.33), while heart rate increased (intravenous: 66, intra-arterial: 53 beats/min, P = 0.09), then decreased (intravenous: 50, intra-arterial: 54 beats/min, P= 0.30). 3. Arterial and venous plasma levels of Et-1LI were not significantly different, venous levels increasing from 30 ± 3 pg/ mL (12 ± 1 pmol/ L) at 1 pmol/ kg per min to 770 ± 78 pg/ mL (308 ± 31 pmol/L) at 16 pmol/kg per min (n = 5). Mean initial plasma half-life was 0.6 min (range: 0.25–1.1 min). 4. It was concluded that there is no significant net pulmonary clearance of exogenously administered endothelin-1 in the conscious rabbit, and that any vaso-active factors released in the lungs by endothelin-1 do not have a significant effect on systemic arterial pressure.     

EFFECTS OF ENDOTHELIN-1 ON ARTERIAL PRESSURE AND MYOCARDIAL CONTRACTILITY IN THE CONSCIOUS NORMOTENSIVE RABBIT

1. We studied the effects of an intravenous bolus of endothelin-1 on arterial pressure and myocardial contractility in the conscious rabbit. 2. Endothelin produced an initial fall in arterial pressure accompanied by an increase in heart rate. This was followed by a dose-dependent increase in arterial pressure, peaking about 7 min after injection, accompanied by a reciprocal fall in heart rate. 3. Left ventricular rate of change of pressure (LV dP dt) increased with endothelin except at higher doses (0.8 and 1.6 nmol/kg), where in some animals it decreased.     

SIMULATION OF ACUTE HAEMORRHAGE IN UNANAESTHETIZED RABBITS

1. We have shown that it is feasible to match the linear rate of fall of cardiac output that occurs during haemorrhage at 2.7 ml/kg per min in unanaesthetized rabbits by constricting the thoracic inferior vena cava so as to decrease venous return. 2. The changes in systemic vascular resistance, arterial pressure and heart rate that occurred during haemorrhage were mimicked by simulated haemorrhage. They were reproducible when simulated haemorrhage was performed three times at 90 min intervals, and when it was repeated four times over 12 days. 3. Simulated haemorrhage caused rises in plasma renin activity (PRA) and plasma arginine vasopressin concentration (AVP) that were similar to those reported after haemorrhage. The response of PRA was unaffected by repeated simulated haemorrhage, but the response of AVP was less on the third occasion. 4. When the shed blood was re-infused after haemorrhage, cardiac output tended to remain low and systemic vascular resistance high. After simulated haemorrhage, all haemodynamic variables returned to normal within 2 min of releasing the caval cuff. 5. Haematocrit fell during haemorrhage, and remained low for at least 5 days after replacement of the shed blood. Haematocrit was unaffected by simulated haemorrhage. 6. Venous pressure below the inflatable cuff rose by 6 mmHg in the course of simulated haemorrhage. 7. We conclude that the central haemodynamic effects of haemorrhage can be closely and repeatedly simulated by inflating a cuff on the inferior vena cava. This provides a useful technique for repeatedly studying the effects of acute reduction of central blood volume in conscious animals.     

RENAL SYMPATHETIC AND HEART RATE BAROREFLEX FUNCTION IN CONSCIOUS AND ISOFLURANE ANAESTHETIZED NORMOTENSIVE AND CHRONICALLY HYPERTENSIVE RABBITS

