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1 Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia, Università del Piemonte Orientale ‘A. Avogadro’, via Solaroli 17, I-28100 Novara, Italy
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Abstract |
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-nitro-L-arginine methyl ester (L-NAME). The subsequent intra-arterial infusion of human placental lactogen did not cause any significant changes in measured blood flows, even when performed after reversing the increase in arterial blood pressure and coronary, renal and iliac resistance caused by L-NAME with continuous intravenous infusion of papaverine. These results indicate that the coronary, renal and iliac vasoconstriction caused by human placental lactogen, known to involve antagonism of ß2-adrenergic vasodilatory effects, was mediated by inhibition of nitric oxide release.
(Received 11 November 2005;
accepted after revision 27 February 2006; first published online 2 March 2006)
Corresponding author C. Molinari: Facoltà di Medicina e Chirurgia, via Solaroli 17, I-28100 Novara, Italy. Email: molinari{at}med.unipmn.it
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Introduction |
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The present work in anaesthetized pigs was therefore designed to establish the role of nitric oxide in the coronary, renal and iliac vasoconstriction caused by human placental lactogen that is mediated through inhibition of the vasodilatory effects of ß2-adrenergic receptors. This was achieved by comparing the response of coronary, renal and iliac blood flow to intra-arterial infusion of human placental lactogen before and after blockade of nitric oxide synthase whilst preventing the secondary interference caused by changes in heart rate and arterial blood pressure.
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Methods |
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Blood pressures in the ascending aorta and in the right atrium were recorded via catheters connected to pressure transducers (Statham P23 XL, Gould, Valley View, OH, USA) inserted into the right femoral artery and the right external jugular vein, respectively. The abdomen was opened by a mid-line incision, and an electromagnetic flowmeter probe (model BL 613, Biotronex Laboratory Inc., Chester, MD, USA) was positioned near the origin of the left renal and left external iliac arteries. The chest was opened in the left fourth intercostal space, the pericardium was cut, and an electromagnetic flowmeter probe was positioned around the proximal part of the anterior descending coronary artery. Distal to the probe, a plastic snare was placed around each artery for the assessment of zero blood flow. Each probe was calibrated in vitro at the end of every experiment.
Left ventricular pressure was measured by means of a catheter connected to a pressure transducer (Statham P23 XL) inserted through the left atrium. The frequency response of the catheter–manometer system was found to be flat (± 5%) up to 40 Hz. To pace the heart, electrodes were sewn on the left atrial appendage and connected to a stimulator (Model S8800, Grass Instruments, Quincy, MA, USA) delivering pulses of 3–5 V with 2 ms duration at the required frequency. Arterial blood pH and partial pressures of O2 and CO2 were measured using a blood gas analyser (IL 1304, IL Instrumentation Laboratory, Lexington, MA, USA). The haematocrit was also measured. The acid–base status of the animals was kept within normal limits during the experiments by the infusion of a solution of 2.8% sodium bicarbonate and by adjusting the respiratory stroke volume, when necessary (Linden & Mary, 1983).
To prevent changes in arterial blood pressure during the experiments, a large-bore cannula was introduced into the left internal mammary artery and connected to a reservoir containing Ringer solution kept at 38°C. The reservoir was pressurized using compressed air, which was controlled with a Starling resistance, and the pressure within the reservoir was measured by a mercury manometer. This method has been shown in anaesthetized pigs to allow the aortic blood pressure to be maintained at steady levels without significant changes in right atrial and left ventricular pressures or the haematocrit (e.g. Molinari et al. 2002, 2004). Blood coagulation was avoided by the intravenous injection of heparin (Parke-Davis; initial dose of 500 i.u. kg–1, and subsequent doses of 50 i.u. kg–1 every 30 min). The rectal temperature of the pigs was monitored and kept between 38 and 40°C using an electric heating pad.
