Role of vasopressin in blood pressure regulation in conscious water-deprived dogs

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.     

Blood pressure control in arterial- and cardiopulmonary receptor denervated dogs.

The mechanisms influencing arterial blood pressure and heart rate were studied in conscious foxhounds after chronic sino-aortic and cardiopulmonary denervation (N = 6). In previous investigations it was shown, that this denervation produces hypertension and tachycardia, which is confirmed by the present study: Mean arterial blood pressure increased from 101 +/- 3 to 123 +/- 6 mmHg (P less than 0.05), and heart rate rose from 85 +/- 6 to 124 +/- 5 beats min-1 (P less than 0.001). The variability of mean arterial blood pressure, but not that of heart rate increased (from 6 +/- 1 to 22 +/- 2 mmHg (P less than 0.001). The administration of the alpha-adrenergic blocker prazosin reduced both mean arterial blood pressure (-33 +/- 8 mmHg, P less than 0.01) and its variability (-12 +/- 1 mmHg, P less than 0.01), thus suggesting an alpha-adrenergic mediated hypertension. beta-blockade by propranolol blunted the heart rate increase (-24 +/- 5 beats min-1, P less than 0.05). Although plasma renin activity increased in the denervated dogs, converting enzyme inhibition had little effect on mean arterial blood pressure and heart rate. In conclusion, chronic sino-aortic and cardiopulmonary denervation enhances the alpha and beta-adrenergic component of cardiovascular control in a different fashion. While the alpha-adrenergic component induces fluctuations around an elevated arterial blood pressure level, the beta-adrenergic tone to the heart increases without any significant increase in variability.     

alpha- and beta-Adrenergic effects of epinephrine on ventricular pacemakers in dogs

We studied the effects of epinephrine on idioventricular rhythm in 15 adult dogs with chronic complete heart block induced by the injection of formalin into the His bundle. Atropine (0.1 mg/kg) was given intravenously to attenuate any potential vagal effects, and epinephrine was infused in graded doses of 0.01-10.0 micrograms.kg-1.min-1. Two different responses were seen. In 12 dogs there was a concentration-dependent increase in ventricular rate following epinephrine infusion. These animals then were given the beta-blocker propranolol (0.5 mg/kg iv), and the epinephrine infusions were repeated. In this situation epinephrine concentrations less than 0.1 micrograms.kg-1.min-1 induced a decrease in ventricular rate with no associated change in arterial pressure. In four additional dogs this decrease in ventricular rate was prevented by alpha-blockade with phentolamine. In three dogs epinephrine less than 0.1 micrograms.kg-1.min-1 induced a decrease in ventricular rate without an associated change in arterial blood pressure. This decrease in rate was abolished by the alpha-blocker phentolamine. It therefore appears that an alpha-adrenergic effect on ventricular automaticity can occur in the intact animals. When this does not occur initially, it can be unmasked by propranolol and results in a slowing of ventricular rate unrelated to changes in blood pressure.     

The separate and combined influences of common carotid occlusion and nonhypotensive hemorrhage on kidney blood flow

The separate and combined effects of bilateral common carotid occlusion (C.C.O.) and hemorrhage on renal blood flow (R.B.F.) were studied in 11 unanesthetized dogs.C.C.O. increased arterial blood pressure (4.4 kPa; 33 mm Hg) and heart rate (10 beats/min) while R.B.F. remained unchanged. When kidney perfusion pressure was maintained at its resting level during C.C.O. (implanted pneumatic cuff) there was also no change in R.B.F.After cutting the aortic nerves in 2 dogs the increase in blood pressure and heart rate with C.C.O. was greater (10.6 kPa; 80 mm Hg and 72 beats/min); however, there was no change in R.B.F.A blood loss of 16% (13.6 ml/kg) reduced central venous pressure (0.3 kPa; 2 mm Hg), increased heart rate (8–14 beats/min) and decreased arterial mean pressure by a maximum of 0.7 kPa (5 mm Hg) (nonhypotensive hemorrhage, N.H.H.). R.B.F. showed a tendency to rise and 90 min after the onset of bleeding was slightly increased (12% of control).After N.H.H. carotid occlusion had no effect on R.B.F. when kidney perfusion pressure increased; when perfusion pressure was controlled during C.C.O. the maximum observed decrease of R.B.F. was 15 ml/min (5% of control).It is concluded that the control of R.B.F. during the baroreceptor reflex under normovolemia and after a blood loss of 16% in the conscious dog at rest does not involve sympathetic vasoconstrictor effects which result in a significant changes in total blood flow.This study was supported by the German Research Foundation within the S.F.B. 90, Heidelberg     

