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Prolactin Induces Regional Vasoconstriction through the ß₂-Adrenergic and Nitric Oxide Mechanisms

Laboratorio di Fisiologia, Dipartimento di Medicina Clinica e Sperimentale, Facoltà di Medicina e Chirurgia, Università del Piemonte Orientale "A. Avogadro," I-28100 Novara, Italy

Address all correspondence and requests for reprints to: Prof. C. Molinari, Facoltà di Medicina e Chirurgia, via Solaroli 17, I-28100 Novara, Italy. E-mail: molinari{at}med.unipmn.it.

Prolactin has been associated with many effects and has been implicated in the pathogenesis of pregnancy-related hypertensive disorders, although little is known about its vascular effects. The present study was designed to determine the primary effect of prolactin on regional vascular beds and the mechanisms involved. In 37 anesthetized pigs, the infusion of 0.17 µg/kg·min of prolactin at constant heart rate and arterial pressure decreased coronary, mesenteric, renal, and iliac blood flow. This response was graded in further five pigs by increasing the infused dose of the hormone between 0.017 and 1 µg/kg·min. In 22 of the 37 pigs, blockade of cholinergic receptors (five pigs) and of -adrenoceptors (five pigs) did not affect the prolactin-induced vascular response, which was abolished by blockade of ß₂-adrenoceptors (five pigs) and by blockade of vascular nitric oxide (NO) synthase (seven pigs). In 15 of the 37 pigs the increases in measured blood flows caused by iv infusion of isoproterenol (five pigs) and by intraarterial administration of acetylcholine (five pigs) and of sodium nitroprusside (five pigs) were significantly reduced by infusion of prolactin. Moreover, the treatment of porcine aortic endothelial cells by prolactin caused a reduction of NO production and of the phosphorylation of ERK, Akt, and p38, which was prevented by the concomitant treatment by the ß₂-adrenergic agonist albuterol. The present study showed that iv infusion of prolactin primarily caused coronary, mesenteric, renal, and iliac vasoconstriction. These effects were brought about by the inhibition of a vasodilatory ß₂-adrenergic receptor-mediated effect related to the NO intracellular pathway.

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