Mean and phasic aortic blood pressures, right atrial pressure, left ventricular pressure, mean and phasic coronary, renal and iliac blood flows were monitored and recorded together with heart rate and the maximum rate of change of left ventricular systolic pressure (dP/dtmax) on an electrostatic strip chart recorder (Gould ES 2000). The heart rate was obtained from the electrocardiogram. The frequency response of the differentiator used to obtain left ventricular dP/dtmax was flat (± 5%) up to 150 Hz.
To calculate coronary vascular resistance, the difference between mean aortic blood pressure (which was prevented from changing) and mean left ventricular pressure during diastole was considered as the coronary pressure gradient. Coronary vascular resistance was calculated as the ratio between this pressure gradient and mean diastolic coronary blood flow during the steady state. The diastolic period of measurement was defined as starting when ventricular pressure reached its minimum value after systole and ending when it increased at the end of diastole. Renal and iliac vascular resistance was calculated as the ratio between mean aortic blood pressure and mean renal and iliac blood flows.
At the end of each experiment, each animal was killed by an intravenous injection of 90 mg kg–1 sodium pentobarbitone.
Experimental protocol
The experiments were begun after at least 30 min of steady-state conditions with respect to measured haemodynamic variables. To avoid interference by any possible changes in heart rate and aortic blood pressure during the experiments, the heart was paced to a frequency higher, by 20 beats min–1, than that observed during the steady state, and the arterial system was connected to the pressurized reservoir. After at least 10 min of steady-state conditions, the experiments were carried out by intra-arterially infusing either a solution of human placental lactogen obtained by diluting in saline 1 mg of the hormone dissolved in 1.5 ml of serum or 1.5 ml of serum diluted in saline as a control. Human placental lactogen was infused for a period of 5 min into the coronary, renal or iliac arteries at a dose of 0.2 µg for each millilitre per minute of measured blood flow with an infusion pump (Model 22, Harvard Apparatus), working at constant rate of 1 ml min–1, by using a catheter connected to a butterfly needle inserted into the arteries distal to the flowmeter probes. The dose of hormone to be infused was calculated from its reported rate of secretion in pregnant women of about 1–3 g day–1 (Walker et al. 1991) and has been previously demonstrated in the same experimental model to cause coronary, renal and iliac vasoconstriction (Grossini et al. 2006). Recordings taken for 10 min during the steady state before each infusion of human placental lactogen were used as controls. Measurements of haemodynamic variables were obtained during the last minute of infusion in the steady state and compared with control values. Changes in blood flow caused by each dose were compared with control values obtained before starting the infusion. After each infusion was stopped, observations were continued for 20 min. It has previously been shown that the coronary, renal and iliac vasoconstriction caused by human placental lactogen begins within 2 min after starting the infusion, reaches a steady state in about 3 min and is completely over within 10 min after the end of infusion.
In each pig, a first experiment of intra-arterial infusion of human placental lactogen was performed to demonstrate and quantify the effect of coronary, renal and iliac vasoconstriction caused by the hormone. In each pig, human placental lactogen was first infused into the coronary artery. When coronary blood flow returned to control values before infusion, the hormone was infused into the renal artery. When renal blood flow returned to control values before infusion, the hormone was infused into the iliac artery. The role of nitric oxide in the responses obtained was studied by repeating the experiment of intra-arterial infusion after blockade of coronary, renal and iliac nitric oxide synthase with intra-arterial administration of N-nitro-L-arginine methyl ester (L-NAME) at a dose of 2 mg for each millilitre per minute of measured blood flow. This dose of L-NAME has previously been shown in anaesthetized pigs to abolish the coronary, renal and iliac vasodilatation caused by intra-arterial infusion of testosterone and the coronary, renal and iliac vasoconstriction caused by intravenous infusion of dehydroepiandrosterone (Molinari et al. 2002, 2003, 2004). L-NAME was administered in the absence of pacing of the heart and without controlling arterial blood pressure. After assessing the effects of this agent, the heart was paced to the same frequency as before, and changes in arterial blood pressure were prevented. In six of the eight pigs, human placental lactogen was first infused into each of the three arteries after injecting L-NAME into the coronary artery. In the same pigs, the hormone was then infused into the renal and iliac arteries after injecting L-NAME into the renal artery. Finally, human placental lactogen was infused into the iliac artery after injecting L-NAME into the same artery. In the remaining two pigs, infusions of human placental lactogen were performed after injecting L-NAME into the three arteries when a steady state had been attained during continuous intravenous infusion of papaverine (3.5–4.5 mg kg–1 h–1; Sigma) to reverse the increase in arterial blood pressure and coronary, renal and iliac vascular resistance caused by L-NAME.