Reflex responses in plasma catecholamines caused by static contraction of skeletal muscle.

To examine a hypothesis of whether static muscle contraction produces a release of catecholamines from the adrenal medulla via reflex stimulation of preganglionic adrenal sympathetic nerve activity induced by receptors in the contracting muscle, we compared the reflex responses in a concentration of epinephrine (Ep) and norepinephrine (NEp) in arterial plasma during static contraction and during a mechanical stretch of the hindlimb triceps surae muscle in anesthetized cats. Static contraction was evoked by electrically stimulating the peripheral ends of the cut L(7) and S(1) ventral roots at 20 or 40 Hz. Mean arterial pressure (MAP) and heart rate (HR) increased 23 +/- 3.1 mmHg and 19 +/- 4.3 beats/min during static contraction. Ep in arterial plasma increased 0.18 +/- 0.072 ng/ml over the control of 0.14 +/- 0.051 ng/ml within 1 min from the onset of static contraction, and NEp increased 0.47 +/- 0.087 ng/ml over the control of 0.71 +/- 0.108 ng/ml. Following a neuromuscular blockade, although the same ventral root stimulation failed to produce the cardiovascular and plasma catecholamine responses, the mechanical stretch of the muscle increased MAP, HR, and plasma Ep, but not plasma NEp. With bilateral adrenalectomy, the baseline Ep became negligible (0.012 +/- 0.001 ng/ml) and the baseline NEp was lowered to 0.52 +/- 0.109 ng/ml. Neither static contraction nor mechanical stretch produced significant responses in plasma Ep and NEp following the adrenalectomy. These results suggest that static muscle contraction augments preganglionic adrenal sympathetic nerve activity, which in turn secretes epinephrine from the adrenal medulla into plasma. A muscle mechanoreflex from the contracting muscle may play a role in stimulation of the adrenal sympathetic nerve activity.     

Depressed responsiveness of the carotid sinus reflex in conscious newborn animals.

The responsiveness of the carotid sinus reflex was evaluated by comparing the effects of bilateral carotid occlusion (BCO) in conscious adult dogs and puppies on measurements of arterial pressure, cardiac output, heart rate, and calculations of total peripheral resistance (TPR). In eight adult dogs, BCO increased mean arterial pressure by 57 +/- 6%, TPR by 48 +/- 5%, and heart rate by 45 +/- 15%. In puppies, BCO induced smaller increases (P less than 0.05) in mean arterial pressure (30 +/- 5%) and TPR (29 +/- 4%), while heart rate did not change. After elimination of opposing vagal and aortic baroreceptor reflexes, the differences in responses to BCO of mean arterial pressure and TPR between adults and newborns were even greater. Thus, the carotid baroreceptor reflex appears to be depressed in the newborn when compared with the fully developed reflex in the normal, conscious adult.     

