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1 Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania 15260; 2 Department of Physiology and Medical Biophysics, Uppsala University, 75123 Uppsala, Sweden; and 3 Department of Physiology, University of Odense, 5000 Odense, Denmark
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Previous experiments have indicated that arterial hypotension increases plasma oxytocin (OT) levels in rats and that OT infused intravenously causes an increase in plasma renin activity (PRA). The goal of the present study was to determine whether systemic administration of an OT receptor antagonist would attenuate the increase in PRA that is normally evoked by arterial hypotension in rats. In conscious male rats, intravenous injection of hydralazine or diazoxide produced sustained hypotension and evoked a significant increase in PRA, as expected. Intravenous infusion of an OT receptor antagonist did not alter the hypotension induced by hydralazine or diazoxide, but it did markedly blunt the induced increase in PRA. The OT receptor antagonist also blunted the hypotension-evoked increase in heart rate and plasma vasopressin levels, suggesting that the antagonist may have generally disrupted afferent signaling of hypotension. Thus hypotension-evoked OT secretion may contribute to cardiovascular homeostasis by enhancing baroreceptor signals that stimulate increases in renin secretion, vasopressin secretion, and heart rate during arterial hypotension in rats.
diazoxide; heart rate; hydralazine; vasopressin
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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NEUROHYPOPHYSIAL OXYTOCIN (OT) is secreted into the circulation in response to arterial hypotension and hypovolemia. Although these responses have been well documented in rats (10, 19, 23), the physiological function of increased circulating OT under these conditions is unclear. In this regard, we recently reported (9, 21) that intravenous infusion of OT in rats, given in doses to produce plasma OT levels similar to those that occur in response to hypotension or hypovolemia, caused a significant increase in plasma renin activity (PRA) that was not secondary to the natriuretic action of OT. This observation led us to propose that increased OT secretion during hypotension or hypovolemia contributes to activation of the renin-angiotensin system, which is well-known to participate in the support of arterial pressure (AP) under these conditions. To test this hypothesis, we have now examined the effect of an OT antagonist, administered systemically, on hypotension-evoked renin secretion in rats. In addition, to evaluate whether the effects of the OT antagonist were selective for renin secretion or generalized to other responses, we also measured the tachycardia and vasopressin (VP) secretion that is evoked by arterial hypotension.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Adult male Sprague-Dawley rats (Zivic Laboratories, Zeleinople, PA), weighing 320-370 g, were housed individually in wire mesh cages in a temperature-controlled colony room (22-24°C, lights on from 8:00 AM-8:00 PM). Rats had ad libitum access to food (Purina #5001 Rat Chow) and tap water for at least 7 days before use in experiments.
On the day before experiments, rats were anesthetized with Brevital (50 mg/kg ip, Jones Medical Industries, St. Louis, MO). A catheter (PE-50 tubing) was implanted in the right femoral artery for blood sampling and for monitoring mean arterial pressure (MAP) and heart rate (HR). Another catheter (PV3 tubing) was implanted in the right femoral vein for administration of drugs. The catheters were filled with saline containing 50 U/ml heparin. The free ends of the two catheters were guided subcutaneously along the back. Upon exiting between the scapulae, the catheters were encased in a steel spring to prevent them from being damaged. The rats were returned to their home cages, and the catheters were connected to a swivel system outside the cage that allowed the rat unrestrained movement.
On the following morning, water and food were removed from each cage. The arterial catheter was connected to a pressure transducer (Statham P23ID) for the recording of MAP and HR on a physiograph (model 7, Grass Instruments, Quincy, MA). The venous catheter was connected to an infusion pump (Harvard Apparatus, South Natick, MA). Rats were then used in one of the following two protocols.
The first protocol tested the effect of the OT antagonist (OT-ant;
Atosiban, [1-(3-mercaptopropionic acid),
2-O-ethyl-D-Tyr,Thr4,Orn8]-OT,
Ferring, Sweden) on renin secretion, VP secretion, and tachycardia evoked by the hypotension caused by systemic treatment with the vasodilating drug hydralazine (HDZ, Sigma Chemical, St Louis, MO). After a 30-min period during which each rat received an
infusion of isotonic saline (5 ml · kg
1 · h1) and baseline
MAP and HR were recorded, a blood sample (1 ml) was collected via the
arterial catheter. Then in one group of rats (n = 8;
the "HDZ + OT-Ant" group), the OT-Ant was infused at the rate
of 40 µg · kg1 · h1 in a
volume of 5 ml · kg1 · h1.
