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Published on: January 19, 2020
Regulation of arginine vasopressin in the human heart
Ikuyoshi Watanabe1, Shigemasa Tani, Ken Nagao
1Division of Cardiovascular Medicine, Surugadai Nihon University Hospital, Tokyo, Japan. ikuwata@med.nihon-u.ac.jp
Insights
Arginine vasopressin (AVP) is regulated in the human heart. Increased AVP levels correlate with enhanced cardiac function, suggesting localized AVP production and receptor synthesis in response to volume load.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
Background:
- The role of arginine vasopressin (AVP) in cardiac function remains unclear.
- Investigating local regulation of AVP within the human heart is crucial.
Purpose of the Study:
- To determine if arginine vasopressin (AVP) is regulated within the human heart.
- To explore the relationship between AVP levels and cardiac function.
Main Methods:
- Analyzed plasma AVP levels in 93 patients at the aortic root and coronary sinus.
- Correlated AVP levels with cardiac function parameters including left ventricular volumes and stroke volume.
- Grouped patients based on AVP level changes (increased vs. non-increased).
Main Results:
- Significant differences in left ventricular end-diastolic volume index between groups (p<0.0234).
- Significant differences in left ventricular stroke volume index between groups (p<0.0137).
- Patients with increased AVP showed enhanced cardiac function parameters.
Conclusions:
- Suggests local production and synthesis of AVP and its receptors in the human heart.
- Indicates enhanced AVP activity in the heart under conditions of volume load.
- Highlights a potential role for AVP in modulating cardiac function regionally.
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.
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