Physiological and behavioral responses of New Zealand hypertensive and normotensive rats to stress

A chronic catheter was inserted into the ventral tail artery of adult male New Zealand hypertensive (NZH) and normotensive (NZN) rats to allow for repeated sampling of blood and measurement of blood pressure and heart rate in conscious animals without handling. Two days after surgery, plasma levels of norepinephrine (NE) and epinephrine (EPI) were similar in NZH and NZN rats while resting and undisturbed in their home cages. Mean arterial blood pressure was significantly higher in NZH rats (166±9 mm Hg) than in NZN rats (124±4 mm Hg) but basal heart rates did not differ (345±8 and 342±14 beats/min, respectively). Increments in plasma levels of NE and EPI and in mean arterial blood pressure and heart rate were similar in NZH and NZN rats following transfer to a shock box and immediately and 10 minutes after exposure to 1 minute of intermittent footshock. Male rats of the two strains also did not differ in their behaviors during tests in an open field arena. These results indicated that NZH and NZN rats do not differ with respect to basal or stress-induced increments in sympathetic-adrenal medullary activity or in several behavioral measures. These results are in striking contrast to previous studies with the Okamoto strain of spontaneously hypertensive (SHR) rats and indicate that genetically determined increases in arterial blood pressure are not necessarily associated with sympathetic-adrenal medullary and behavioral hyperresponsivity to stress.     

Decrease in repetitive extrasystole threshold during epinephrine infusion is enhanced in conscious dogs with perinephritic hypertension.

Hypertension is associated with myocardial hypertrophy as well as increased adrenergic responsiveness, both of which can predispose to malignant ventricular arrhythmias. This study was designed to test the effects of subpressor doses of epinephrine (0.15 and 0.3 micrograms/kg/min x 30 min) on vulnerability to ventricular arrhythmia in normotensive and perinephritic hypertensive dogs. Two groups of 6 dogs each were chronically instrumented with aortic catheters to measure mean arterial pressure and bipolar pacing catheters in the apex of the right ventricle to measure repetitive extrasystole threshold, an index of vulnerability to ventricular fibrillation. In the normotensive dogs, the low dose of epinephrine (0.15 micrograms/kg/min IV) had no significant effects on mean arterial pressure, heart rate of repetitive extrasystole threshold. However, in the hypertensive dogs, the same dose caused a significant 39% increase in heart rate (p less than 0.05) and 41% decrease in repetitive extrasystole threshold (p less than 0.05). These findings suggest that electrophysiological vulnerability of the myocardium caused by epinephrine infusion is enhanced in the hypertensive animal.     

Intrinsic heart rate in the dog determined by pharmacologic denervation

Intrinsic heart rate was measured in 19 dogs in 76 experiments after autonomic blockade, using various forms of anesthesia. Measurements were made in conscious dogs (n = 16) and in dogs in neuroleptanesthesia (n = 54) or under pentobarbital sodium (n = 6). Temperature, arterial pH, and blood gases were kept within narrow limits. Adrenergic blockade was achieved by phenoxybenzamine (2 mg X kg-1) and propranolol (2 mg X kg-1, followed by 2 mg X kg-1 X h-1). The parasympathetic system was blocked either by atropine (0.5 mg X kg-1, followed by 0.5 mg X kg-1 X h-1) and hexamethonium (20 mg X kg-1, followed by 10 mg X kg-1 X h-1) or by atropine and bilateral cervical vagotomy. Administration of hexamethonium or vagotomy was needed to block the vagal cardioacceleration unmasked by the administration of muscarinic blocking agents in conscious dogs and in dogs in neuroleptanesthesia. The mean denervated heart rate was 142.8 beats/min. This value is higher than that reported for surgically denervated hearts, the difference very likely reflecting the activity of the intact parasympathetic intrinsic cardiac innervation in surgical preparations. The estimated intraindividual and interindividual SD were 9.7 and 19.4 beats/min, respectively. The highly significant interindividual variation (P less than 0.01) contradicts the concept of an intrinsic heart rate as a practically constant species-dependent quantity.     