Student's paired t test was used to examine changes in measured variables caused by human placental lactogen infusion. A value of P < 0.05 was considered statistically significant. Group data or their changes are presented as means ±S.D. (range).
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Results |
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Effects of intra-arterial infusion of human placental lactogen
In the eight pigs, intra-arterial infusions of the vehicle did not cause any changes in the control values of measured haemodynamic variables. Control values of heart rate, mean aortic blood pressure, left ventricular dP/dtmax, mean right atrial pressure and left ventricular end-diastolic pressure, respectively, were 106.3 ± 8.1 (98–121) beats min–1, 91.9 ± 9.3 (79–105) mmHg, 2390 ± 280 (2057–2913) mmHg s–1, 3.4 ± 0.6 (2.4–4.1) mmHg and 6.1 ± 1 (4.9–7.6) mmHg. Infusion of human placental lactogen caused no significant changes (at least P > 0.10) in these variables. Group changes in coronary, renal and iliac blood flow caused by intra-arterial infusion of the hormone are shown in Table 1 and individual changes are shown in Fig. 1.
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Role of nitric oxide
In the eight pigs, intra-arterial administration of L-NAME increased heart rate, mean aortic blood pressure and left ventricular dP/dtmax by 6.1 ± 3.2 (1–10) beats min–1 (P < 0.0005), 16.4 ± 6.9 (8–29) mmHg (P < 0.0005) and 73 ± 21 (32–98) mmHg s–1 (P < 0.0005), respectively. Injection of L-NAME into the coronary artery did not significantly (P > 0.10) change (–1.3 ± 3.1 ml min–1; –6.4 to +3.1) mean coronary blood flow. Injection of L-NAME into the renal artery decreased renal blood flow by 66 ± 30 (34–102) ml min–1 (P < 0.0005). Injection of L-NAME into the iliac artery decreased iliac blood flow by 5 ± 3 (1–11) ml min–1 (P < 0.0025). In two of the eight pigs in which L-NAME was injected into the three arteries before the intra-arterial infusions of human placental lactogen, infusion of papaverine reversed the effect of L-NAME in that the infusion decreased mean aortic blood pressure by 15 and 19 mmHg, coronary vascular resistance by 0.28 and 0.35 mmHg ml min–1, renal vascular resistance by 0.07 and 0.08 mmHg ml min–1, and iliac vascular resistance by 0.22 and 0.25 mmHg ml min–1.
In the same pigs, the increases in coronary, renal and iliac vascular resistance caused by L-NAME were, respectively, 0.29 and 0.24 mmHg ml min–1, 0.07 and 0.07 mmHg ml min–1, and 0.20 and 0.22 mmHg ml min–1.
L-NAME injection into the coronary artery. In each of the eight pigs, blockade of nitric oxide synthase abolished the response of coronary blood flow to the subsequent intracoronary infusion of human placental lactogen (Fig. 2), without affecting the responses of renal and iliac blood flow to the infusion of human placental lactogen into the renal and iliac arteries. Intracoronary infusion of human placental lactogen did not significantly (P > 0.30) change coronary blood flow, which was altered only by –0.1 ± 0.7 (–1.1 to +0.9) ml min–1 from control values of 61.9 ± 4.6 (56–68) ml min–1. In the six pigs in which L-NAME was injected only into the coronary artery, the differences between the responses of renal and iliac blood flow to intra-arterial infusion of human placental lactogen before and after injection of L-NAME into the coronary artery were not significant (P > 0.15 and P > 0.20, respectively). During these experiments, only insignificant changes (at least P > 0.15) occurred in left ventricular dP/dtmax, mean right atrial pressure and left ventricular end-diastolic pressure.