1. Baroreflex control of heart rate (HR) has been studied in normotensive (NT) and hypertensive (HT) awake and anaesthetized animals and man, but baroreflex control of sympathetic nerve activity has not been well studied. We investigated baroreflex control of HR and renal sympathetic nerve activity (RSNA) over a wide range of arterial pressure (AP) in conscious and isoflurane (ISO) anaesthetized NT and HT rabbits. 2. Animals were instrumented to record AP, HR and RSNA. Hypertension was accomplished by renal encapsulation. AP-HR and AP-RSNA baroreflex function curves were obtained while awake and after 1.0, 1.5, 2.0 and 2.5% ISO. All baroreflex curves were fit to sigmoid or exponential functions. 3. In conscious rabbits, HT for 3–5 weeks, AP was significantly higher (75.6 ± 0.8 vs 102.3 ± 8.9 mmHg); HR significantly lower (218.0 ± 5.5 vs 189.5 ± 5.5 beats/min); and RSNA not different than NT rabbits (14.9 ± 2.2 vs 9.9 ± 3.2% max RSNA). 4. ISO shifted AP-HR and AP-RSNA baroreflex curves to the left in NT and HT animals, and significantly attenuated baroreflex range and slope. At low ISO concentrations, baroreflex compensation for decreases in AP is limited to small increases in HR and sympathetic nerve activity. At higher ISO concentrations, baroreflex responses to decreases in AP are lost. RSNA responses to increases in AP are preserved with increasing ISO concentrations while HR responses are progressively attenuated. The sole effect of chronic hypertension was to shift the AP-HR and AP-RSNA barocurves to the right along the pressure axis in both conscious and ISO anaesthetized animals with no additional change in range or slope. 5. At this stage of hypertension development, ISO anaesthesia affects baroreflex function equally in normotensive and hypertensive rabbits.     

INTERACTIONS BETWEEN THE CIRCULATORY EFFECTS OF CENTRAL HYPOVOLAEMIA AND ARTERIAL HYPOXIA IN CONSCIOUS RABBITS

1. Eight conscious rabbits were repeatedly subjected to progressive reduction in central blood volume by gradually inflating a thoracic inferior vena caval-cuff so cardiac index (CI) fell at a constant 8.5% of baseline/min. 2. Caval-cuff inflations were performed after 10 min exposure to 100, 21, 12–14 and 8–10% O₂, with and without the addition of 3–4% CO₂, in randomized order. 3. The haemodynamic response to progressive reduction in central blood volume was biphasic. In Phase I, systemic vascular conductance index (SVCI) fell linearly, supporting mean arterial pressure (MAP). When CI had fallen to a critical level, Phase II occurred in which SVCI rose abruptly, MAP plummeted and respiratory drive progressively increased. 4. During Phase I, there were independent linear relationships between Pao₂ (but not Pao₂) and the rates at which SVCI and MAP changed during the progressive fall of CI. The higher the level of Pao₂, the greater was the rate of fall of SVCI and the less the rate of fall of MAP. 5. There was an inverted U-shaped effect of Pao₂, on the level of CI at which Phase II occurred: (a) during hyperoxia (100% O₂), Phase II occurred later than during normoxia (21% O₂); and (b) across the normoxic and hypoxic gas mixtures (21–8% O₂, with and without added CO₂), there was an independent linear relationship between Pao₂ (but not Pao₂ or Pao₂×Pao₂) and the level of CI at which Phase II occurred. That is, the lower the level of Pao₂, the later was the onset of Phase II. This interaction is best explained by an increased level of central sympathetic vasoconstrictor drive during hypoxia.     

EFFECTS OF RESPIRATION ON BLOOD PRESSURE AND HEART RATE VARIABILITY IN HUMANS

1. Non-invasive continuous finger blood pressure (BP) measurement and a spectral technique based on the Fourier transform (FT) were recently combined to quantify short-term fluctuations in haemodynamic variables. 2. Systolic BP (SBP) recording combined low frequency (LF, Mayer waves) plus high frequency (HF, respiratory) oscillations. The presence of HF oscillations of SBP probably reflects fluctuations in cardiac output. Heart rate (HR) also exhibited a combination of low and HF (respiratory) oscillations. The vagus nerve mediates the efferent control of the respiratory sinus arrhythmia (RSA). 3. During controlled breathing in a supine position, a change in SBP is associated with an opposite consequent change in HR. Respiratory sinus arrhythmia could therefore depend on the baroreceptor-HR response to underlying SBP oscillations. 4. The fast regulation of R-R interval by SBP through the baroreceptor-HR reflex may explain why the respiratory variations in the diastolic BP are small.     

