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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanically and chemically sensitive receptors in the ventricle have been described histologically and electrophysiologically. Early experiments documented the hypotension and bradycardia that resulted from the intracoronary administration of one of the veratrum alkaloids (the Bezold-Jarisch reflex). Mechanical distension of the ventricles also results in a reflex decrease in heart rate and a reduction in peripheral resistance. Skeletal muscle and coronary vascular resistance appear to be most prominently affected by stimulation of ventricular receptors. Coronary ischemia has also been shown to evoke reflex effects which are attributable to stimulation of ventricular receptors. The resultant bradycardia can be especially ominous in acute myocardial infarction. Changes in myocardial inotropic state have been shown to alter ventricular receptor discharge in experimental animals. This stimulus may evoke reflex changes in peripheral hemodynamics. A variety of humoral substances can alter ventricular receptor discharge and evoke Bezold-Jarisch like responses. These include bradykinin and prostaglandins. PGI2, when given intracoronary in small doses or intravenously in larger doses will lower blood pressure while inhibiting the baroreflex induced tachycardia. It has also been shown in some experiments that PGI2 and arachidonic acid can evoke overt bradycardia and hypotension via a reflex mechanism. The role of prostaglandins in cardiovascular reflex control may be important in pathophysiologic states such as coronary ischemia and heart failure. Ventricular receptors can interact centrally with the arterial baroreceptors to attenuate the baroreflex control of both heart rate and peripheral resistance. Finally, the stimulation of ventricular receptors can alter a variety of humoral substances which are important regulators of cardiovascular and fluid volume homeostasis. These include vasopressin, renin and catecholamines. Those studies which have been done within the last 10 years or so, especially in unanesthetized animals, have demonstrated that the Bezold-Jarisch reflex is more important to cardiovascular control than previously thought. Future work will be necessary to determine the precise role ventricular receptors play in various pathological situations.
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PMID:Left ventricular receptors: physiological controllers or pathological curiosities? 354 77

The concept of depressor reflexes originating in the heart was introduced by von Bezold in 1867 and was later revived by Jarisch. The Bezold-Jarisch reflex originates in cardiac sensory receptors with nonmyelinated vagal afferent pathways. The left ventricle, particularly the inferoposterior wall, is a principal location for these sensory receptors. Stimulation of these inhibitory cardiac receptors by stretch, chemical substances or drugs increases parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion. Conversely, decreases in the activity of these inhibitory sensory receptors reflexly increase sympathetic activity, vascular resistance, plasma renin activity and vasopressin. Long regarded as pharmacologic curiosities, it is now clear that reflexes originating in these inhibitory cardiac sensory receptors are important to the pathophysiology of many cardiovascular disorders. This paper reviews the role of inhibitory cardiac sensory receptors in several clinical states including 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.
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PMID:The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. 682 48

Vasovagal syncope is associated with an abnormal reflex and the physiopathological mechanisms of the phenomenon overall are only partially known. Experimental and clinical studies suggest that the main factor which triggers the syncope is the brusque interruption of the alpha-adrenergic tone with marked, sudden peripheral vasodilation. Although documented, vagal hypertony, with consequent bradycardia and asystolia, is only occasional and is almost always a secondary phenomenon. The most commonly suggested cause of vasovagal syncope is a Bezold-Jarish reflex starting from the cardiac receptors in the walls of the ventricle, mediated by the paradoxical activation of afferent vagal fibres. However, recent studies are suggesting that there may be other pathogenetic mechanisms such as the paradoxical activation of the venous-atrial baroceptors and other "extracardiac" vascular receptors. The neuro-endocrine aspect of the vasovagal reaction is very complex and in spite of the many studies carried out on the catecholamine, renal-angiotensive system, arginine-vasopressin, and b-endorphine trends, there are still many points awaiting clarification. The response of the autonomous nervous system linked to age also require further research.
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PMID:[Physiopathology of vasovagal syncope: review of the most endorsed theories and recent findings]. 755 40