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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 8 2828-2831
Copyright © 2000 by The Endocrine Society

Original Studies

Exercise-Induced Increase in Circulating Adrenomedullin Is Related to Mean Blood Pressure in Heart Transplant Recipients

François Piquard, Anne Charloux, Bertrand Mettauer, Eric Epailly, Evelyne Lonsdorfer, Sorin Popescu, Jean Lonsdorfer and Bernard Geny

Laboratoire des Régulations Physiologiques et des Rythmes Biologiques chez l’Homme et Service de Chirurgie Cardio-Vasculaire, Faculté de Médecine, 67085 Strasbourg, France

Address correspondence and requests for reprints to: Dr. François Piquard, Institut de Physiologie, Faculté de Médecine, 67085 Strasbourg Cedex, France. E-mail: Francois.Piquard{at}physio-ulp.u-strasbg.fr


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Adrenomedullin (ADM) is a newly discovered potent vasorelaxing and natriuretic peptide that recently has been shown to be increased after heart transplantation. To investigate the hemodynamic factors modulating its release and the eventual role of ADM in blood pressure regulation after heart transplantation, seven matched heart-transplant recipients (Htx) and seven normal subjects performed a maximal bicycle exercise test while monitoring for heart rate, blood pressure, and circulating ADM. Baseline heart rate and systemic blood pressure were higher in Htx; left ventricular mass index and ADM tended to be higher after heart transplantation and correlated positively in Htx (r = 0.79, P = 0.03). As expected, exercise-induced increase in heart rate was lower in Htx than in controls (60 ± 11 % vs. 121 ± 14 %, respectively) and blood pressure increase was similar in both groups. Maximal exercise increased significantly plasma ADM in both groups (from 25.3 ± 3.1 to 30.7 ± 3.5 pmol/L, P < 0.05 and from 15.2 ± 1.4 to 29.1 ± 4.4 pmol/L, P = 0.02 in Htx and controls, respectively), the hypotensive peptide level remaining elevated until the 30th min of recovery. A significant inverse relationship was observed between peak mean blood pressure and circulating ADM in Htx (r = -0.86, P < 0.02). Besides showing that circulating ADM is increased after heart transplantation, the present study demonstrates a positive relationship between baseline ADM and left ventricular mass index. Furthermore, maximal exercise-induced increase in ADM is inversely related to mean blood pressure in Htx, suggesting that ADM might participate in blood pressure regulation during exercise after heart transplantation.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
ADRENOMEDULLIN (ADM), produced by vascular smooth muscle cells and by vascular endothelial cells, is a newly discovered potent vasorelaxing and natriuretic peptide (1, 2, 3). Plasma ADM increases in patients with congestive heart failure in proportion to the severity of the disease and has been observed to be elevated in patients or animals with pulmonary or systemic hypertension (4, 5, 6, 7, 8, 9, 10). Secreted by the failing human heart like other cardiac natriuretic peptides (11, 12, 13), circulating ADM recently has been shown to be increased in hypertensive heart-transplant patients (Htx), further supporting its involvement in circulation control (14).

However, the factors modulating ADM release and the physiological role of this new hypotensive peptide after heart transplantation remain to be determined. Because dynamic exercise challenges greatly circulatory homeostasis, it may allow to investigate both the hemodynamic parameters stimulating ADM release and the potential contribution of ADM on blood pressure regulation. Particularly, Htx’s response to exercise is characterized by a blunted heart rate increase secondary to the surgical cardiac denervation (11, 15). This may be useful to determine an eventual specific effect of heart rate increase on ADM release during exercise, by comparing Htx to normal subjects’ responses to exercise. Furthermore, if exercise-induced blood pressure increase is generally similar in Htx and controls, there are very few data on ADM response to exercise (16, 17, 18) and, to date, the effect of exercise on ADM after heart transplantation is unknown.

The three objectives of this study were, therefore: 1) to determine for the first time the effect of maximal dynamic exercise on plasma ADM in Htx, as compared with normal subjects; 2) to investigate the specific contribution of heart rate on exercise-induced ADM release; and 3) to test the hypothesis that increased ADM during exercise might reduce Htx’s cardiac afterload through its hypotensive action.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Subjects

Fourteen male subjects, matched for age and body mass index, gave informed consent and participated in the study, which was approved by the University Review Board for Human Studies. The clinical characteristics of the subjects, cardiac symptom free and in-sinus rhythm, are presented in Table 1Go. The seven Htx were under the usual triple immunosuppressive therapy with cyclosporine (blood residual level at 170 ± 21 ng/mL), prednisolone (10.0 ± 1.5 mg/day), and azathioprine (23.2 ± 7.9 mg/day). Other medications included calcium antagonists (n = 1), nitrate (n = 2), angiotensin conversion inhibitors (n = 2), and/or furosemide (n = 3). The seven matched controls were healthy, not taking medication.