Changes in blood pressure and heart rate induced by movements of normal and inflamed knee joints

The effects of passive movements of normal and inflamed knee joints on blood pressure and heart rate were recorded in baroreceptor denervated cats anesthetized with halothane, and these effects were compared with those obtained by severe noxious squeezing of the hind paw. Rhythmic flexions and extensions as well as rhythmic inward and outward rotations of a normal knee joint in its physiological working range did not have any significant influence on blood pressure and heart rate. However, on the inflamed side, the same movements caused definite increases in blood pressure and heart rate (e.g. mean increases for flexion-extension movements were 13 mmHg and 4 beats/min, respectively, P less than 0.01). Static outward rotations in the normal working range were ineffective in both joints, but as soon as these static rotations were extended into the noxious range significant increases in blood pressure and heart rate were elicited. The respective mean increases induced from the normal and inflamed sides were 17 and 38 mmHg for the blood pressure and 4 and 8 beats/min for the heart rate. The increases in blood pressure and heart rate induced by noxious outward rotation of the inflamed joint regularly exceeded those elicited by noxious squeezing of the hind paw. It is concluded that impulses in articular nociceptors and possibly other fine articular afferent units activate sympathetic outflow to the cardiovascular system, and that these effects are particularly prominent when the joint receptors are sensitized by     

Effects of bilateral carotid occlusion and auditory stimulation on renal blood flow and sympathetic nerve activity in the conscious dog

In conscious foxhounds with intact aortic baroreceptors the effects of common carotid occlusion (C. C. O.; 3 dogs) or excitement (elicited by a sudden loud noise due to firing a pistol; 7 dogs) on renal blood flow (R.B.F.) were studied. C.C.O. increased arterial blood pressure by 40–50 mm Hg and heart rate by 22 beats/min while R.B.F. remained unchanged. When kidney perfusion pressure was maintained during C.C.O. there was also no change in R.B.F. Excitement increased mean aortic blood pressure by 35 mm Hg and heart rate by 84 beats/min; R.B.F. was transiently reduced by 40% of control.In another 3 foxhounds successful recordings of renal sympathetic nerve activity (R.S.N.A.) were obtained in the conscious state for 2–7 postoperative days. The effects of C.C.O. or excitement — elicited by whistling or hand-clapping — on R.S.N.A. were tested. There was pulse-synchronous nerve activity in the resting conscious animal. C.C.O. induced a steady state increase of averaged R.S.N.A. by 62% of control. Excitement was associated with transient bursts of activation of averaged R.S.N.A. by 500% of control.It is concluded that total R.B.F. is not changed during the baroreceptor short-term adjustment of blood pressure although changes in sympathetic outflow to the kidney are observed under comparable conditions. In contrast, excitement causes a much higher degree of sympathetic activation; this is probably responsible for the intense, transient renal vasoconstriction.This study was supported by the German Research Foundation within the S.F.B. 90 Heidelberg     

Adrenal blood flow response to adrenocorticotrophic hormone and other stimuli in the dog

Summary Measured with heated thermocouples, intravenous ACTH was found to increase adrenal blood flow within 1 min in anaesthetized as well as in conscious dogs. Repeated injections continued to increase flow at a time when corticoid secretion was no longer increasing. Hypotension induced by bleeding and vasoconstriction elicited with vasopressin produced less substantial reductions in adrenal than in renal and thyroidal blood flow. Thyroidal blood flow failed to respond to thyrotrophic hormone within the observation period. — The rubidium⁸⁶ method yielded after ACTH the same results in dogs as those obtained by Sapirstein in rats.With 4 Figures in the Text     

Increase in renin release after sionaortic denervation and cervical vagotomy.

The role of the vagi in the control of renin secretion was investigated in dogs maintained on a high-salt diet. Renal perfusion pressure was maintained relatively constant by the manipulation of a suprarenal aortic snare. Mean arterial blood pressure (MAP), plasma renin activity (PRA), and packed cell volume (PCV) increased after sinoaortic denervation and cervical vagotomy. Cooling of cervical vagi to 3-5 degrees C had the same effect as vagotomy. There was no change in MAP, PRA, and PCV in sham-operated animals. Propranolol prevented the increase in PRA following sinoaortic denervation and vagotomy, but not that in MAP or PCV. In splenectomized dogs, PCV still showed increases after sinoaortic denervation and vagotomy. It is suggested that the removal of sinoaortic and/or vagal inhibitory effects on the vasomotor center causes increases in sympathetic discharge to the adrenal medulla and the peripheral vessels, and that this in turn leads to the increase in MAP. The increase in sympathetic discharge to the adrenal medulla and the kidney causes the increases in PRA.     

