Cardiac Effects of Vasopressin

Abstract

Vasopressin is an essential hormone involved in the maintenance of cardiovascular homeostasis. It has been in use therapeutically for many decades, with an emphasis on its vasoconstrictive and antidiuretic properties. However, this hormone has a ubiquitous influence and has specific effects on the heart. Although difficult to separate from its powerful vascular effects in the clinical setting, a better understanding of vasopressin's direct cardiac effects could lead to its more effective clinical use for a variety of shock states by maximizing its therapeutic benefit. The cardiac-specific effects of vasopressin are complex and require further elucidation. Complicating our understanding include the various receptors and secondary messengers involved in vasopressin's effects, which may lead to various results based on differing doses and varying environmental conditions. Thus, there have been contradictory reports on vasopressin's action on the coronary vasculature and on its effect on inotropy. However, beneficial results have been found and warrant further study to expand the potential therapeutic role of vasopressin. This review outlines the effect of vasopressin on the coronary vasculature, cardiac contractility, and on hypertrophy and cardioprotection. These cardiac-specific effects of vasopressin represent an interesting area for further study for potentially important therapeutic benefits.

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“…In addition, it has been demonstrated that the heart muscle has the capacity also to release VP [44,45]. Added to this is the number of studies which have shown that administration of VP in shock added to the endogenous release of VP often causes decreases in cardiac output and decreases in perfusion of the intestinal tract, kidneys and liver [43][44][45]. These affects can and often lead to lifethreatening situations.…”

“…This controversy might be related to different actions on the major, surface coronaries versus the smaller arterioles deep within the walls of the ventricles. Another factor that has to be considered in all forms of circulatory shock, is that there is a massive release of VP from the paraventricular and supraoptic nuclei of the hypothalamus which often will reach levels in the blood which are from 20-200 times normal [45]. In addition, it has been demonstrated that the heart muscle has the capacity also to release VP [44,45].…”

“…Another factor that has to be considered in all forms of circulatory shock, is that there is a massive release of VP from the paraventricular and supraoptic nuclei of the hypothalamus which often will reach levels in the blood which are from 20-200 times normal [45]. In addition, it has been demonstrated that the heart muscle has the capacity also to release VP [44,45]. Added to this is the number of studies which have shown that administration of VP in shock added to the endogenous release of VP often causes decreases in cardiac output and decreases in perfusion of the intestinal tract, kidneys and liver [43][44][45].…”

“…These affects can and often lead to lifethreatening situations. On a molar basis, VP is one of the most powerful peripheral vasoconstrictor agents, even more powerful than angiotensin II [43][44][45]. Most arteries and arterioles (including coronary vessels), in the body, show greater contractile sensitivity to VP compared to angiotensin II, in terms of both affinity and intrinsic activity [19,21,33,35,36].…”

“…VP has been shown, in numerous animal and human studies, to cause reductions in coronary arterial flows that become severe, resulting in ischemia [37][38][39][40][41][42][43][44][45]. However, some studies suggest that this may not either happen or VP may induce vasodilatation (in pulmonary and cerebral vascular beds [45], despite evidence to the contrary [37][38][39][40][41][42][43][44][45]. This controversy might be related to different actions on the major, surface coronaries versus the smaller arterioles deep within the walls of the ventricles.…”