Analysis of Pulmonary Vascular Responses in Cats to Sympathetic Nerve Stimulation Under Elevated Tone Conditions Evidence That Neuronally Released Norepinephrine Acts on α1-, α2-, and β2-Adrenoceptors

• Published in: Circulation research 1990-10, Vol.67 (4), p.862-870
• Main Authors: Hyman, Albert L, Lippton, Howard L, Kadowitz, Philip J
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Blood vessels and receptors; Fundamental and applied biological sciences. Psychology; Vertebrates: cardiovascular system
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.RES.67.4.862

The influence of an increase in vascular tone on responses to sympathetic nerve stimulation and the receptors mediating these responses were investigated in the pulmonary vascular bed of the cat. Under conditions of controlled blood flow and constant left atrial pressure, stimulation of the sympathetic nerves to the lung elicited a biphasic response characterized by an initial increase in lobar arterial pressure followed closely by a decrease. The response to nerve stimulation was reproducible with respect to time and was not altered when a delay coil was added to the perfusion circuit, indicating that the response was directly mediated. The increase in pressure was reduced by prazosin and by yohimbine, whereas the decrease in pressure was blocked by propranolol or ICI 118551. These data suggest that the pressor component of the response is mediated by α1- and postjunctional α2-adrenoceptors, whereas the depressor response is mediated by ß2-receptors. The pressor response was enhanced by propranolol or ICI 118551, whereas the depressor response was enhanced by prazosin or yohimbine, suggesting that the response to nerve stimulation represents the net effect of the actions of neuronally released norepinephrine on α- and β-receptors. The pressor response to nerve stimulation was enhanced when tone was elevated with a prostaglandin endoperoxide analogue and when βreceptors were blocked. The effects of an increase in tone and a passive increase in pressure on responses to sympathetic nerve stimulation were different. When lobar arterial pressure was raised by obstructing lobar venous outflow, the pressor component was attenuated, and a depressor response could not be elicited. The present data suggest that neuronally released norepinephrine can act on α1-, α2-, and β2-adrenoceptors and that the response to sympathetic nerve stimulation represents the summation of the effects of the adrenergic transmitter on α1-, postjunctional α2-, and β2-adrenoceptors.