EFFECTS OF NEUROPEPTIDE Y ON LEFT VENTRICULAR FUNCTION IN THE CONSCIOUS RABBIT

1. Changes in arterial pressure, heart rate and left ventricular contractility induced by intravenous injections of neuropeptide Y (NPY; 1-30 micrograms/kg) were studied in the conscious rabbit. 2. NPY has a brief pressor effect associated with a bradycardia, an increase in left ventricular end diastolic pressure, and a prolonged fall in peak left ventricular dP/dt (LVdP/dt). 3. The haemodynamic changes increase substantially with increasing doses up to 10 micrograms/kg. Beyond 10 micrograms/kg there are only slight effects on heart rate or peak LV dP/dt.     

NALOXONE BLOCKS THE CARDIAC EFFECTS OF MYOCARDIAL ISCHAEMIA AND REPERFUSION IN THE RAT ISOLATED HEART

The effects of naloxone on contractility and cardiac rhythm were studied in the rat isolated perfused heart during myocardial ischaemia and reperfusion. Pretreatment of the rat isolated perfused heart with naloxone abolished the reduction in left ventricular pressures and attenuated greatly the arrhythmias due to myocardial ischaemia and reperfusion. Administration of naloxone into the fibrillating rat isolated heart induced by myocardial ischaemia and reperfusion also attenuated the arrhythmias in a dose-dependent manner. The results indicate a possible involvement of the endogenous opioid peptides in the cardiac effects due to myocardial ischaemia and reperfusion. The antiarrhythmic effect of naloxone has great clinical implications.     

EFFECT OF ACUTE ADMINISTRATION OF PRAZOSIN ON BLOOD PRESSURE, HEART RATE AND PLASMA RENIN LEVEL IN THE CONSCIOUS NORMOTENSIVE RAT

This study investigated whether the specific alpha-antagonist, prazosin, stimulated basal plasma renin levels and heart rate. Furthermore the beta-adrenergic nervous system was also investigated to ascertain whether it was involved in this effect. Prazosin (0.1 or 1 mg/kg) was injected subcutaneously (s.c.) to conscious normotensive rats, either alone or in combination with the beta-adrenoceptor antagonist, DL-propranolol (1 or 3 mg/kg). Rats bore chronically implanted dorsal aorta cannula for measurement of blood pressure and heart rate and blood sampling for renin determinations. Acute administration of prazosin (1 mg/kg, s.c.) produced a fall in mean arterial pressure accompanied by renin release and tachycardia. A tenfold lower dose of prazosin did not alter blood pressure or heart rate but did stimulate renin release. Acute administration of DL-propranolol, (1 or 3 mg/kg, s.c.) produced falls in blood pressure and heart rate but did not affect plasma renin level. Combinations of prazosin with propranolol gave falls in blood pressure similar to those predicted on the basis of a simple addition of the effects of the two drugs given separately. Prazosin-induced tachycardia and renin release were attenuated by propranolol. It appears that prazosin produces renin release and tachycardia via stimulation of the beta-adrenergic adrenoceptor.     

EFFECTS OF P-CHLOROPHENYLALANINE ON BLOOD PRESSURE AND HEART RATE IN NORMAL RABBITS AND RABBITS WITH NEUROGENIC HYPERTENSION

SUMMARY 1. Intraperitoneal administration of p -chlorophenylalanine ( p CPA: 100–400 mg/kg per day) reduced central serotonin concentrations to 20–50% of control in the rabbit.
2. Intraperitoneal administration of a single dose of p CPA (400 mg/kg) decreased heart rate by 14% for a period of 1–2 days, but did not affect arterial pressure.
3. Repeated intraperitoneal administration of p CPA (100 mg/kg per day) caused a gradual reduction in arterial pressure to about 90% of control values over a 10 day period, but had no consistent effect on heart rate.
4. In rabbits that received repeated intraperitoneal injections of p CPA (100 mg/kg per day), the tachycardia that followed sinoaortic denervation was not as well sustained as in normal rabbits; the development of neurogenic hypertension was unaltered.
5. Intracisternal administration of p CPA was particularly toxic in the rabbit; the maximum doses tolerated did not succeed in lowering central serotonin concentration and had no effect on blood pressure or heart rate.     

