Biomedical subjects

D C Randall

Publications and source records attributed to D C Randall.

At least 37 records · Page 2Linked to original sources

PubMed1992

Inspection of veterinary biologics in the United States.

Inspection of veterinary biologics in the United States (U.S.) has changed significantly over the years since the Virus-Serum-Toxin Act (V-S-T) was passed by the U.S. Congress in 1913. At first, government inspectors were appointed to every production location, observing the preparation, testing and initial shipment of veterinary biologics. In the 1950s, a new plan was developed to provide a more scientific basis of inspection. Over a 10-year period, a programme to test finished products at the National Veterinary Services Laboratories and a new procedure for inspecting facilities and products was implemented. Our current programme retains our extensive pre-licensing review of products, labeling, facilities and personnel and adds the new inspection system of random checking of finished batches, unannounced in-depth inspections, control of product batches and post-licensing monitoring. This combination of activities ensures that pure, safe, effective and economical veterinary biologics are available for use in the U.S.

Animals↗

PubMed1991

SA nodal parasympathectomy delineates autonomic control of heart rate power spectrum.

The purpose of this study was to quantify the relative roles of the canine cardiac parasympathetic and sympathetic nerves in controlling the distribution of power within the heart rate (HR) power spectrum using a highly selective surgical technique to parasympathectomize the SA node. DAta were recorded in awake dogs (n = 6) before and after the selective denervation; the animals were isolated from human contact and their behavior carefully monitored during the measurements. The average amplitude in the high-frequency (approximately 0.32 Hz) peak in the HR power spectrum decreased from a predenervation control of 2.68 +/- 1.54 (mean +/- SD, arbitrary units) to 0.07 +/- 0.06 (P less than 0.05). Corresponding resting HR increased from 80 +/- 9 to 106 +/- 16 beats/min (P less than 0.05). The low-frequency peak (approximately 0.02 Hz) also decreased from a control of 2.45 +/- 1.18 to a postparasympathectomy value of 1.25 +/- 0.92 (P less than 0.05). beta-Adrenergic blockade (propranolol, 1 mg/kg) further decreased the latter peak to 0.59 +/- 0.52 (P less than 0.05). These data directly demonstrate that the high-frequency peak of the HR power spectrum 1) results from parasympathetic control of SA nodal automaticity, while 2) the low-frequency peak reflects activity in both divisions of the autonomic nervous system.

Adrenergic beta-Antagonists↗

PubMed1991

Angiotensin II does not contribute to rapid reflex control of arterial pressure.

Pharmacological blockade of the renin-angiotensin converting enzyme reportedly alters the heart rate (HR) power spectrum in conscious dogs, suggesting that these hormones contribute to the short-term regulation of arterial blood pressure. We tested this possibility using four independent procedures. First, HR power spectrum was determined in seven awake dogs before and after administration of enalaprilat (300 ng/kg), a converting-enzyme inhibitor. There were no significant changes in the average amplitude for the spectral peak between 0.003 and 0.1 Hz (i.e., the "low-frequency peak"). Second, the HR power spectrum was measured in 11 awake rabbits before and after treatment with deoxycorticosterone acetate (1 mg.kg-1.day-1) and salt (0.9% saline ad libitum) for 7 days to depress plasma renin levels. There were no significant changes in the amplitude of the HR power spectrum, although mean HR decreased from 206 +/- 3 to 184 +/- 4 beats/min after treatment. In the third experiment, another group of rabbits (n = 8) was tested after 2 wk on a low-salt diet to elevate plasma angiotensin levels and then after 2 wk on a normal salt diet. Once again there were no significant effects on the HR power spectrum. Finally, tranquilized dogs (n = 9) were subjected to sinusoidally varying lower body negative pressure at selected frequencies of 0.008-0.12 Hz. Tests were conducted in the control state and after administration of an angiotensin receptor antagonist (saralasin, 1 microgram.kg-1.min-1). Lower body negative pressure-induced fluctuations in arterial blood pressure were similar in both states. We find no evidence for the role of the renin-angiotensin system in the moment-to-moment regulation of arterial pressure and HR.

Angiotensin II↗

PubMed1990

A temporally detailed reanalysis of the conditional heart rate response in dog.