This dose of OT-Ant has been shown to block the increase in PRA evoked
by OT infusion (9); furthermore, the drug is known to
block the natriuretic effect of OT but not the pressor effect of VP
(7). After a 1-h pretreatment with the OT-Ant, a blood sample (time 0) was taken, and then HDZ was injected
intravenously (10 mg/kg in 1 ml/kg saline plus an additional 0.4 ml
saline to flush the catheter). An additional blood sample was taken 30 min after the injection of HDZ. Then the 
-adrenergic receptor
agonist isoproterenol [ISP, 10 µg/kg in 1 ml/kg saline
(9)] was injected, and 5 min later the final blood sample
was taken. Infusion of the OT-Ant was maintained throughout the
experiment. MAP and HR were monitored continuously except during the
collection of each blood sample. The volume of each blood sample (1.0 ml) was replaced with an equal volume of warmed isotonic saline
containing the erythrocytes from the previous sample. Control rats
(n = 6, "HDZ + Vehicle") were treated in the
same way as rats in the HDZ + OT-Ant group except that the OT-Ant
was replaced with saline. All blood samples were withdrawn from the
arterial catheters into chilled tubes containing EDTA (Vacutainer,
Becton Dickinson, Franklin Lakes, NJ) and immediately centrifuged
(1,100 g for 8 min at 4°C). The plasma was removed and
stored at 
80°C before the assay of PRA and VP.
The second protocol was identical to the first except that diazoxide (DZX, 20 mg/kg) was used to produce arterial hypotension. Thus rats in the DZX + OT-Ant group (n = 7) received a 1-h pretreatment with OT-Ant and then were injected with DZX, whereas control rats (n = 5, "DZX + Vehicle") received saline instead of OT-Ant.
PRA was measured by radioimmunoassay of angiotensin I generated during a 1-h incubation at 37°C, in which the plasma samples were diluted 1:1 with maleate buffer (20). All values included in this report were obtained in the same assay. VP levels were measured in duplicate 250-µl aliquots of plasma as described previously (19). Plasma samples were extracted using Sep-Pak C18 cartridges (1 ml, 50 mg, Waters, Milford, MA), and VP was measured in duplicate in aliquots of each plasma extract. The assay sensitivity was 2.5 pg/ml, and all samples included in this report were run in a single assay.
Results are presented as means ± SE. Data were analyzed by two-way ANOVA (Systat, Evanston IL) with repeated measures in the time parameter. The error terms and degrees of freedom from the ANOVA were used in t-tests to compare treatment values to baseline values within each group. Tukey's honestly significant difference test was used for comparisons between groups at specific time points. Comparisons between groups receiving HDZ and DZX were done using two-way ANOVA with repeated measures. A P value <0.05 was considered to be statistically significant.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Systemic infusion of OT-Ant did not alter the basal values of PRA,
but it did significantly attenuate the HDZ-evoked increase in PRA (Fig.
1). This blunting of the HDZ-evoked
increase in PRA by OT-Ant did not result from a decreased level of
arterial hypotension, because HDZ treatment decreased MAP from ~115
to ~75 mmHg regardless of whether rats also were treated with OT-Ant
(Fig. 2). However, although OT-Ant did
not significantly affect basal HR or the initial tachycardia evoked by
HDZ, it did blunt subsequent HDZ-evoked increases in HR (Fig. 2).
OT-Ant also did not significantly alter baseline VP levels but it did
attenuate the HDZ-evoked increase in VP (Fig.
3).
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To determine whether the attenuated increase in PRA was due to a
general interference by the OT-Ant with renin secretion, HDZ-treated
rats were injected with the -adrenergic agonist ISP (10 µg/kg),
and a blood sample was collected 5 min later. ISP further increased PRA
and HR and decreased MAP in HDZ-treated rats (Table
1). These additional effects were
comparable whether or not rats were given OT-Ant (Table 1).
