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Histamine is a basic amine stored in mast cells, with its release capable of activating one of four histamine receptors. The histamine 3 receptor (H 3 R) is known to be cardioprotective during acute ischemia by acting to limit norepinephrine release. However, a recent study reported that myofibroblasts isolated from the infarct zone of rat hearts responded to H 3 R activation by up-regulating collagen production. Thus, it is necessary to clarify the potential role of the H 3 R in relation to fibrosis in the heart. We identified that the mouse left ventricle (LV) expresses the H 3 R. Isolation of mouse cardiac fibroblasts determined that while angiotensin II (Ang II) increased levels of the H 3 R, these cells did not produce excess collagen in response to H 3 R activation. Using the Ang II mouse model of adverse cardiac remodeling, we found that while H 3 R blockade had little effect on cardiac fibrosis, activation of the H 3 R reduced cardiac fibrosis and macrophage infiltration. These findings suggest that when activated, the H 3 R is anti-inflammatory and anti-fibrotic in the mouse heart and may be a promising target for protecting against cardiac fibrosis.

The Histamine 3 Receptor Is Expressed in the Heart and Its Activation Opposes Adverse Cardiac Remodeling in the Angiotensin II Mouse Model