THE INFLUENCE OF CAPTOPRIL AND NALOXONE ON THE VALSALVA MANOEUVRE AND SYSTOLIC TIME INTERVALS IN HEALTHY VOLUNTEERS

1. The aim of the study was to ascertain whether the inhibition of the sympathetic nervous system by angiotensin-converting enzyme (ACE) inhibitors is mediated by endogenous opioids. Naloxone was used to evaluate the effects of the latter on systolic time intervals (STI) and Valsalva manoeuvre-induced blood pressure and heart rate changes. 2. Baseline recordings were done in 12 healthy male volunteers and repeated 2h after oral administration of 75 mg of captopril and again after naloxone 0.4 mg/kg was administered intravenously over 10 min. 3. After captopril there was a significant reduction in systolic (P<0.02) and mean blood pressure (P<0.04) without any changes in heart rate. Furthermore, captopril increased the Valsalva ratio (P<0.06) but did not influence inotropism as indicated by STI. Naloxone did not influence any of these findings. 4. The changes in the Valsalva ratio after captopril were mediated by an increase in the maximum bradycardia in nine of the 12 subjects. 5. The results indicate that endogenous opioids do not play a role in the putative sympatholytic effect of ACE inhibition.     

COMPARISON OF METHODS FOR ELICITING THE BARORECEPTOR-HEART RATE REFLEX IN CONSCIOUS RABBITS

1. Two methods were used for altering blood pressure in conscious rabbits by up to ± 30 mmHg from the resting level in order to characterize the barorecep-tor-heart rate reflex. These were to inflate descending aortic or inferior vena caval cuffs, or to give brief intravenous infusions of phenylephrine or glycerol trinitrate. The relation of change in blood pressure to change in heart interval was examined, both during the initial ‘ramp’ changes of these variables and when they had reached a ‘steady-state'. 2. Both methods allowed the construction of'steady-state’ sigmoid stimulus-response curves whose parameters were reproducible within animals, and which were attended by a relatively small variance between animals. The inflatable-cuff method gave a higher average value for maximum gain than the vasoactive drug method (10.0 v 5-4 ms/mmHg) and a narrower pressure range between the threshold and saturation points of the response, but values for the other parameters were similar. Corresponding parameters obtained by the two methods correlated closely. 3. After denervating all arterial baroreceptors except one carotid sinus, ‘steady-state’ maximum gain by cuff-inflation was reduced to 3.1 ms/mmHg, and to 2-6 ms/mmHg by the vasoactive drug method. The heart interval range between upper and lower plateau levels was reduced, but the pressure range between threshold and saturation points was widened, with both methods. 4. During the initial ‘ramp’ changes of blood pressure the sensitivity of the reflex was described by the slope of the linear regression of heart interval on ‘mean blood pressure. The slopes obtained by aortic cuff inflation, and by infusion of either vasoactive drug, correlated positively with ‘steady-state’ maximum gain. However, the reproducibility of the ‘ramp’ method was inferior to that of the ‘steady-state’ method with respect to reflex sensitivity, and other parameters of the stimulus-response relation cannot be estimated. 5. Complete baroreceptor denervation virtually eliminated heart rate changes over the range of blood pressures usually employed. However, when blood pressure was increased by more than 40 mmHg a profound reflex bradycardia and hypopnoea were then evoked.     