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L-NAME injection into the iliac artery. In each of the eight pigs, blockade of nitric oxide synthase abolished the response of iliac blood flow to the subsequent infusion of human placental lactogen into the iliac artery (Fig. 2). Infusion of human placental lactogen into the iliac artery did not significantly (P > 0.25) change iliac blood flow, which was altered by only –0.4 ± 2.0 (–3 to +3) ml min–1 from control values of 101 ± 8 (88–112) ml min–1. During these experiments, only insignificant (at least P > 0.25) changes occurred in left ventricular dP/dtmax, mean right atrial pressure and left ventricular end-diastolic pressure.
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Discussion |
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To enable the observed changes of coronary, renal and iliac blood flow to be related primarily to the administration of human placental lactogen, care was taken during the experiments to avoid secondary interference by other concomitant variables. Firstly, the heart rate and arterial blood pressure were prevented from changing, to avoid the influence of reflex, local metabolic and physical factors. Secondly, during the experiments there were no significant changes in left ventricular dP/dtmax, mean right atrial pressure and left ventricular end-diastolic pressure, thereby excluding metabolic changes related to changes in left ventricular contractility or reflexes caused by involvement of mechanoreceptors situated in the heart. Thirdly, human placental lactogen was infused into the appropriate region and not systemically. Indeed, the observed changes in blood flow were confined to the examined region without affecting other parts of the body. In these experimental conditions, intra-arterial infusion of human placental lactogen caused in each pig of this study a decrease in coronary, renal and iliac blood flow, while intra-arterial infusion of the vehicle at the same rate as that of the human placental lactogen did not cause any changes in the baseline values of the same flows. These results confirm previously reported findings obtained in the same experimental model showing that human placental lactogen causes coronary, renal and iliac vasoconstriction (Grossini et al. 2006).
In our previous study, we showed that the coronary, renal and iliac vasoconstriction elicited by intra-arterial infusion of human placental lactogen involved ß2-adrenergic receptors, since it was abolished by intravenous administration of butoxamine but not by intravenous administration of atropine or phentolamine. The administration of butoxamine caused an increase in arterial blood pressure and in coronary, renal and iliac vascular resistance, indicating the presence of tonic vasodilatory effects attributable to ß2-adrenergic receptors. These findings were consistent with previously reported findings showing a ß2-adrenergic receptor-mediated vasodilatation in several peripheral vascular beds in the same experimental anaesthetized preparation (e.g. Vacca et al. 1996) and indicated that human placental lactogen blocks these tonic vasodilatory effects involving ß2-adrenergic receptors. In the present study, the intra-arterial administration of L-NAME abolished the coronary, renal and iliac vasoconstriction caused by human placental lactogen. The intra-arterial injection of L-NAME caused an increase in arterial blood pressure and in coronary, renal and iliac vascular resistance. This effect could be argued to mask the vasoconstrictive effects of the subsequent intra-arterial infusion of human placental lactogen. However, when the arterial blood pressure and vascular resistance increases caused by L-NAME were reversed by papaverine, the intra-arterial infusion of human placental lactogen did not cause significant changes in coronary, renal and iliac blood flow. This indicated that the effects of L-NAME on the baseline values of arterial blood pressure and vascular resistance were not involved in the blockade of the coronary, renal and iliac response to human placental lactogen. Since it is known that L-NAME prevents the formation of nitric oxide (Henderson, 1991), the present results indicate that blockade of tonic vasodilatory effects attributable to ß2-adrenergic receptors caused by human placental lactogen involves the release of nitric oxide from endothelium.