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OT-Ant had similar effects in a separate group of rats in which
hypotension was elicited by injection of DZX instead of HDZ. Specifically, OT-Ant did not significantly affect the decrease in MAP
caused by injection of DZX, but it did blunt the increase in PRA and HR
that occurred (Figs. 4A and
5) and completely blocked the increase in
VP levels (Fig. 4B). Furthermore, OT-Ant did not significantly alter the ISP-evoked increase in PRA (Table 1). Note that
in the doses used in this study, DZX and HDZ treatments produced
similar decreases in MAP and increases in HR, but HDZ caused
significantly greater increases in PRA and in VP levels than did DZX
(both P values < 0.01).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The key findings of the present study are that systemic infusion of OT-Ant blunted the increase in PRA, plasma VP levels, and HR in rats made hypotensive by systemic treatment with either HDZ or DZX. Because arterial hypotension increases neurohypophysial OT secretion in rats (19), these data suggest that OT contributes to several adaptive responses to hypotension in rats.
In the present studies the OT analog Atosiban was infused intravenously
to block OT receptors. Interpretation of the obtained results presumes
that this drug is an effective and selective antagonist of OT
receptors. In this regard, Atosiban has been shown to block the actions
of OT on uterine smooth muscle while having no effect on the
antidiuretic or pressor effects of VP (13), although it
does block VP receptors when given in higher doses (13).
Furthermore, the dose of Atosiban used in the present studies has been
shown to block the increase in PRA (9) and the natriuresis
evoked by infusion of OT, without altering urinary water excretion or
the pressor response to VP infused intravenously (7, 8).
Of particular relevance to the present studies is the observation that
the OT-Ant does not interfere with increases in PRA or HR evoked by the
-adrenergic receptor agonist ISP (9), a finding that we
now confirm, because it indicates that Atosiban does not generally
interfere with renin secretion or increases in HR. Presumably, these
effects of ISP are caused by direct stimulation of -adrenergic
receptors in the kidneys and heart, respectively.
The present studies derived from our previous observation that PRA was increased by infusion of OT given in doses that increased plasma OT levels to the range seen in response to arterial hypotension (9, 21). Furthermore, the OT-evoked increase in PRA was independent of the natriuretic effect of OT (21). These findings raised the possibility that during hypotension, neurohypophysial OT secretion may contribute to the increase in PRA that also occurs then. In support of this hypothesis, the present data show clearly that pretreatment with OT-Ant significantly blunted the increase in PRA evoked by two different hypotensive drugs, DZX and HDZ. Treatment with the OT-Ant attenuated the increase in PRA caused by DZX and HDZ by two- to threefold, which is quantitatively similar to the two- to threefold increase in PRA produced by infusion of OT (9). However, when viewed as the absolute change in PRA, the magnitude of the drug's effect is more substantial; OT infusion increased PRA by ~5 ng angiotensin I ml/h, whereas the OT-Ant reduced HDZ- and DZX-evoked increases in PRA by 15-45 ng angiotensin I ml/h. These results suggest that the contribution of OT to hypotension-evoked renin secretion is greater than that estimated from the effects of OT administered alone, possibly as a result of OT interacting with other stimuli for renin secretion that are present during hypotension.
Previous studies have shown that the increase in PRA evoked by
nonhypovolemic hypotension can be largely blocked by injection of a
-adrenergic receptor antagonist (11). These findings
suggest that the evoked increase in renin secretion is mediated largely by increased sympathoadrenal activity. However, it should be noted that
OT-evoked renin secretion is also blocked by a -adrenergic receptor
antagonist (9). Thus it seems likely that OT influences renin secretion through an action involving the sympathetic nervous system.
The observation that OT-Ant interfered with tachycardia evoked by DZX or HDZ also suggests an interaction of OT with the sympathoadrenal system. Hypotension causes a rapid tachycardia that is mediated predominantly by increases in sympathetic activity associated with the baroreceptor reflex (6). Interestingly, whereas the tachycardia that occurred during the first few minutes of hypotension was not altered by OT-Ant, the sustained tachycardia that otherwise was induced by DZX or HDZ was significantly reduced by OT-Ant. These observations suggest that the initial and sustained periods of tachycardia during hypotension may not be mediated by similar mechanisms. In agreement with this possibility, although rats with chronic sinoaortic baroreceptor denervation lack the rapid reflex tachycardia evoked by acute hypotension, sustained hypotension still elicits a tachycardia that develops gradually over ~10 min (Sved, unpublished observations).