We used rapid (500 Hz) digital sampling to derive a detailed analysis of the HR conditional response in dog (n = 11) to a 30-sec tone (CS+) followed by a 1/2-sec shock. We found an initial bradycardia at 1.5 +/- 1.0 sec in 6 of 11 dogs from a pre-CS+ control of 85 +/- 26 bpm (mean +/- SD) to 74 +/- 25 bpm (p less than 0.05). In 9 of the 11 dogs there was a subsequent rapid (19.9 +/- 6.7 bpm/sec) increase (+26 +/- 10 bpm) in HR lasting from 1.3 +/- 0.9 to 2.7 +/- 1.0 sec. This was followed by a second, larger (+41 +/- 16, p less than 0.05), but slower (4.0 +/- 2.4 bpm/sec, p less than 0.05) tachycardia which lasted from 4.9 +/- 1.0 to 13.5 +/- 2.6 sec. The peak HR (131 +/- 27 bpm) was attained at 15.0 +/- 3.8 sec, after which HR fell slowly (-2.4 +/- 1.4 bpm/sec) to an average of 92 +/- 29 bpm at 28.6 +/- 1.4 sec (i.e., approximately 1.4 sec prior to shock delivery). This analysis revealed trends in the conditional HR response which were not discernible in individual trials and were obscured in the more traditional analyses of the conditional HR response.

Animals↗

PubMed1990

Hemodynamic and arrhythmogenic effects of aversive stress during myocardial ischemia.

Pavlovian conditioning was accomplished in two groups of dogs by following a 30-s tone (the CS+) with a short (less than or equal to 1 s) electric shock). An inflatable occluder was implanted around the left circumflex coronary artery in all animals. The CS+ was presented to Group I dogs (n = 6) during control (i.e., no coronary occlusion) and at 30 s and 3 min after the onset of a 4-min left circumflex coronary occlusion. The CS+ evoked a robust increase in heart rate and blood pressure in the control state. A conditional cardiovascular response was still evoked during the acute coronary occlusion despite the evolving myocardial ischemia. No increase in ventricular ectopic beats occurred during the CS+. An anterior myocardial infarction (16.8 +/- 1.7% of left ventricular mass, mean +/- SEM) was created in Group II dogs (n = 8) at the time of surgery. A CS+ was presented, as above, both alone and 1 min after the beginning of a 2-min left circumflex coronary occlusion. There were significant differences in the conditional response in heart rate, left ventricular (systolic) pressure (LVP) and d(LVP)/dt for trials given during the coronary occlusion compared with no occlusion. These dogs were then classified as 'resistant' or 'susceptible' to ventricular arrhythmias approx. 4 weeks later using an exercise and coronary occlusion test. Three of five susceptible dogs, but none of three resistant dogs, evidenced increased severity of arrhythmias during the CS+. We conclude that the nature of the cardiovascular response to behavioral stress during myocardial ischemia depends in part upon the timing of the CS+, the presence or absence of a resident myocardial infarction and the status of the autonomic reflexes controlling the heart.

Animals↗

PubMed1990

Coronary alpha-adrenergic tone and contraction of ischemic myocardium in awake dog.

The effect of neurogenic coronary vasomotor tone upon contraction in ischemic myocardium was investigated in awake, mongrel dogs. The animals were chronically instrumented with a hydraulic occluder around the left circumflex coronary artery; a small catheter was also implanted within the vessel. Ultra-sound crystal pairs were placed distal to the occluder in myocardium perfused by the left circumflex artery. Pacing electrodes were sutured onto the right ventricular conus. During the experiment (n = 6) the occluder was inflated to stenose the vessel; the imposition of cardiac pacing (210/min) in conjunction with this stenosis resulted in depressed contraction of the myocardium distal to the occluder as assessed by the ultra-sound crystals: Segmental shortening decreased to 45.4 +/- 5.4% of unpaced control. Phentolamine, an alpha-antagonist, was then infused into the left circumflex catheter for ten minutes (0.1 mg/min) and the experiment repeated. After the alpha-blockade the combination of coronary stenosis and heart rate pacing decreased segmental shortening to only 84.6 +/- 10.1% of control, which was significantly (P less than 0.01) improved relative to the unblocked condition. In another experiment (n = 4), a less severe stenosis was imposed upon the left circumflex vessel. During pacing, muscle shortening decreased to 94 +/- 8.5% of control. Infusion of phenylephrine, an alpha-agonist, for ten minutes (0.1 mg/min) resulted in a 56.7 +/- 5.9% decrease in shortening during pacing; this was significantly greater (P less than 0.01) than the previous decrease. These data indicate that coronary alpha-adrenergic tone can significantly compromise regional myocardial function even in ischemic muscle whose coronary blood flow reserve has been exhausted.