The present results are consistent with previously reported findings showing that the release of nitric oxide from the endothelium can mediate or modulate ß-adrenergic effects in the coronary and peripheral vasculature though there are reports that did not confirm such effects in isolated coronary arteries (Macdonald et al. 1987; Xu & Huang, 2000). In the dog it has been shown that the responses of the coronary arteries to the ß-agonist isoprenaline require an intact endothelim (Rubanyi & Vanhoutte, 1985), that endothelium-derived relaxing factor formation contributes to the dilatation of coronary resistance vessels elicited by ß2-adrenergic effects (Parent et al. 1993), and that the limb vasodilatory response to adrenaline depends on intact endothelium of the iliac artery (Young & Vatner, 1986). Also, ß-adrenergic vasodilatory responses of the hindlimb of chronically instrumented conscious rats were found to be modulated by endothelium-derived relaxing factor release, which is mediated by adrenoceptors (DiCarlo et al. 1995). In the pig heart, nitric oxide synthase has been shown to be present mainly in the endothelium of the coronary vessels (Ursell & Mayes, 1993), and coronary microvessels have been demonstrated to be dilated both by ß-adrenergic activation and by stimulation of nitric oxide release (Quillen et al. 1992). Moreover, in the same experimental model as the present study, the release of nitric oxide has been shown to be involved in the coronary vasoconstriction caused by growth hormone (Molinari et al. 2000) and in the coronary, mesenteric, renal and iliac vasoconstriction caused by dehydroepiandrosterone (Molinari et al. 2003, 2004), vascular effects which were demonstrated to be elicited by blockade of a tonic vasodilatory effect attributable to ß2-adrenergic receptors.
The involvement of nitric oxide in the widespread vasoconstriction elicited by human placental lactogen can be argued to contribute to the physiological control of regional blood flow during pregnancy. Previous reports on the haemodynamic effects of 17ß-oestradiol and progesterone in anaesthetized pigs have shown that these hormones cause widespread vasodilatation through mechanisms which involve the endothelial release of nitric oxide (Vacca et al. 1999; Molinari et al. 2001a,b). The increase in the endothelial release of nitric oxide caused by the increase in maternal peripheral serum levels of oestrogens and progesterone as pregnancy advances could be argued to be balanced by the inhibition of nitric oxide release caused by the concomitant progressive increase in maternal peripheral serum levels of human placental lactogen (Walker et al. 1991). This hypothesis is supported by the fact that the vasoconstrictive effect of human placental lactogen and the vasodilating effects of 17ß-oestradiol and progesterone have been found to be greater in the coronary vascular bed than in the renal and iliac beds.
The decrease in the endothelial release of nitric oxide and the consequent vasoconstriction caused by human placental lactogen raises the possibility that this hormone may be involved in pathological conditions during pregnancy. Although human placental lactogen has been associated with pregnancy-induced hypertension and pre-eclampsia, an increased (Obiekwe et al. 1984; Murai et al. 1997) or a decreased level (Westergaard et al. 1984; Bersinger et al. 2002) of this hormone has been reported in these conditions. The present findings, showing that the peripheral vasoconstriction caused by human placental lactogen involves the inhibition of the endothelial release of nitric oxide, are consistent with the possibility that human placental lactogen contributes to the pathogenesis of pregnancy-related hypertension and pre-eclampsia.
In conclusion, the present study has shown that the coronary, renal and iliac vasoconstrictor effect of human placental lactogen, known to involve antagonism of ß2-adrenergic receptors, was mediated by inhibition of endothelial release of nitric oxide.
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References |
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) and iliac artery (
) 
, data from the two pigs which also received papaverine. The values obtained during the test period of measurement are plotted on the ordinate against the control values before the infusions on the abscissa. The continuous line is the line of equality.