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1Department of Kinesiology, Leisure, and Sport Sciences, East Tennessee State University, Johnson City, Tennessee; 2Division of Exercise Physiology, Department of Physiology and Pharmacology, and the Center for Interdisciplinary Research in Cardiovascular Sciences, West Virginia University School of Medicine, Morgantown, West Virginia; and 3Department of Applied Physiology and Kinesiology and the Center for Exercise Science, University of Florida, Gainesville, Florida
Submitted 13 June 2007 ; accepted in final form 30 August 2007
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ABSTRACT |
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orthostatic hypotension; blood flow; tilt; visceral fat
Head-up tilt (HUT) has been utilized extensively to study cardiovascular system responsiveness to orthostatic stress in humans and animals (8, 13, 14, 16, 26, 31). Postural changes from the supine position to the upright posture elicit a blood volume shift from the thoracic cavity to the lower limbs (29), which results in reduced venous return and, subsequently, decreased stroke volume. The resultant decrease in cardiac output must be offset by a decrease in peripheral vascular conductance (PVC) to maintain arterial blood pressure (29). Since there is a greater incidence of orthostatic hypotension with advancing age (16, 25, 31, 38), the primary purpose of the present study was to determine whether a diminished ability to maintain MAP during an orthostatic stress is manifest in aged Fischer-344 rats and to identify whether alterations in regional vascular conductance correspond to a putative orthostatic hypotension. Specifically, we hypothesized that with HUT, aged animals will demonstrate a diminished vasoconstriction in some tissues, as evidenced by higher blood flows and vascular conductance relative to that in young adult rats. The results indicated an inability of old rats to diminish vascular conductance in several tissues, including white adipose tissue, during HUT. Therefore, a secondary purpose was to test the hypothesis that aging diminishes myogenic and adrenergic vasoconstriction of resistance vessels from white visceral adipose tissue. The results from this series of experiments may indicate an underlying mechanism for the old age-related orthostatic intolerance. Given that adipose tissue makes up a greater proportion of body composition with aging in rats (7) and humans (1), a reduced vasoconstriction of resistance vessels from this tissue could have significant ramifications on the ability to decrease peripheral vascular conductance during orthostatic challenges and with exercise among the elderly.
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METHODS |
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Young adult (4–6 mo; n = 19) and aged (24–26 mo; n = 17) male Fischer-344 rats were obtained from the National Institute of Aging colony. The 4- to 6-mo-old ages represent young sexually mature adult animals, and 
24-mo-old animals are considered senescent rats (10). Rats were housed individually at 23°C, maintained on a 12:12-h light-dark cycle, and fed rat chow and water ad libitum. All procedures were approved by the Institutional Animal Care and Use Committees at Texas A&M and West Virginia Universities.
Surgical Procedures
Before the surgical procedure, animals were habituated to the tilt apparatus at 0° tilt for 15 min/day for at least 5 days. At the conclusion of the habituation regimen, the rats were anesthetized with isoflurane (2%/O2 balance), and a catheter (Dow Corning, Silastic; ID 0.6 mm, OD 1.0 mm) filled with heparinized saline solution (Elkins-Sinn; 100 U/ml) was advanced into the ascending aorta via the right carotid artery as previously described (4, 20). This catheter was used for infusion of radiolabeled microspheres for tissue blood flow measurements and for monitoring MAP. The carotid catheter was externalized at the base of the tail and secured on the underside of the tail. A second polyurethane catheter (Braintree Scientific; ID 0.36 mm, OD 0.84 mm) was implanted in the caudal tail artery as described previously (4) and externalized at the tail. This catheter was used to obtain a reference blood sample that serves as an artificial organ for calculating tissue flows. Externalizing the catheters at the base of the tail allowed for a shorter length of catheter in the caudal tail artery and, therefore, less resistance to the withdrawal of blood from this catheter for the reference blood sample. The catheters were secured in place with sutures and covered with a Vetwrap self-adhesive support bandage.
