left ventricular receptor

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Left ventricular receptor : 

Left ventricular receptor

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Mechanically and chemically sensitive receptors in the ventricle have been described histologically and electrophysiologically

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Early experiments documented the hypotension and bradycardia that resulted from the intracoronary administration of one of the veratrum alkaloids (the Bezold- Jarisch reflex).

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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

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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

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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.

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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

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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

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When the left ventricle is distended in experimental animals, there is a fall in systemic arterial pressure and heart rate. It takes considerable ventricular distention to produce this response, and its physiologic significance is uncertain.

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However, left ventricular stretch receptors may play a role in the maintenance of the vagal tone that keeps the heart rate low at rest. In experimental animals, injections of serotonin, ver- atridine, capsaicin, phenyldiguanide, and some other drugs into the coronary arteries supplying the left ventricle cause apnea followed by rapid breathing, hypotension, and bradycardia (the coronary chemoreflex or Bezold-Jarisch reflex).

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The receptors are probably C fiber endings, and the afferents are vagal. The response is not produced by injections into the blood supply of the atria or the right ventricle. Its physiologic role is uncertain, but in patients with myocardial infarcts, substances released from the infarcted tissue may stimulate ventricular receptors, contributing to the hypotension that is not infrequently a stubborn complication of this disease.

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