Sensitization of cardiac vagal afferent reflexes at the sensory receptor level: an overview.
The gain or sensitivity of reflexes originating in cardiac sensory receptors with vagal afferent pathways is highly dynamic. This modulation is usually attributed to central nervous system or efferent mechanisms. This paper briefly reviews evidence that modulation of reflexes originating in the heart can also occur at the sensory or afferent level. Five examples are cited: calcium antagonists, cardiac glycosides, arginine vasopressin, atrial natriuretic peptides, and changes in dietary sodium. These examples emphasize the role of ionic and humoral factors in regulation of cardiac vagal afferent function. This concept of sensory modulation of cardiac vagal afferents has implications for cardiovascular pharmacology and for pathophysiological states such as heart failure and hypertension.
D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002301:Cardiac Glycosides / Q000494:pharmacology; D002628:Chemoreceptor Cells / Q000187:drug effects*; D004285:Dogs; D009475:Neurons, Afferent / Q000187:drug effects; D011311:Pressoreceptors / Q000187:drug effects*; D051381:Rats; D012018:Reflex / Q000187:drug effects*; D012964:Sodium / Q000502:physiology; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*
D002121:Calcium Channel Blockers; D002301:Cardiac Glycosides; D001127:Arginine Vasopressin; D009320:Atrial Natriuretic Factor; D012964:Sodium