This is not the first study to suggest that OT may enhance baroreceptor-evoked changes in HR. Russ and Walker (17) reported that intravenous infusion of OT in rats, at a rate that would be expected to increase plasma OT to levels much higher than those attained in the present study (21), significantly potentiated the reflex bradycardia evoked by increased AP. That response was antagonized by an OT receptor antagonist similar to the one used in the present study. In contrast, intravenous infusion of OT in rabbits has been reported to have no effect on the baroreceptor reflex control of HR (12). Thus the influence of increased circulating levels of OT on baroreceptor reflex responses may not be the same across mammalian species; this issue requires further study.
In addition to blunting hypotension-evoked increases in PRA and HR, OT-Ant also significantly attenuated the induced increases in VP secretion. Unlike hypotension-evoked increases in PRA and HR, which are largely sympathetically mediated responses, hypotension-evoked VP secretion is not dependent on the sympathetic nervous system. Thus, in considering the mechanisms by which OT-Ant blunts all three of these hypotension-evoked responses, it seems plausible that OT-Ant acts on the afferent signaling of these responses. The effect of OT to increase baroreceptor-evoked bradycardia in rats (17) is also consistent with the possibility that OT may influence afferent processing of baroreceptor responses. Alternatively, it is possible that OT influences these responses to hypotension in different ways.
An alternative site of action for OT and OT-Ant to influence these variables may be within the central nervous system. Although the peptide structure of OT-Ant would generally preclude its passage through the blood-brain barrier, it could enter the brain via circumventricular organs or by specific transport mechanisms. If systemic administration of OT-Ant did access central OT receptors, then it could have influenced each of the parameters that were studied. Within the spinal cord, OT has been reported to increase the activity of sympathetic preganglionic neurons (3), and therefore it could lead to increased PRA and HR. Indeed, intrathecal injection of OT increases HR in rats (24). Also intriguing are reports that central injection of an OT receptor antagonist or disruption of central OT systems blocks stress-evoked tachycardia (1, 14).
The OT-Ant blunted hypotension-evoked increases in plasma VP levels and PRA, two adaptive responses evoked by hypotension. Nonetheless, the decrease in AP produced by HDZ or DZX was not enhanced by the OT-Ant. This result likely occurred because both DZX and HDZ act directly on vascular smooth muscle cells and thereby interfere with the actions of vasoconstrictor agents such as angiotensin II and VP, whose receptors are located on vascular smooth muscle cell membranes (2, 4, 15, 16).
Another observation of interest was that DZX and HDZ caused the same decrease in AP yet very different increases in PRA and VP secretion. Differences in renin secretion in response to DZX and HDZ have been noted previously and attributed to inhibition by HDZ of the formation of angiotensin II from renin, thereby diminishing the angiotensin-mediated feedback inhibition of renin secretion (22). A related mechanism may underlie the greater increase in plasma VP levels in response to HDZ. If HDZ interferes with the generation of angiotensin II but not the generation of angiotensin I, then HDZ treatment might be associated with a marked increase in the formation of angiotensin-(1-7) (5), which is known to stimulate VP secretion (18).
In summary, the present experiments show that systemic infusion of an OT receptor antagonist markedly attenuates hypotension-evoked renin secretion, tachycardia, and VP secretion. These results suggest that increased release of OT caused by arterial hypotension or hypovolemia is another member of the family of adaptive physiological responses that collectively serve to restore and maintain cardiovascular homeostasis.
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ACKNOWLEDGEMENTS |
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The technical assistance of R. Bandaranayake and M. Fredenslund is greatly appreciated. Dr. P. Melin (Ferring, Sweden) generously donated the OT antagonist used in these studies.
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FOOTNOTES |
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These studies were supported by National Institutes of Health Grants MH-25140 and HL-55687, the Swedish Medical Research Council (Project 00140), the Danish Health Sciences Research Council, and the NOVO-Nordisk Foundation.
A preliminary version of this work was presented at the annual meeting of the Society for the Study of Ingestive Behavior, Pecs, Hungary, July 1998 (Appetite 31: 238, 1998) and the American Physiological Society meeting on the hypothalamic paraventricular nucleus, December 1998 (Physiologist 41: 381, 1998).
Address for reprint requests and other correspondence: A. F. Sved, Dept. of Neuroscience, Univ. of Pittsburgh, 446 Crawford Hall, Pittsburgh, PA 15260 (E-mail sved{at}bns.pitt.edu).
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.
Received 5 June 2000; accepted in final form 1 November 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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