Experimental Protocol
After a 24-h recovery period, the animals were placed in the tilt apparatus in a horizontal standing position (0° tilt). The rats were allowed 20 min of quiet standing before the first microsphere infusion. Arterial pressure and heart rate were measured in each rat at 0° tilt for baseline data and every minute up to 10 min immediately after the onset of tilt at 70°. Tissue blood flows were measured during 0° tilt and after 10 min of 70° tilt. At the end of the experiment, the animals were euthanized with an overdose of pentobarbital sodium (>80 mg/kg ia) via the carotid catheter. Visceral tissues (kidneys, spleen, stomach, duodenum, large intestine, adrenal glands, liver), hindlimb skin, white adipose tissue (subcutaneous, visceral, epididymal), reproductive tissues (testis and prostate), and 11 hindlimb muscles or muscle groups were excised, weighed, and placed into counting vials for blood flow determination and calculation of tissue vascular conductance. Several muscles were further sectioned into red, white, or mixed portions to determine whether putative old age-associated alterations in muscle blood flow and vascular conductance are based on muscle fiber composition or oxidative capacity (6). The knee flexor muscle group consisted of biceps femoris, semitendinosus, and semimembranosus muscles.
Simulated Orthostatism
Animals were gently restrained in a Plexiglas canopy (Rodent ECU; Braintree Scientific) hinged to a tilting Plexiglas support base. The animals were placed so that the thorax was at the same level as the tilting axis. The concept for the tilting apparatus is based on that previously employed with rats (24, 42). The head end of the canopy had a tapered opaque plastic hood to protect the rodents from visual disturbances. This served to minimize the ocular postural input, which may alter cardiovascular reflex responses. Tilt time was 
1–2 s from the level (0°) baseline condition to 70° HUT. During the experiments animals remained in the tilted position for 10 min before infusion of the microspheres. Preliminary studies (n = 10) indicated that baseline MAP did not differ between the young and aged rats but that during the 70° HUT, MAP fell in the aged animals and reached a steady state after 2–5 min of tilt onset. Thus the 10-min period of tilt represented a relative steady-state measure of the cardiovascular response to HUT for the young and aged animals.
Blood Flow and Vascular Conductance Measures
Radiolabeled (46Sc and 85Sr) microspheres (Perkin Elmer NEN) with a 15.5 ± 0.2-µm diameter were used for blood flow measurements as previously described (4, 20). Specifically, microspheres were suspended in physiological saline with <0.5% Tween 80 and mixed before infusion by 10 min of sonication (FS20 Sonicator; Fisher Scientific). A reference blood sample was taken from the caudal artery at a rate of 0.618 ml/min with a Harvard withdrawal pump (model 907; Cambridge, MA) while simultaneously, 2.5 x 105 microspheres suspended in 0.2 ml of saline were infused into the carotid catheter over a 10- to 15-s period. Warm (37°C) saline (0.5 ml) was infused over a 30-s period immediately after microsphere infusion to clear the catheter of residual microspheres; withdrawal of the reference blood sample continued for 20 s after the saline flush. After euthanasia and tissue dissection, tissue samples were counted in a gamma counter (Packard Auto Gamma Spectrometer, model 5780), and flows were computed from counts per min and tissue wet weights (blood flows reported in ml·min–1·100 g–1). Adequate mixing of the microspheres was verified by demonstrating a <15% difference in blood flows to the right and left kidneys. MAP and heart rate were electronically averaged from pulsatile pressure measurements via a pressure transducer (BP100; ADInstruments). Regional vascular conductance (ml·min–1·100 g–1·mmHg–1) was calculated by dividing tissue flows (ml·min–1·100 g–1) by the MAP (mmHg).
