Chronic heart failure is a complex clinical syndrome characterized by many neuroendocrine manifestations by which the organism responds to the reduced cardiac output--the reduced minute volume. In order to ensure the blood flow to vitally important organs in several regions of the circulation vasoconstriction occurs. The plasma noradrenaline (NA) level rises and this correlates with the stage of chronic heart failure. In chronic heart failure the renin production in the kidney and vascular wall rises and thus also the angiotensin II (AG II) formation is increased. AG II is an affective direct arterial constrictor which facilitates NA release from terminal nerve endings and stimulates aldosterone secretion. AG II conditions also myocardial hypertrophy. Arginine vasopressin (AVP) is usually also elevated in chronic heart failure. In vasoconstriction associated with chronic heart failure participates also endothelin, an effective vasoconstrictor substance which modulates the renin-angiotensin-aldosterone system and has also an antinatriuretic effect. As a compensating response to the increased formation of vasoconstrictor substance during chronic heart failure endogenous vasodilatating and natriuretic substances are formed. Another vasodilatating factor is the atrial natriuretic factor (ANF) which is secreted by atrial myocytes as a result of atrial distension, hypernatremia or tachycardia. ANF inhibits renin, aldosterone and AVP formation. The ANF level correlates closely with the grade of chronic heart failure. With advancing heart failure also down regulation of receptors for ANF occurs. Dopamine, a natural precursor of NA, is also a vasodilatating substance and is secreted during stimulation of the sympathetic nerve. In chronic heart failure the formation of vasoconstrictor substances predominates above vasodilating ones.(ABSTRACT TRUNCATED AT 250 WORDS)

Keywords: Heart Failure /physiopathology/; Humans; Natriuretic Agents /physiology/; Neurotransmitter Agents /physiology/; Vasomotor System /physiology/