Abstract
Prostaglandins are released into the circulation from several organs when the sympathetic nerves are stimulated, or vasoconstrictors are infused (Bergstrom et al, 1968; Davies et al, 1968; Gilmore et al, 1968; McGiff et al, 1970; Sweet et al, 1971; Dunham and Zimmerman, 1970). Prostaglandins of the E and A series are potent vasodilators in most vascular beds and the vasodilator action is not blocked by classical pharmacological blocking agents such as atropine, propranolol, or antihistamines (Nakano and McCurdy, 1967; Dougherty, 1971; Strong and Bohr, 1967; Nakano, 1968). PGE(1) has been reported to decrease vasoconstrictor responses to catecholamines in several vascular beds in the dog (Kadowitz et al, 1971a; Kadowitz et al, in press; Hedwall et al, 1971), the cat (Holmes et al, 1963), and the rat (Weiner and Kaley, 1969; Viguera and Sunahara, 1969). PGE(2) has been reported to inhibit constrictor responses to nerve stimulation and norepinephrine in the isolated cat spleen (Hedqvist, 197 0) but in high concentrations enhances the response to nerve stimulation in the cutaneous vascular bed of the dog (Kadowitz et al, 1971a).
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References
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Kadowitz, P.J., Sweet, C.S., Brody, M.J. (1972). Effect of Prostaglandins on Adrenergic Neurotransmission to Vascular Smooth Muscle. In: Ramwell, P.W., Pharriss, B.B. (eds) Prostaglandins in Cellular Biology. Alza Conference Series, vol 1. Springer, New York, NY. https://doi.org/10.1007/978-1-4684-2844-5_23
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DOI: https://doi.org/10.1007/978-1-4684-2844-5_23
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