Adipose Microvessel Preparation
White visceral adipose tissue microvessel studies were preformed in a separate group of young (n = 7; 322 ± 11 g) and aged rats (n = 7; 395 ± 12 g). Animals were anesthetized with pentobarbital sodium (50 mg/kg ip) and euthanized via rapid removal of the heart to minimize loss of blood in the microcirculation. The visceral fat pad was carefully excised and placed in cold (4°C) physiological saline solution (PSS) containing 145.0 mM NaCl, 4.7 mM KCl, 2.0 mM CaCl2, 1.17 mM MgSO4, 1.2 mM NaH2PO4, 5.0 mM glucose, 2.0 mM pyruvate, 0.02 mM EDTA, 3.0 mM MOPS buffer, and 1 g/100 ml BSA at pH 7.4. Resistance arteries (i.e., <300 µm maximal luminal diameter) were then isolated with the aid of a dissecting microscope (Olympus SVH10). The arteries were cleared of surrounding adipocytes and placed in a Lucite chamber containing PSS equilibrated to room air. The vessels were cannulated on both ends to glass micropipettes and secured with nylon monofilament suture (Alcon 11-0). After cannulation, the chambers were transferred to the stage of an inverted microscope (Olympus IX70) equipped with a video camera (Panasonic BP310), video caliper (Microcirculation Research Institute, Texas A&M), and data acquisition system (MacLab) for recording of luminal diameter. Intraluminal pressure was set at 75 mmHg. Vessels that exhibited leaks were discarded. Vessels free of leaks were warmed to 37°C and allowed to develop spontaneous tone during a 60-min equilibration period. To determine vasoconstrictor responsiveness to norepinephrine (NE) and phenylephrine (PE), the cumulative addition of either NE (10–9–10–4 M) or PE (10–9–10–4 M) was performed in separate sets of vessels (3, 27). Following these vasoconstrictor tests, the vessels were then incubated in Ca2+-free PSS containing 2.0 mM EDTA to determine maximal passive lumen diameter at 75 mmHg. To determine myogenic vasoconstrictor responsiveness, intraluminal pressure in a separate group of adipose resistance arteries was increased from 0 to 135 cmH2O in 15-cmH2O increments, with diameter recorded continuously for 5 min with each pressure change (3, 27). To determine the passive pressure-diameter relation, the vessels were then incubated at 37°C for 60 min in Ca2+-free PSS containing 2.0 mM EDTA with the bathing medium changed every 15 min. The same protocol as described above for the active myogenic response was used to determine the passive vessel characteristics.
Statistical Analysis
Hemodynamics during HUT.
A two-way repeated-measures ANOVA was used to compare MAP, heart rate, tissue blood flow, and vascular conductance between groups (young vs. aged) and within groups across conditions (level vs. 70° HUT). Duncan's multiple range test was used to determine the significance of difference between treatment means. All data are means ± SE. Significance was set at P 
0.05.
Isolated adipose vessel statistical analysis. The development of spontaneous tone was expressed as the percent constriction relative to maximal diameter and was calculated as spontaneous tone (%) = (Dmax – Db)/Dmax x 100, where Dmax is the maximal diameter recorded at a pressure of 75 mmHg in Ca2+-free PSS and Db is the steady-state baseline diameter (3, 27). Vasoconstrictor responses to NE and PE were expressed as a percent change from baseline diameter according to the formula vasoconstriction (%) = (Db – Ds)/Db x 100, where Db is the initial baseline diameter recorded immediately before the addition of the vasoconstrictor agonist and Ds is the steady-state diameter measured after each dose of the adrenergic agonist (3, 27). Active myogenic responses and passive diameter measurements recorded after each step pressure change were normalized according to the formula normalized diameter = Ds/Dmax, where Ds is the steady-state diameter measured after each incremental pressure change. The data are expressed as normalized diameter to account for differences in vessel size between young and aged animals (3, 27). Two-way repeated-measures ANOVA was used to detect differences between (young vs. old) and within factors (drug concentration or pressure level). Post hoc analyses were performed using Duncan's multiple range test. The agonist concentration that produced 50% of the maximal vasoconstrictor response was designated EC50. All EC50 values were converted to log values for statistical comparison.
A one-way ANOVA was used to determine the significance of differences between groups in animal mass and vessel characteristics. Duncan's multiple range test was used to determine the significance of difference among treatment means. All data are means ± SE. Significance was set at P 0.05.
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RESULTS |
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Blood flow experiments were successfully completed in 12 young and 10 aged animals. Body mass was significantly greater in the aged (405 ± 7 g) compared with young animals (341 ± 7 g).