Animals↗

PubMed1990

Experience with a physiology workshop for high school and college teachers.

Science education in the United States at all academic levels is widely perceived to need direct assistance from professional scientists. The current dearth of quality applicants from this country to medical and graduate schools suggests that our existing undergraduate and high school science curriculum is failing to provide the necessary stimulus for gifted students to seek careers in the health sciences. Recognizing the need to become more directly helpful to high school and college science teachers, members of the faculty of the Department of Physiology and Biophysics at the University of Kentucky College of Medicine held a 5.5-day Physiology Summer Workshop during June, 1989. Participants included 25 college teachers from Kentucky and 5 other states plus 22 Kentucky high school teachers. The presence of the two levels of educators provided communication about curricular concerns that would be best addressed by mutual action and/or interaction. Each day's activities included morning lectures on selected aspects of organ system and cellular physiology, a series on integrative physiology, and afternoon laboratory sessions. The laboratory setting allowed the instructor to expand on principles covered in lecture as well as provided the opportunity for in-depth discussion. A selection of evening sessions was presented on 1) grants available for research projects, 2) obtaining funds for laboratory equipment, and 3) graduate education in physiology.

Capital Financing↗

PubMed1990

Influence of cardiac innervation on intrinsic heart rate in dogs.

Intrinsic heart rate is defined as the rate at which the heart beats when all cardiac neural and hormonal inputs are removed. We determined the effect of prevailing autonomic innervation of the heart on the intrinsic heart rate in chronically maintained, sedated, normally innervated dogs (n = 14), and in 14 other dogs that had previously (greater than 12 day) undergone complete surgical cardiac denervation. Intrinsic rate was determined in both groups using the following two procedures: 1) pharmacological effector blockade; and 2) pharmacological ganglionic blockade. The intrinsic rate determined by effector blockade was 142.9 +/- 7.2 (SE) beats/min in the dogs with intact cardiac innervation. When the same treatment was given after total surgical cardiac denervation, intrinsic rate was 97.9 +/- 4.8 beats/min. Intrinsic heart rate was significantly (P less than 0.05) lower in surgically denervated dogs. Ganglionic blockade in surgically denervated animals yielded an intrinsic rate of 90.0 +/- 8.5 beats/min, which was again significantly lower than the corresponding value of 128.4 +/- 5.5 beats/min in normal dogs. There was no difference in the intrinsic heart rate as determined by effector vs. ganglionic blockade in either group of dogs. An additional six dogs were subjected to selective surgical sinoatrial nodal parasympathectomy; their intrinsic rate (effector blockade) in the conscious state was 115.8 +/- 4.3 beats/min; this was significantly lower than the corresponding value for normal dogs and significantly greater than in dogs subject to total surgical cardiac denervation. The lower rate observed in the totally denervated and selectively denervated dogs after effector and/or ganglionic blockades implies that intrinsic heart rate depends on the level or nature of prevailing autonomic activity.

Animals↗

PubMed1990

Modulation of baroreflex by varying insulin and glucose in conscious dogs.

We developed a conscious, chronically instrumented canine preparation (n = 5 dogs) in which insulin concentration was precisely controlled to study the effects of controlled variations of plasma insulin and glucose concentrations on cardiac responses to bilateral carotid occlusion and dobutamine. Endogenous insulin secretion was reduced to negligible levels using alloxan and then replaced by continuous, constant intravenous insulin infusion at a rate (0.625 +/- 0.115 U/h) sufficient to maintain fasting normoglycemia (85 +/- 9 mg/100 ml); plasma immunoreactive insulin (IRI) in this basal "normal insulin, normal glucose" (NI,NG) condition was 0.362 +/- 0.45 ng/ml (NS vs. prealloxan fasting concentration). A fivefold increase of IRI from NI,NG levels with normoglycemia maintained (5 x NI,NG) reduced (P less than 0.05) the maximal first time derivative of left ventricular pressure (LV dP/dtmax) from 3,010 +/- 62 to 2,398 +/- 91 (SE) mmHg/s but had no effect on LV dP/dtmax when plasma glucose was elevated to 298 +/- 25 mg/100 ml (5 x NI,HG). The LV dP/dtmax increase during bilateral carotid occlusion (BCO) in the NI,NG state of 124 +/- 17 mmHg/s was significantly reduced (P less than 0.05) in the 5 x NI,HG state to 58 +/- 18 mmHg/s but was not altered in the 5 x NI,NG state. Reduction of plasma insulin to one-fifth of the normal fasting level had no effect on basal cardiac function or the responses to BCO. There were no other statistically significant effects of insulin or glucose concentration on cardiovascular responses to BCO or to infusion of dobutamine. Our data indicate that physiologically realistic variations in plasma IRI and glucose concentrations interact and may modulate cardiovascular responses to changes in autonomic nervous activity, even though previously reported effects of pharmacological doses of insulin were not observed.

