B-type natriuretic peptide (BNP) is a new biomarker expressed from the myocytes located in the ventricle. When heart failure (HF) progresses, the change of compensatory mechanisms that result in the pathophysiological process of HF develops such as sympathetic stimulation and volume overload. Those changes in pathophysiological responses finally become detrimental as HF progresses. The release of BNP results in a variety of physiological changed that confront the compensatory mechanisms. BNP is a counter-regulatory hormone. In the kidneys, BNP increases glomerular filtration rates via efferent arteriolar vasoconstriction and afferent arteriolar vasodilatation. This results in diuresis and sodium loss, which ameliorate fluid balance and congestion. In the cardiovascular system, BNP causes a decrease in blood pressure and preload by causing vasodilatation. In the nervous system, there is a suppression of sympathetic activity as a result of BNP release, resulting in improvement in heart rate with reduction of tachycardia. BNP is now widely used in cardiovascular clinical practice and research throughout the world. This report reviews the relationship between heart failure and BNP for providing information in the care of heart failure.