Heart Rate and MAP
Baseline values for heart rate were not different between young and aged rats (402 ± 8 vs. 407 ± 5 beats/min, respectively). At the end of the HUT protocol, young rats had significantly elevated heart rate (419 ± 7 beats/min), whereas aged rats had a lower heart rate (397 ± 5 beats/min) compared with baseline values. Young and aged animals also demonstrated directionally different changes in MAP with HUT; young rats increased MAP by 7% (136 ± 5 mmHg at baseline to 145 ± 3 mmHg during tilt, P 0.05), whereas MAP was reduced by 7% in aged rats (127 ± 5 mmHg at baseline to 118 ± 3 mmHg during tilt, P 0.05). During tilt, MAP was greater in the young rats relative to that in the aged animals (P 0.05).
Skeletal Muscle Blood Flow and Vascular Conductance
Blood flow to most skeletal muscles was not affected by aging or tilt (Table 1). However, during level standing, cremaster muscle perfusion was higher in the aged rats (Table 1). During tilt, blood flow to the red portion of the tibialis anterior muscle from the young animals was reduced (Fig. 1A).
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During level standing, aged animals demonstrated lower blood flow to the spleen, stomach, jejunum, cecum, large intestines, mesentery, adrenal cortex, kidneys, hindlimb skin, and prostate (Table 3). In response to HUT, young animals reduced blood flow in 15 of the 18 tissues, whereas only 6 of these 18 tissues exhibited reduced blood flow in aged animals (Table 3). Blood flow to the visceral, subcutaneous, and epididymal white adipose tissues was reduced during HUT in young rats but was unaltered by tilt in the aged animals; blood flow was lower in visceral and epididymal fat of young rats during tilt relative to that in the aged animals (Fig. 2).
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Vascular conductance in response to HUT was diminished in 16 of the 18 tissues in young rats (Table 4), whereas only 4 of the 18 tissues demonstrated reduced vascular conductance in the aged animals (Table 4). In the adipose tissue from three distinct anatomical locations, vascular conductance was reduced in young animals with HUT (Fig. 3). In the aged animals, however, vascular conductance did not change during the orthostatic stress condition and was significantly greater in visceral and epididymal fat during tilt than that in young rats (Fig. 3). Vascular conductance in the adrenal medulla and testis was also significantly higher during tilt in the aged rats (Table 4).
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The maximal intraluminal diameter of resistance arteries from white visceral fat of aged rats (288 ± 11 µm) tended to be larger than that of vessels from young animals (250 ± 15 µm; P < 0.1). However, there were no differences in the wall-to-lumen ratio between groups (young, 0.129 ± 0.006 vs. aged, 0.103 ± 0.008; P > 0.05). Vessels from both young and aged rats demonstrated spontaneous tone, although tone in vessels from aged rats was less than that from young animals (young, 28 ± 2% vs. aged, 10 ± 2%; P < 0.05).
Vasoconstrictor Responses
NE elicited concentration-dependent decreases in intraluminal diameter in adipose resistance arteries from both young and aged animals. Contractile responses evoked by NE (Fig. 4A) and sensitivity to NE (EC50; young, 8.44 x 10–7 ± 3.80 x 10–7 M; aged, 1.33 x 10–5 ± 5.04 x 10–6 M; P < 0.05) were lower in adipose vessels from aged rats. Similarly, PE produced concentration-dependent decreases in intraluminal diameter in vessels from both groups. Contractile responses evoked by PE (Fig. 4B) and sensitivity to PE (EC50; young, 3.64 x 10–7 ± 1.53 x 10–7 M; aged, 1.18 x 10–5 ± 3.93 x 10–6 M; P < 0.05) were lower in adipose resistance arteries from aged rats.
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Elevations in intraluminal pressure of visceral adipose fat resistance arteries resulted in a pressure-dependent increase in intraluminal diameter (Fig. 5). At all pressures above zero active diameter was larger in vessels from the aged group (Fig. 5). However, in Ca2+-free solution there was no difference in the passive pressure-diameter response between groups (Fig. 5).