Atrial natriuretic peptide during head-up tilt induced hypovolaemic shock in man

To evaluate the importance of right atrial filling pressure versus central blood volume for the plasma concentration of atrial natriuretic peptide in man, head-up tilt to 50 degrees maintained until the appearance of presyncopal symptoms was carried out in six healthy males. Head-up tilt increased thoracic electrical impedance from 35.4 +/- 0.9 (mean and SE) to 39.2 +/- 0.9 ohm, mean arterial pressure from 64.5 +/- 3.6 to 76.6 +/- 3.0 mmHg and heart rate from 51 +/- 3 to 85 +/- 4 beats min-1 (P less than 0.01). After 35 +/- 7 min presyncopal symptoms appeared, together with a decrease in mean arterial pressure to 51 +/- 4 mmHg and in heart rate to 59 +/- 7 beats min-1 (P less than 0.01). Central venous pressure (2.1 +/- 1.0 mmHg) did not change significantly, but atrial natriuretic peptide decreased from 9.4 +/- 1.6 to 4.2 +/- 1.3 pmol l-1 (P less than 0.01) and was inversely related to thoracic impedance (r = -0.65, n = 44, P less than 0.001). The results indicate that changes in the central blood volume rather than in central venous pressure determine the secretion of atrial natriuretic peptide in man.     

Sympatho-adrenal responses of spontaneously hypertensive rats to immobilization stress.

Blood pressure, heart rate, and circulating levels of norepinephrine, epinephrine, and corticosterone were measured before and during the first or seventh period of immobilization stress (150 min per day) in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive male rats. A catheter was inserted into the tail artery of each rat to permit direct measurement of blood pressure and heart rate and serial sampling of blood in conscious, unhandled animals. During the first immobilization, SHR rats had significantly higher circulating levels of norepinephrine, epinephrine, and corticosterone than did WKY rats. One day after the sixth immobilization, basal levels of norepinephrine and epinephrine were significantly higher and mean blood pressure was significantly lower in repeatedly stressed SHRs compared to unstressed SHRs. In addition, adaptation to the repeated stress in SHRs was attended by reduced adrenomedullary secretion and an increased blood pressure response. These results demonstrate that adaptive changes in the cardiovascular and sympatho-adrenal medullary systems of repeatedly immobilized rats are greater in SHR than in WKY rats.     

Role of arterial baroreceptors in mediating cardiovascular response to exercise.

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.     

Comparison of the effects of 2-deoxyglucose and immobilization on secretion and synthesis rate of catecholamines in the adrenal gland: a microdialysis study in conscious rats

Using microdialysis, extracellular 3,4-dihydroxyphenylalanine (DOPA), noradrenaline (NA) and adrenaline (AD) concentrations in the adrenal gland were monitored in conscious rats during and after 60 min of immobilization (IMM) as well as after injection of 500 mg kg^-1 2-deoxyglucose (2-DG). IMM produced a rapid and transient increase in secretion of AD (20-fold), NA (13-fold) and DOPA (3.6-fold). This was accompanied by an increase in blood pressure (+ 18 mmHg) and heart rate (- 146 b. p.m.). Repeated exposure to IMM (daily 60 min, for 5 days) had no influence on either catecholamine secretion of haemodynamic profiles, indicating the lack of habituation to stressful conditions. Unlike IMM, the stress of 2-DG-induced centralneuroglucopenia stimulated the release of AD without affecting NA secretion. AD levels peaked (5.1-fold increase) 4&60 min after 2-DG injection and then slowly declined. 2-DG induced no changes in blood pressure but reduced the heart rate (-48 b. p.m.). In separate experiments, steady-state dialysate DOPA levels, reached during continuous infusion of decarboxylase inhibitor NSD 1015 into adrenal gland tissue through the dialysis probe, served as an index of adrenomedullary tyrosine hydroxylase (TH) activity. IMM evoked a marked increase in TH activity (DOPA formation increased 2.7-fold), which remained elevated 60 min after the cessation of stress when AD and NA secretion had already fallen to baseline. After 2-DG, despite significant hormonal response, adrenal TH activity was unchanged. These results give clear evidence that IMM and 2-DG-induced neuroglucopenia may be considered as two different types of stressful stimuli.     