EFFECT OF BREATHING PATTERN ON BLOOD PRESSURE AND HEART RATE OSCILLATIONS IN HUMANS

1. The relationships of respiratory sinus arrhythmia (RS A) and respiratory changes in systolic blood pressure (SBP) to tidal volume (V_T) and breathing frequency (BF), were quantified during voluntary control of V_T and BF in healthy subjects. 2. Respiration was measured non-invasively with a respiratory inductive plethysmograph, which was calibrated prior to each study while breathing through a pneumotachygraph. Finger arterial blood pressure was measured non-invasively by the Finapres. 3. Heart rate (HR) increased during inspiration, with a nearly fixed time delay for most V_T and BF approximating 0.9 s. The magnitude of RS A increased with increases in V_T and with decreases in BF. SBP decreased during inspiration, with a time delay which increased as BF decreased, resulting in a phase delay approximating 160°. The magnitude of the inspiratory fall in SBP increased with increases in V_T. Increased amplitudes of RSA and SBP variation occurred at the lowest BF, consistent with the possibility of interactions between respiratory-related influences and those due to ‘slow waves’ of vasomotor tone. 4. The present results are consistent with the conclusion that respiratory effects on SBP are caused by a mechanism other that simply changes in HR.     

TIME COURSE OF CHANGES IN BARORECEPTOR REFLEX CONTROL OF HEART RATE IN CONSCIOUS SHR AND WKY: CONTRIBUTION OF THE CARDIAC VAGUS AND SYMPATHETIC NERVES

1. The aim of this study was to assess the vagal and sympathetic nerve contribution to the relationship between mean arterial pressure (MAP) and heart rate (HR) at 6, 9, 14 and 20 weeks of age in conscious Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) with methoxamine- and nitroprusside-induced steady-state changes in blood pressure. 2. MAP increased with age in both strains but was 17-23% higher in SHR. 3. By contrast baroreflex parameters (HR range: difference between upper and lower HR plateaus, and gain: average slope between inflection points of the logistic MAP-HR relationship) decreased with age in SHR but increased in WKY. 4. After methylatropine, no differences in the cardiac sympathetic baroreflex range or gain parameters were observed between strains or ages. 5. It was concluded that older SHR have normal sympathetic but reduced vagal capacity to control HR in response to changes in MAP, but that this deficit was not dependent on the absolute level of blood pressure. 6. Because the differences were confined to one effector, SHR may have different central rather than arterial baroreceptor afferent mechanisms.     

THE EFFECT OF EPANOLOL ON INTRA-ARTERIAL AMBULATORY BLOOD PRESSURE AND BARORECEPTOR HEART RATE REFLEX IN ESSENTIAL HYPERTENSION

1. The effect of chronic treatment with epanolol, a new cardioselective beta-adrenoreceptor antagonist with moderate beta 1-selective intrinsic sympathomimetic activity (ISA), on 24 h ambulatory intra-arterial blood pressure (24 h IABP) and the sino-aortic baroreceptor heart rate (SAB/HR) reflex was investigated in six hypertensive subjects. 2. All subjects demonstrated a greater than 10% reduction in mean arterial pressure with atenolol therapy (100 mg once daily) before entering a randomized, double-blind, placebo-controlled, crossover protocol with epanolol (100 mg twice daily for 4 weeks). 3. Epanolol treatment at this dose was not associated with significant reduction in systolic or diastolic 24 h IABP or heart rate. There was no change in SAB/HR reflex set point, sensitivity or latency with epanolol. 4. beta 1-selective ISA may be undesirable in beta-adrenoceptor antagonists used to treat hypertension.     

EFFECTS OF CLONIDINE ON BLOOD PRESSURE AND HEART RATE RESPONSES TO AN EMOTIONAL STRESS IN THE RAT: A SPECTRAL STUDY

1. The fluctuations that underlie the spontaneous variability of blood pressure (BP) and heart rate (HR) were investigated in conscious normotensive rats using power spectral analysis. 2. Air jet stimulation determined a significant BP rise associated with a tachycardia. This environmental mild stressor amplified the 195-605 mHz oscillations of HR which are under autonomic control. No habituation to this stressor was observed since a second stimulation determined similar responses. 3. Clonidine (10 micrograms/kg, i.v.) prevented the BP rise normally associated with air jet stimulation. In addition, clonidine dramatically reduced the amplitude of BP and HR oscillations in the frequency region of 195-605 mHz. 4. It is concluded that a mild emotional stressor elicits in normotensive rats a rise in BP and HR associated with modified spectral profiles reflecting sympathetic hyperactivity. Clonidine minored the effects of stress on BP and HR variability and also prevented BP elevation.