Cardiovascular reflex responses induced by epicardial chemoreceptor stimulation

Abstract

The cardiac mechano- and chemoreceptors are broadly distributed in the myocardium and coronary vessels. A portion of these receptors extends over the epicardium and pericardium and therefore can be excited by mechanical or chemical stimuli directly applied to the surface of the heart. Excitation of epicardial receptors by topical application of chemical compounds elicits a variety of reflex cardiovascular responses, without the vascular or systemic effects of the drug administered systemically. A considerable number of studies has used the epicardial sensory field as a tool to delineate the functional characteristics of the cardiac afferent neurones in normal as well as in pathological conditions. In this review we analyze the cardiovascular reflex responses induced by epicardial application of a variety of substances like bradykinin, nicotine, muscarine, isoprenaline, adenosine, potassium chloride, capsaicin, prostaglandins or substance P in physiological models and also in models with acute myocardial ischemia or heart failure. The data highlight the contribution of the epicardial sensory neurites to the overall control of the cardiovascular system and, on the other hand, strengthen the need for further investigations directed to better elucidate the reflex cardiovascular responses that may develop in patients with pericardial abnormalities.

Interplay between cardiac function and heart development

“…Stable hemodynamic forces are needed to preserve normal ventricular dimensions and functional parameters, and to avoid heart adaptation [114] . The pericardium fulfills an important role in stabilizing several mechanical parameters: it limits heart dilatation during diastole, reduces endomyocardial tension, prevents cardiac hypertrophy in pressure overload conditions, prevents ventricular-atrial blood retrogression under high end-diastolic ventricular pressure, preserves negative endothoracic pressure (crucial for atrial blood filling) and regulates cardiac frequency and arterial blood pressure [27] , [42] , [51] . In the adult, physiological levels of wall shear stress suppress proliferation of endothelial cells and promote their quiescence [112] .…”

Physiology of pericardial fluid production and drainage

“…The normal pericardium contributes in important functions. In is necessary for: (1) lubricating the moving surfaces of the heart, (2) stabilizing the heart anatomic position, (3) isolating the heart from the adjacent anatomical structures, prohibiting the adhesion formation, the inflammatory or neoplastic extention, (4) limiting heart dilatation during diastole, reducing the endomyocardial tension, (5) preventing cardiac hypertrophy in pressure overload conditions, (6) reducing the right ventricular impulse work in left ventricular overload conditions, (7) the ventriculoatrial blood retrogression prevention during high end-diastolic ventricular pressures, (8) the preservation of the negative endothoracic pressure, which is crucial for the atria blood filling, (9) the nervous stimulation response and regulation of the cardiac frequency and arterial blood pressure, (10) the formation of a hydrostatic compensation system ensuring that end-diastolic pressure remains the same at all hydrostatic levels and the Frank–Starling mechanism is functional (Holt, 1970 ; Goto and LeWinter, 1990 ; Cinca and Rodriguez-Sinovas, 2000 ).…”

Cardiac capsaicin‐sensitive sensory nerves regulate myocardial relaxation via S‐nitrosylation of SERCA: role of peroxynitrite

“…Sensory nerve endings may act as potential sensor machinery for ischaemia, as ischaemia, hypoxia, lactate, K + and low pH were shown to stimulate cardiac sensory nerves in association with a release of their transmitters ( Franco‐Cereceda, 1988 ). Sensory nerves may exert a strong influence on cardiac function, cardiac reflexes and adaptive responses due to their nitric oxide (NO) and vasoactive peptide content, such as calcitonin gene‐related peptide and substance P ( Franco‐Cereceda, 1988 ; Ren and Ruda, 1995 ; Sosunov et al , 1995 , 1996 ; Cinca and Rodriguez‐Sinovas, 2000 ). In agreement with the hypotheses outlined above, through the use of capsaicin, we and others have previously shown that cardiac sensory nerves play a role in cardiac adaptation to ischaemic stress ( Li et al , 1996 ; Ferdinandy et al , 1997 ; Wang and Wang, 2005 ; Zhong and Wang, 2007 ), in the regulation of cardiac NO–cGMP system ( Csont et al , 2003 ) and in the mechanism of doxorubicin‐induced heart failure ( Katona et al , 2004 ).…”