Alloxan↗

PubMed1989

Selective vagal postganglionic innervation of the sinoatrial and atrioventricular nodes in the non-human primate.

The distribution of parasympathetic postganglionic nerves to the atrioventricular (AVN) and sinoatrial nodal (SAN) regions was investigated in the non-human primate heart. Eight male monkeys (Macaca fascicularis) weighing 5.5-7.0 kg. were anesthetized (alpha-chloralose, 50 mg/kg and urethane, 500 mg/kg) and instrumented to measure arterial pressure, electrocardiogram, atrial and ventricular electrograms. The cervical vagi were electrically stimulated (20 Hz, 4 V, 2 ms) before and after selective denervation (D) of the AVN and/or SAN. Vagal stimulation was repeated during atrial pacing to assess parasympathetic modulation of AVN conduction. Ablation of parasympathetic pathways to the AVN, accomplished by the disruption of the epicardial fat and surface muscle layer at the junction of the inferior vena cava and inferior left atrium eliminated (P less than 0.01) the dromotropic effects of vagal stimulation without affecting the heart rate response (right vagus, before D, paced: atrial rate 218.0 +/- 6.3, ventricular rate 67.1 +/- 23.7; after D: atrial rate 210.3 +/- 6.4, ventricular rate 210.3 +/- 6.4 beats/min, means +/- S.D.). In sharp contrast, surgical dissection of the fat pad overlying the right pulmonary vein-superior vena cava junction significantly (P greater than 0.01) attenuated negative chronotropic effects of vagal stimulation (left vagus, before D the R-R interval increased by 832.7 +/- 146.4 ms, 209.5% increase; after D 37.4 +/- 18.0 ms, 8.8% increase). These data demonstrate discrete vagal efferent pathways innervate both the SAN and AVN regions of the non-human primate heart.

Animals↗

PubMed1989

Human Pavlovian HR decelerative conditioning with negative tilt as US: a review of some S-R, stimulus-substitution evidence.

Interest in human Pavlovian heart rate (HR) conditioning with conventional shock and loud noise unconditional stimuli has declined, as measured by reports in the literature. Accompanying this decline have been the following views: (a) that HR should be abandoned as a psychophysiological index of the psychological (learning) process of Pavlovian conditioning; (b) that, following psychology's shift to a more cognitive emphasis, the self-regulation (S-R), stimulus-substitution view of pavlovian conditioning is wrong, because there is no equivalence in direction between shock- and loud noise-induced HR-accelerative unconditional response and the conditional response. This paper reviews recent reports of human Pavlovian conditioning of HR deceleration with negative tilt as the unconditional stimulus. The results support an S-R, stimulus-substitution interpretation of conditioning. In addition, these studies have potential therapeutic application in the teaching of (medically desirable) HR deceleration, especially when Pavlovian procedures are combined with instrumental (biofeedback) ones. However, such physiological aspects of the decelerative unconditioned response as the degree of vagal involvement are difficult to investigate in the human preparation.

Arousal↗

PubMed1989

Human Pavlovian HR-decelerative conditioning with negative tilt as US: evidence of vagal and sympathetic influences on the UR in dogs.

