Pulmonary vasodilator responses to catecholamines and sympathetic nerve stimulation in the cat. Evidence that vascular beta-2 adrenoreceptors are innervated.

Abstract

SUMMARYWe investigated the effects of catecholamines and sympathetic nerve stimulation in the feline pulmonary vascular bed under conditions of controlled pulmonary blood flow. Norepinephrine and nerve stimulation caused dose-and stimulus frequency-dependent increases in pulmonary vascular resistance. However, when pulmonary vascular tone was enhanced and a receptors blocked, norepinephrine and nerve stimulation caused dose-and frequency-dependent decreases in pulmonary vascular resistance. The decreases in pulmonary vascular resistance were blocked with propranolol and were of greater magnitude than were constrictor responses observed under basal conditions. Vasodilator responses to nerve stimulation were not modified by atropine. Epinephrine and isoproterenol had marked vasodilator activity in the pulmonary vascular bed when pulmonary vascular tone was elevated. When o receptors were blocked, isoproterenol and epinephrine had similar vasodilator activity, and when fi receptors were blocked, epinephrine and norepinephrine had marked vasoconstrictor activity. Selective /8-1 receptor antagonists had little effect on vasodilator responses to isoproterenol, whereas responses to this substance were blocked by propranolol. These results suggest the presence of a-and f}-2 adrenoreceptors in the feline pulmonary vascular bed and that both types of adrenergic receptors are innervated by the sympathetic nervous system. Circ Res 48: [407][408][409][410][411][412][413][414][415] 1981

Autonomic control of cardiovascular performance and whole body O2 delivery and utilization in swine during treadmill exercise

“…The observation of b-adrenergic vaso- [14,16], or ponies [26]. The phentolamine-induced indilation in the pulmonary bed is in agreement with findings creases in HR and contractility were b-adrenoceptor in several other species, including the cat [49], dog [50] mediated, as they were abolished by propranolol. Phenand sheep [51].…”

Pulmonary vasodilator responses to vagal stimulation and acetylcholine in the cat.

“…The results of the present study indicate that the vagus in the mid-cervical region in the cat carries efferent fibers innervating lung vessels which have adrenergic and cholinergic terminals, and that, in order to demonstrate a vasodilator response to vagal stimulation, it is necessary to interfere with the integrity of the adrenergic nerves and to enhance vasoconstrictor tone, since the pulmonary vascular bed has little, if any, vasoconstrictor tone under resting conditions (Hyman and Kadowitz, 1979;Hyman et al, 1981;Kadowitz et al, 1981). The physiological significance of the cholinergic dilator system is uncertain at resting tone (Fio 2 0.21) conditions.…”

“…Since the magnitude of vasodilator responses in the lung is dependent on the existing level of vasoconstrictor tone which is minimal under baseline conditions [Fio 2 = 0.21] (Hyman and Kadowitz, 1979;Hyman et al, 1981), responses to vagal stimulation and acetylcholine were also investigated when lobar vascular tone was elevated. Intralobar infusion of U-46619, a stable prostaglandin endoperoxide analog, n = 9, or 15-methyl PGF 2n , n = 3, increased lobar arterial pressure from 12 ± 1 to 36 ± 2 mm Hg in the 12 animals.…”

Mechanisms of neurogenic pulmonary edema.

“…These effects of stimulation of a-and /3-adrenergic receptors are observed in isolated-perfused lungs of cats and dogs and in pulmonary vascular smooth muscle strips of cats, rats, and guinea pigs (Bergofsky, 1980). The aadrenergjc receptors of the pulmonary vasculature predominate over the /3-adrenergic receptors (Bergofsky, 1980;Hyman et al, 1983); therefore, pulmonary vasoconstriction occurs in response to agents such as epinephrine that activate both sets of receptors (Bergofsky, 1980). This is similar to the response in kidney, muscle, and splanchnic circulations.…”

“…The pulmonary vascular bed contains both aconstrictor and /3-dilator adrenergic receptors (Bergofsky, 1980;Hyman et al, 1983). These receptors have been identified using specific pharmacological antagonists for these receptors.…”