Calcitonin gene-related peptide (CGRP) and leg vascular resistance during head-up tilt induced hypovolaemic shock in man

Calcitonin gene-related peptide is a potent vasodilator and its distribution in perivascular nerves suggests a role in the regulation of vascular tone. We evaluated leg vascular resistance together with total peripheral resistance and the arterial plasma concentrations of calcitonin gene-related peptide and catecholamines during 50 degrees head-up tilt induced hypotension in 7 males. During tilt mean arterial pressure, heart rate, total peripheral resistance, leg vascular resistance and plasma noradrenaline increased, while cardiac output and leg blood flow decreased. After 45 +/- 9 min (mean +/- SE) presyncopal symptoms appeared together with decreases in mean arterial pressure (81 +/- 6 to 56 +/- 9 mmHg), heart rate (97 +/- 6 to 73 +/- 8 beats min-1), leg vascular resistance (158 +/- 9 to 109 +/- 8 mmHg min l-1) and total peripheral resistance (17 +/- 3 to 10 +/- 2 mmHg min l-1) (P less than 0.01). Plasma calcitonin gene-related peptide increased from 32 +/- 3 to 35 +/- 3 pmol l-1 (P less than 0.01) and adrenaline from 1.1 +/- 0.2 to 1.7 +/- 0.3 nmol l-1 (P less than 0.01), while noradrenaline did not change. The results indicate that presyncopal symptoms induced by head-up tilt are associated with regional as well as total decreases in vascular resistance accompanied by moderate increases in arterial plasma concentrations of calcitonin gene-related peptide and adrenaline.     

Effects of synthetic human atrial natriuretic peptide (hANP) in conscious dogs

The effects of synthetic human atrial natriuretic peptide (hANP) on arterial blood pressure, heart rate, and renal functions were evaluated in conscious trained dogs in moderate sustained water diuresis. Synthetic hANP was given i.v. over 3 min at doses of 0.27-2.16 micrograms kg-1 body wt. It did not cause significant changes in blood pressure or heart rate. The rate of sodium excretion increased 20-fold following 2.16 micrograms kg-1 and 2.5-fold after 0.54 micrograms kg-1. Natriuresis was immediate and vanished after 10 min, regardless of dose. The concomitant increase in diuresis was less than 50%, but significant for a longer period of time. Increases in potassium excretion were significant, but small, that is, by a factor of 1.5-2.8. All natriuretic doses of hANP increased PAH clearance (at constant blood pressure), but some did so without measurably affecting creatinine clearance.     

Elevation of arterial blood pressure in the squirrel monkey at 10 degrees C.

Systemic arterial blood pressure, heart rate, and total body oxygen consumption were measured in seven unanesthetized squirrel monkeys exposed to ambient temperatures of 28 degrees C and 10 degrees C. At 28 degrees C, subjects sat quietly, the average mean arterial blood pressure was 116 +/- 16 (mean +/- SD, n - 7) mmHg, heart rate was 274 +/- 31 beats/min, and oxygen consumption was 14 +/- 1.4 ml/kg-min. At 10 degrees C, the animals shivered vigorously, the average mean arterial blood pressure was 139 +/- 16 mmHg, heart rate was 328 +/- 18 beats/min, and oxygen consumption was 31.6 +/- 3.9 ml/kg-min. Thus, the oxygen consumption more than doubled, the blood pressure rose by approximately 21%, and the heart rate by approximately 20%. Elevations in heart rate as well as systemic mean arterial blood pressure during exposure to low ambient temperature were probably mediated by sympathetic-adrenal discharges as well as by activity of skeletal muscles.