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  		Table 1. Baseline clinical and biological characteristics

 
Study protocol

Maximal exercise testing was performed on a bicycle ergometer (Medifit 1000 S; Maaren, The Netherlands) until exhaustion. After an initial workload of 20 watts during 3 min, the workload was increased every minute to reach the maximal tolerated power, as previously determined, in 10 min. Heart rate, systemic blood pressure (Critikon, Paris, France), and oxygen consumption (Medisoft partnair, Dyn’air, France) were determined noninvasively at rest and at peak exercise. Venous blood samples were obtained in both study groups at the same time points and at the 30th min of recovery.

Echocardiographic data

Echographic data were obtained, in normal subjects and Htx, after a 10-min rest with the subject in left decubitus position, using an Advanced Technology Laboratories (Bothrell, WA) Ultramark 9 echodoppler and a 2.25-MHz transducer. Left ventricular end-diastolic dimension (LVD), interventricular septum thickness (IVST), and left ventricular posterior wall thickness (PWT) were determined by using the left parasternal long axis view, according to the recommendations of the American Society of Echocardiography. Left ventricular mass (LVM) was then calculated from the Penn convention, according to the equation of Devereux and Reichek (19): LVM = 1.04 [(IVST + PWT + LVD)3 - LVD3] - 13.6. Left ventricular mass index (LVMI) was calculated by dividing LVM by body surface area.

Plasma measurements

Blood was collected on ice in EDTA tubes, separated at 4C, and plasma was stored at -80C for subsequent analysis. Plasma ADM concentration was determined by RIA, as described previously, using kits from Peninsula Laboratories (Belmont, CA) after extraction on Sep.Pak C18 cartridges (Waters Corp., Milford, MA) (14). There is no evidence of cross-reactivity between ADM and atrial natriuretic peptide (20).

Statistical analysis

All the results are expressed as means ± SEM. Differences between means were assessed using, as necessary, a one-way (effect of transplantation) or a two-way ANOVA (effect of transplantation and effect of exercise) with repeated measures. When ANOVA was significant, comparisons between individual means were performed using the a posteriori Tukey’s test. The relationship between two variables was examined by regression analysis. Partial correlation was used to test the relationship between ADM and LVMI with adjustment for blood pressure and the relationship between ADM and blood pressure with adjustment for LVMI. The results were considered significant at a level of P < 0.05.


   Results
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 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Baseline period

The characteristics of the two groups are summarized in Tables 1Go and 2Go. Subjects were matched for age and body mass index. Baseline heart rate and mean systemic blood pressure were significantly higher in Htx as compared with controls. As inferred from the fractional shortening, the systolic ventricular function was similar in both groups. LVMI and circulating ADM (25.3 ± 4.1 vs. 15.2 ± 1.4 pmol/L, P = 0.08) tended to be higher after transplantation. A positive relationship was observed between ADM and LVMI (r = 0.79, P = 0.03) in Htx, which remained similar after adjustement for blood pressure (r = 0.78, P = 0.03). No correlation was observed between ADM and blood pressure, at rest.


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  		Table 2. Baseline and peak exercise hemodynamic and respiratory characteristics

 
Exercise period

As expected, maximal tolerated power (122 ± 14 vs. 203 ± 16 watts, P < 0.002) and oxygen consumption (Table 2Go) were lower in Htx than in controls and exercise-induced increase in heart rate was greater in controls (121 ± 14 vs. 60 ± 5%, P = 0.001). Exercise increased mean systemic blood pressure similarly in both groups (22.1 ± 4.2 mm Hg, paired t test P < 0.01, in controls, and 18.1 ± 5.6 mm Hg, P < 0.02, in Htx).

Maximal exercise increased significantly plasma ADM in both groups (from 25.3 ± 4.1 to 30.7 ± 3.5 pmol/L, P < 0.05, in Htx, and from 15.2 ± 1.4 to 29.1 ± 4.4 pmol/L, P = 0.02, in controls), the hypotensive peptide level remaining elevated until the 30th min of recovery (Fig. 1Go). Interestingly, a significant and inverse relationship was observed between peak mean blood pressure and circulating ADM in Htx (r = -0.86; P = 0.02, Fig. 2Go). Such a relationship was improved when adjusting for LVMI (r = -0.97, P < 0.001).



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  		Figure 1. Time course of plasma adrenomedullin in control subjects ({square}) and Htx ({blacksquare}) during rest, at the peak of an exhausting exercise (ExPeak), and after 30 min of recovery (Rec30).

 


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  		Figure 2. Inverse relationship between plasma adrenomedullin and peak mean blood pressure (mBP) in Htx. r = -0.86, P < 0.02.

 

   Discussion
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 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
The present study demonstrates a relationship between elevated baseline ADM and LVMI and that maximal exercise-induced increase in ADM is inversely related to mean blood pressure after heart transplantation.