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DISCUSSION |
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While quadrupeds have been used extensively in head-up tilt studies (4, 8, 13, 14, 42), there is a paucity of literature comparing cardiovascular responses of aged and young animals. However, there is experimental support for a diminished cardiovascular response to orthostatic challenges in aged humans (23, 30, 38). For example, in a study by Shi et al. (31), aged individuals demonstrated significant reductions in systolic blood pressure in response to 10 min of –40 Torr lower body negative pressure, whereas young subjects maintained pressure; this difference was attributed to a higher heart rate in the young. A lower heart rate response during tilt with advancing age has also been described in other human studies (16, 26, 31, 33, 35). The lack of cardioacceleration in the aged animals during tilt in the present study is consistent with these observations in humans, and this appears to be related to a lower cardiac output during head-up tilt with aging (19, 21, 35, 41).
The results of the present investigation demonstrate that aged animals do not decrease peripheral vascular conductance in a number of tissues relative to that at baseline during orthostatic stress. Therefore, a compromised ability to elevate cardiac output coupled with a diminished capacity to lower peripheral vascular conductance would make the elderly more susceptible to episodes of hypotension. Such appears to be the case in the present study of aged rats during head-up tilt.
In young animals, vascular conductance decreased during tilt in the majority of tissues (19 of 21; Table 4 and Fig. 3), whereas vascular conductance decreased in only 4 of 21 tissues in aged rats. This could be interpreted as a lack of vasoconstrictor responsiveness in the aged animals. However, the reason for the lack of vasoconstriction in many of these tissues from the aged animals was a greater relative constriction in the normal standing condition preceding tilt, so during tilt there was no further change in vascular conductance. To assess old age-related decrements in vasoconstrictor capacity, absolute vascular conductance during tilt can be compared between young and old rats rather than considering whether a change occurred from the standing to tilted condition. The data demonstrate that two skeletal muscles (tibialis anterior and vastus medialis), the adrenal medulla, testes, and visceral and epididymal fat were the only tissues in which vascular conductance was higher in the aged rats during tilt relative to that in the young rats. These results indicate that the greater vasoconstrictor tone during normal standing in aged animals diminishes the vasoconstrictor reserve in many of the tissues, so further vasoconstriction to support the maintenance of arterial pressure during orthostatic stress is not possible. Furthermore, the results demonstrate that an old age-associated decrease in vasoconstrictor capacity is evident in a few tissues, which includes the visceral and epididymal fat pads (Fig. 3).
One mechanism for the higher vascular conductance is a reduced vasoconstrictor responsiveness of the resistance vasculature. Thompson et al. demonstrated diminished adrenergic responsiveness of the skin (36) and forearm (37) vasculature in elderly subjects. Furthermore, Wilson et al. (43) found that higher doses of NE were needed to reduce human forearm cutaneous blood flow in old subjects compared with young individuals. This reduced sensitivity to NE in the human forearm may underlie the attenuated ability of elderly subjects to decrease forearm vascular conductance in response to head-up tilt with passive heating (26). Likewise, the diminished sensitivity of the resistance vasculature to NE in aged rats may underlie the higher regional vascular conductance during orthostatic stress (Fig. 3 and Table 4).
The higher vascular conductance during tilt in aged rat white adipose tissue (Fig. 3) led us to test a secondary hypothesis that adrenergic and myogenic vasoconstriction of resistance arteries isolated from white visceral fat would be lower in aged vs. young rats. The primary role of white adipose is the storage and mobilization of lipids. However, white adipose tissue is also regarded as an endocrine organ, since white adipocytes produce mediators that influence metabolism of lipids and glucose, immune responses, and reproduction (39, 40). Although white adipose tissue lacks significant parasympathetic innervation, there is substantial evidence of sympathetic innervation (12, 32). For example, electrical stimulation of nerves innervating canine white adipose tissue results in vasoconstriction that is abolished by 
-adrenergic receptor blockade (28). Adipose tissue also receives a large proportion of cardiac output (8% in young rats, 12% in aged rats) under normal resting conditions (7), so alterations in vascular control mechanisms in this tissue could have significant consequences on the ability to redirect blood flow and augment total vascular resistance. Results from isolated adipose resistance arteries demonstrate that the contractile response and sensitivity to both NE (via 1- and 2-receptors; Fig. 4, top) and PE (via 1-receptors; Fig. 4, bottom), as well as the myogenic vasoconstrictor response (Fig. 5), are significantly diminished in aged animals. Mechanisms underlying this blunted adrenergic vasoconstriction are unknown, although several possibilities exist. First, there could be an old age-associated increase in 2-receptors located on the endothelium that could counteract the 1- and 2-receptor-mediated vasoconstriction from the smooth muscle. This seems unlikely, since an impairment of PE-mediated vasoconstriction through the 1-adrenergic receptor mechanism also occurred, indicating an exclusive 2-receptor mechanism is not involved. Second, there may be chronic elevations in sympathetic activity to white adipose tissue with aging, possibly contributing to a diminution of -adrenergic receptor density in the blood vessels within this tissue. This possibility appears more likely, since a reduction in the number of 1-receptor binding sites (18) and blunted -adrenergic vasoconstriction (5) have been reported in the aorta of aged rats.