Following a review of studies employing negative tilt in human Pavlovian conditioning of heart rate (HR) deceleration (Furedy et al, in press), this paper reports data based on animal subjects on such physiological aspects of the decelerative unconditioned response (UR) as the degree of vagal involvement. Five anesthetized dogs underwent 90 degrees negative body tilts pre- and postbilateral vagotomy, while interbeat interval (IBI), left ventricular pressure (LVP) and its first derivative, d(LVP)/dt, which is a measure of sympathetic cardiac drive, were recorded. Consistent with the vagal interpretation of the tilt-induced decelerative UR, the results indicated that vagotomy markedly changed the tilt-induced bradycardic reflex from a fast-recruiting, large-magnitude (over 45%), and sustained (throughout the 20-27-s tilt) IBI increase, to slower-recruiting, and markedly smaller (less than 5%) IBI increase. However, there was also evidence of an initial sympathetic excitation of about 5 s, as indicated by a 45% increase in d(LVP)/dt, which returned to baseline level by 9 s following tilt onset. Vagotomy increased this tilt-induced sympathetic excitation to about 100%, and it remained at above 70% throughout the tilt. Prevagotomy LVP showed a slight (about 10%) and delayed (about 6 s following tilt onset) depressor response, which was eliminated by vagotomy. Finally, unaveraged data from individual dogs suggested that prevagotomy, LVP changes preceded IBI changes. Regarding implications of these results for human HR deceleration-inducing preparations, we conclude that the different physiological mechanisms that accompany and/or produce a given change in HR need continuing investigation with multiple dependent physiological variables (which are assessed for topographical differences), and in both human and animal preparations.

Animals↗

PubMed1989

Stability of the heart rate power spectrum over time in the conscious dog.

The purpose of this experiment was to test the stability of the heart rate (HR) power spectrum over time in conscious dogs. HR was recorded for 1 h for each of six animals on 2 days. A Fast Fourier transform was used to derive the HR power spectrum for the 12 contiguous 5-min epochs comprising the 1-h recordings. Changes in frequency and amplitude of the various spectral peaks were quantitatively examined. We confirm the presence of two major concentrations of power centered around 0.02 (low frequency peak) and 0.32 Hz (high frequency peak). However, we observed variations in these spectral peaks, especially their amplitudes, both within each hour and from day 1 to day 2. The amplitudes of these two spectral peaks tended to vary reciprocally. HR power spectra based on 5 min of recorded data were also derived from an additional eight animals in both the lying and standing positions; the power spectra from these short recordings were sufficiently sensitive to detect redistributions in power due to changes in posture in all eight dogs. We conclude that: 1) data should be recorded for relatively long periods (e.g., 1 h) to characterize the HR power spectrum; 2) some variability in frequency and amplitude will persist across spectra even when based on longer data bases; 3) care should be taken to ensure that the subject's behavioral state is stable within the recording period; 4) shorter (e.g., 5 min) data bases are not suitable except for detecting relatively robust changes in the HR power spectrum.

Animals↗

PubMed1989

A dynamic analysis of cardiovascular regulation using sinusoidal acceleration in dogs.

Control of cardiovascular function during time-dependent pooling of blood in the upper and lower body was studied in intact dogs (n = 5) and in dogs in which hearts had been surgically denervated (n = 5). The animal was positioned horizontally on a platform mounted on the arm of a centrifuge; rotation of the platform at one of nine rates with a period ranging from 3.3 min to 4 s exposed the subject to a sinusoidally varying force (+/- 2 g) that periodically translocated blood from the chest to the lower quarters and back again. The resulting oscillatory changes in arterial blood pressure (BP), cardiac output, stroke volume, heart rate (HR), and peripheral resistance (PR) were analyzed using a fast Fourier transform. Normal dogs were superior to cardiac-denervated dogs in minimizing arterial BP fluctuations, especially in the midfrequency range (i.e., approximately 0.032 Hz); after pharmacological alpha-, beta-, and muscarinic-receptor blockade, the BP oscillations were similar in the two groups. The unblocked denervated dogs regulated BP poorly primarily because of their inability to 1) make appropriately timed changes in HR and 2) minimize inappropriate oscillations in SV. Both groups of dogs in the unblocked state showed large appropriately timed PR fluctuations at the lower frequencies, which minimized BP oscillations; these became less optimally timed as acceleration frequency increased, thereby potentiating the natural disposition for BP to oscillate at the acceleration frequency. Afferent information from cardiac receptors did not appear to be essential for controlling this aspect of vascular function.

Animals↗

PubMed1989

Microprocessor-based analysis of sympathetic nerve traffic.

Two systems based on microcomputers with analog-to-digital (A/D) converters were developed to measure sympathetic nerve activity. The first utilized a relatively inexpensive computer and A/D converter and an analog technique to count nerve traffic "spikes" above a reference voltage. The second system, which required a more expensive microcomputer and A/D converter, used digital methods exclusively to count spikes and integrate nerve activity. These systems produced accurate and reliable indexes of nerve traffic. The digital system could also be used to store the nerve signal to magnetic disk, thereby allowing the later use of more complex analytical procedures and the possibility of comparing the results of different analyses performed upon a single data set.

