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CLINICAL STUDIES

Adenosine causes the release of active renin and angiotensin II in the coronary circulation of patients with essential hypertension

Agostino Virdis^*, Lorenzo Ghiadoni^*, Mario Marzilli, Enrico Orsini, Stefania Favilla^*, Piero Duranti^*, Stefano Taddei^*, Paolo Marraccini and Antonio Salvetti^*

^* Department of Internal Medicine, University of Pisa, Pisa, Italy
C.N.R. Institute of Clinical Physiology, Pisa, Italy

Manuscript received May 6, 1998; revised manuscript received January 5, 1999, accepted January 21, 1999.

Reprint requests and correspondence: Dr. Agostino Virdis, Department of Internal Medicine, University of Pisa, Via Roma, 67, 56100 Pisa, Italy

OBJECTIVES

The aim of the study was to evaluate whether adenosine infusion can induce production of active renin and angiotensin II in human coronary circulation.

BACKGROUND

Adenosine can activate angiotensin production in the forearm vessels of essential hypertensive patients.

METHODS

In six normotensive subjects and 12 essential hypertensive patients adenosine was infused into the left anterior descending coronary artery (1, 10, 100 and 1,000 µg/min x 5 min each) while active renin (radioimmunometric assay) and angiotensin II (radioimmunoassay after high performance liquid chromatography purification) were measured in venous (great cardiac vein) and coronary arterial blood samples. In five out of 12 hypertensive patients adenosine infusion and plasma samples were repeated during intracoronary angiotensin-converting enzyme inhibitor benazeprilat (25 µg/min) administration. Finally, in adjunctive hypertensive patients, the same procedure was applied during intracoronary sodium nitroprusside (n = 4) or acetylcholine (n = 4).

RESULTS

In hypertensive patients, but not in control subjects, despite a similar increment in coronary blood flow, a significant (p < 0.05) transient increase of venous active renin (from 10.7 ± 1.4 [95% confidence interval 9.4 to 11.8] to a maximum of 13.8 ± 2.1 [12.2 to 15.5] with a consequent drop to 10.9 ± 1.8 [9.7 to 12.1] pg/ml), and angiotensin II (from 14.6 ± 2.0 [12.7 to 16.5] to a maximum of 20.4 ± 2.7 [18.7 to 22.2] with a consequent drop to 16.3 ± 1.8 [13.9 to 18.7] pg/ml) was observed under adenosine infusion, whereas arterial values did not change. Calculated venous–arterial active renin and angiotensin II release showed a strong correlation (r = 0.78 and r = 0.71, respectively; p < 0.001) with circulating active renin. This adenosine-induced venous angiotensin II increase was significantly blunted by benazeprilat. Finally, both sodium nitroprusside and acetylcholine did not affect arterial and venous values of active renin and angiotensin II.

CONCLUSIONS

These data indicate that exogenous adenosine stimulates the release of active renin and angiotensin II in the coronary arteries of essential hypertensive patients, and suggest that this phenomenon is probably due to renin release from tissue stores of renally derived renin.

Abbreviations and Acronyms   ACE = angiotensin-converting enzyme   CBF = coronary blood flow   LAD = left anterior descending coronary artery   RAS = renin–angiotensin system

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