The decrements in vascular responsiveness to both adrenergic and pressure stimuli could culminate in an increased functional compliance within the white adipose vascular bed. Therefore, during conditions of orthostatic stress, where central shunting of blood away from the periphery is requisite for maintaining arterial blood pressure, diminished adipose vasoconstrictor responsiveness would make the elderly more vulnerable to orthostatic hypotension. We are unaware of any other studies that have described old age-associated reductions in adrenergic or myogenic vasoconstriction of resistance vessels isolated from white adipose tissue. This novel finding may provide a plausible mechanism for the hypotensive responses observed in the aged population during an orthostatic challenge.
With normal aging, there is an increasing proportion of body mass that is made up of adipose tissue (1, 7). Correspondingly, there is an 50% increase in the percent of cardiac output going to adipose tissue with advancing age (7). Both the higher proportion of cardiac output going to body fat (7) and the functional deficit of the adipose resistance arteries to vasoconstrict (Figs. 3–5) creates a combination of factors that make the regulation of MAP more vulnerable to significant drops in pressure, including that observed during orthostatic stress.
In previous work we found that myogenic vasoconstrictor responsiveness is diminished in skeletal muscle resistance arterioles with old age (27). Therefore, we hypothesized that skeletal muscle vascular conductance would be higher in aged animals during the HUT. This occurred in the tibialis anterior muscle (Fig. 1) but was not the case in the majority of skeletal muscles (Table 2). We speculate that the old age-associated diminution of this pressure sensitive vasoconstrictor mechanism (27) may be offset in vivo by enhanced vasoconstrictor responsiveness to NE (9) or other vasoconstrictor agents such as endothelin-1 (10) in skeletal muscle arterioles. Thus the net effect of these changes in vasoconstrictor responsiveness during head-up tilt is no change in vascular conductance.
In conclusion, advancing age results in cardiovascular dysfunction that is characterized by orthostatic intolerance (2, 17, 22). The present study demonstrates that within the aged vasculature there is diminished vasoconstrictor reserve that produces an attenuated ability to lower vascular conductance during an orthostatic challenge that consequently results in arterial hypotension. One novel observation was the lack of ability to lower vascular conductance during orthostatic stress in white adipose tissue (Fig. 3). In vitro experimentation with isolated resistance arteries from white visceral fat demonstrated an old age-associated decrement in -adrenergic and myogenic vasoconstrictor responsiveness. This diminished vasoconstrictor response of white adipose tissue coupled with the increased percentage of body fat with old age (7) provides a clinically relevant mechanism that may contribute to the orthostatic hypotension that is prevalent among the elderly.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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O2 max. J Appl Physiol 65: 1147–1151, 1988.This article has been cited by other articles:
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  L. S. Kang, S. Kim, J. M. Dominguez II, A. L. Sindler, G. M. Dick, and J. M. Muller-Delp Aging and muscle fiber type alter K+ channel contributions to the myogenic response in skeletal muscle arterioles J Appl Physiol, August 1, 2009; 107(2): 389 - 398. [Abstract] [Full Text] [PDF]
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 M. P. Tan, J. L. Newton, T. J. Chadwick, and S. W. Parry The relationship between carotid sinus hypersensitivity, orthostatic hypotension, and vasovagal syncope: a case-control study Europace, December 1, 2008; 10(12): 1400 - 1405. [Abstract] [Full Text] [PDF]
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P < 0.05, mean during tilt different from that at the level in animals of the same age group.
