This paper presents a physiological long-term model of the cardiovascular system. It integrates the previous models developed by Guyton, Uttamsingh and Coleman. Additionally it introduces mechanisms of direct effects of the renal sympathetic nerve activity (rsna) on tubular sodium reabsorption and renin secretion in accordance with experimental data from literature. The resulting mathematical model constitutes the first long-term model of the cardiovascular system accounting for the effects of rsna on kidney functions in such detail. The objective of developing such a model is to observe the consequences of long-term rsna increase and impairment of rsna inhibition under volume loading. This model provides an understanding of the rsna-related mechanisms, which cause mean arterial pressure increase in hypertension and total sodium amount increase (sodium retention) in congestive heart failure, nephrotic syndrome and cirrhosis.