BACKGROUND: The role of arginine vasopressin (AVP) in the heart has yet to be determined. The present study was designed to examine whether AVP is regulated in the human heart. METHODS AND RESULTS: The subjects were 93 patients who underwent coronary angiography and left ventriculography. Blood samples were collected at the aortic root (AO) and the coronary sinus (CS) to measure the plasma levels of AVP. The patients who showed increases in AVP levels at the CS and AO were assigned to the increased AVP group and those who showed no change or a decrease were assigned to the non-increased AVP group. Cardiac function was compared between these 2 groups. There was a significant difference (p<0.0234) in left ventricular end-diastolic volume index between the increased AVP group (125.5 +/-53.4 ml/m2) and the non-increased AVP group (102.2+/-30.6 ml/m2). There was also a significant difference (p<0.0137) in left ventricular stroke volume index between the increased AVP group (66.6+/-23.2 ml/m2) and the non-increased AVP group (54.4+/-18.6 ml/m2). CONCLUSION: These results suggest that both the production of AVP and synthesis with its receptors may be enhanced at regional sites of the human heart in the volume load.
BACKGROUND: The role of arginine vasopressin (AVP) in the heart has yet to be determined. The present study was designed to examine whether AVP is regulated in the human heart. METHODS AND RESULTS: The subjects were 93 patients who underwent coronary angiography and left ventriculography. Blood samples were collected at the aortic root (AO) and the coronary sinus (CS) to measure the plasma levels of AVP. The patients who showed increases in AVP levels at the CS and AO were assigned to the increased AVP group and those who showed no change or a decrease were assigned to the non-increased AVP group. Cardiac function was compared between these 2 groups. There was a significant difference (p<0.0234) in left ventricular end-diastolic volume index between the increased AVP group (125.5 +/-53.4 ml/m2) and the non-increased AVP group (102.2+/-30.6 ml/m2). There was also a significant difference (p<0.0137) in left ventricular stroke volume index between the increased AVP group (66.6+/-23.2 ml/m2) and the non-increased AVP group (54.4+/-18.6 ml/m2). CONCLUSION: These results suggest that both the production of AVP and synthesis with its receptors may be enhanced at regional sites of the human heart in the volume load.