Previous studies demonstrated that circulating ADM is elevated in case of hypertension and ADM increase has been proposed to be related to cardiac hypertrophy in both animals and humans (7, 8, 9). Accordingly, we have recently reported that ADM is similarly increased in renal patients and Htx and in hypertensive subjects (14). The present study, besides confirming ADM increases after heart transplantation (14, 21), further supports that such an elevation is related to increased LVM. This is consistent with a recent report demonstrating that ventricular ADM levels correlate with the extent of cardiac hypertrophy in a time-dependent manner in rats with pressure overload (22). However, many mechanisms, including hemodynamic overload and humoral factors, are involved in the process of cardiac ventricular hypertrophy (23). Because circulating ADM still correlates with Htx’s LVMI, even after adjustement for blood pressure, it further supports that cardiac hypertrophy per se might play a key role in ADM increase. Thus, although not excluding a role for increased blood pressure, it suggests that other factors leading to cardiac hypertrophy participate likely in ADM increase after heart transplantation. In this view, it is interesting to point out that ADM has been shown to inhibit protein synthesis of cardiomyocytes, regulating, thus, cardiac growth (23).

Because systemic hypertension induces cardiac hypertrophy and because ADM has well described hypotensive properties, it is tempting to speculate that increased circulating ADM may participate in blood pressure regulation after cardiac transplantation. Particularly, both circulating ADM and ADM gene expression being stimulated by acute pressure overload (9), one may raise the hypothesis that ADM release could be enhanced and play a physiological role during exercise-induced increase in blood pressure in hypertensive Htx.

In fact, from the few data available concerning the ADM response to exercise, it seems that submaximal exercise failed to modify plasma ADM in normal subjects and in patients with myocardial infarction (17). Similarly, no significant plasma ADM change was observed in hypertensive patients during submaximal exercise (16). However, maximal exercise significantly increased plasma ADM both in our normal subjects and Htx. This is consistent with a previous report in normal humans, supporting that exercise intensity rather than duration may stimulate ADM release (18).

Whether increased ADM during exercise originated from myocardial source or from other sources is unknown, but the heart is likely to participate in such ADM increase. Indeed, ADM is secreted in multiple sites by vascular endothelial cells and smooth muscles cells, including the heart (24). Particularly, an increased cardiac production and secretion of ADM has been reported from the failing heart (4, 25) and, besides its normal systolic function, the transplanted heart is generally characterized by a mildly impaired diastolic function that worsens during exercise (26).

ADM production in endothelial cells is regulated by a variety of factors. In this view, heart rate did not seem to play a key role in ADM release during exercise. Indeed, although we observed a blunted heart rate increase during maximal exercise after heart transplantation, secondary to the surgical sinus node denervation (11, 15, 27), no relationship between heart rate and ADM was observed either in controls or in Htx. These data also support that, if any, an eventual partial and heteregeneous cardiac reinnervation (28) would have little influence on the exercise-induced ADM release after heart transplantation.

Catecholamines are known to stimulate ADM release by endothelial cells (24, 29) and could, thus, participate in exercise-induced ADM increase. This issue will need further investigations, but relationships between circulating ADM and catecholamines has not been consistently reported (25, 30, 31). On the other hand, only proadrenomedullin but not ADM has been shown to inhibit adrenal catecholamine release in vivo (32).

Increased blood pressure through increased mechanical stress might stimulate ADM production in vascular endothelial cells (33). Furthermore, the rapid change of ADM suggests it could participate in short-term hemodynamic adaptation to dynamic exercise. Thus, Tanaka et al. (18) observed an inverse relationship between systemic blood pressure and ADM increase during maximal exercise in normal humans and proposed that ADM might exert a fall of systemic pressure by its vasodilation effect. Consistently, although correlation does not imply causation, the highly significant inverse relationship we observed between maximal ADM value and peak mean blood pressure supports that ADM might blunt the exercise-induced systemic pressure increase. Particularly, taken in mind that ADM increases local blood flow in heart and kidneys, it may act similarly, on a paracrine manner, on the muscular bed during exercise (34).

ADM was increased by exercise to a similar level both in controls and patients after heart transplantation. Such increase was, thus, relatively blunted in Htx, in view of their higher resting level. The fact that this was not associated with an enhanced blood pressure increase during exercise, as compared with normal subjects, does not rule out a physiological role of ADM in Htx. Indeed, blood pressure increase was adequate for the physical work intensity performed by the patients (11, 15). Interestingly, attenuated ADM increase has also been observed in hypertensive rats after acute pressure overload, suggesting an impaired adaptional response to hemodynamic load. Nonetheless, like in our study, the blood pressure increase was similar in the control and the hypertensive animal groups and, thus, although blunted, ADM increase in response to pressure overload seemed also to be adequate in this study. As proposed by the authors, such ADM deficiency could contribute to the pathogenesis of resting hypertension in rats (9). Additional studies will nevertheless be needed to determine whether such hypotheses may be extended to hypertensive Htx.

In summary, besides showing that resting elevated ADM plasma level is related to LVMI in Htx, this study supports that ADM might participate in blood pressure regulation during exercise after heart transplantation. Because hypertension is very common and difficult to treat in Htx, additional studies could be warranted to determine whether new therapeutic strategies aiming to increase ADM after heart transplantation might be useful.

Received January 5, 2000.

Revised May 11, 2000.

Accepted May 14, 2000.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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