Animals↗

PubMed1988

Effect of Innovar upon the autonomic control of the heart in intact dog.

This experiment compares the regulation of cardiac function in dogs before and after administration of a drug (Innovar-Vet, 0.05 ml/kg) that produces a state of 'neuroleptanalgesia'. All animals (n = 21) were chronically instrumented to measure arterial blood pressure (BP) and heart rate (HR); left ventricular pressure (LVP, n = 10) and ascending aortic flow (n = 4) were also recorded in some animals. After Innovar, the dogs became somnolent and tolerated minor surgical procedures. The paO2 decreased (95 +/- 11 vs 90 +/- 8 mm Hg, pre- vs post-Innovar, mean +/- S.D.; P less than 0.05) while paCO2 increased (33 +/- 5 vs 36 +/- 5 mm Hg; P less than 0.05) when measured (n = 6) 10 min after drug administration. The changes in HR and BP during a 5-min, left circumflex coronary artery occlusion (n = 15) were virtually identical in the awake and sedated states; likewise, no significant differences were detected in the occlusion-induced changes in BP, HR, d(LVP)/dt and stroke volume in the subset of more fully instrumented dogs. However, some significant effects were seen when the Innovar dose was increased to 5 times normal. The effects of bilateral carotid occlusion and dobutamine infusion (8, 16 and 30 mg/kg) were tested in another 7 dogs. Once again, the analysis of variance interaction terms testing the reflex or drug-induced changes in HR, BP and d(LVP)/dt before vs after sedation were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

An analysis of the haemodynamic effects of tolbutamide in conscious dogs.

1. In conscious chronically instrumented dogs, tolbutamide (5-45 mg/kg) induced significant dose-related increases in mean arterial pressure and left ventricular end-diastolic pressure. 2. Cardiac output was decreased while heart rate, d(LVP)/dt, and regional myocardial performance at the left ventricle were not significantly affected. Computed total peripheral resistance was increased. 3. Pretreatment with the alpha-antagonist phentolamine (1-1.5 mg/kg) abolished the pressor response. Furthermore, the pressor response to norepinephrine (0.1 microgram/kg) was enhanced by pretreatment with tolbutamide (45 mg/kg). 4. In an isolated tissue preparation using ring segments of canine femoral arteries, neither tolbutamide nor its major hepatic metabolites (carboxytolbutamide, p-toluene-sulfonamide and p-toluene-sulfonylurea) caused any smooth muscle contraction. However, pretreatment of these tissues with 10(-4), 10(-3), or 10(-2) mol/l tolbutamide potentiated the contractile response to norepinephrine by up to 19% and to phenylephrine by up to 8%. 5. It was concluded that the pressor effect of tolbutamide arises by potentiating the alpha-adrenoceptor mediated vasoconstrictor action of circulating endogenous catecholamines.

Adrenergic alpha-Antagonists↗

PubMed1988

Endurance training in dogs increases vascular responsiveness to an alpha 1-agonist.

The effects of endurance training on vascular responsiveness to an alpha 1-agonist and the associated changes in baroreflex modulation of heart rate and vascular resistance were studied. Graded dosages of phenylephrine were given to eight treadmill-trained dogs and to eight untrained dogs; both groups were chronically instrumented and were sedated and resting when tested. These dosages were repeated after ganglionic blockade. Aortic pressure, cardiac output, central venous pressure, peripheral resistance, and heart rate were each averaged over 30 s before injection and 90 s after injection. The slope of the peripheral resistance-dose relationship was significantly increased in trained compared with untrained dogs in both the unblocked and blocked cases [unblocked: trained 0.89, untrained 0.47; blocked: trained 4.30, untrained 2.05 (mmHg.l-1.min)/(microgram.kg-1)]. The unblocked resistance slopes were reduced with respect to the blocked slopes by 77 (untrained) and 79% (trained). The slope of the heart rate-aortic pressure response was reduced, but not significantly, by endurance training. We conclude that 6 wk of endurance training in dogs resulted in a doubling of the vascular responsiveness to an alpha 1-agonist, with no significant change in the baroreflex regulation of resistance or heart rate.

Animals↗