Hepatic microvascular regulatory mechanisms. I. Adrenergic mechanisms

• Published in: Microvascular research Vol. 21; no. 1; pp. 103 - 116
• Main Authors: Reilly, Frank D., McCuskey, Robert S., Cilento, Eugene V.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 1981
• Subjects: Administration, Topical; Animals; Butoxamine - pharmacology; Electric Stimulation; Isoproterenol - administration & dosage; Isoproterenol - pharmacology; Liver - blood supply; Liver - innervation; Male; Microcirculation; Norepinephrine - administration & dosage; Norepinephrine - pharmacology; Practolol - pharmacology; Rats; Receptors, Adrenergic - pharmacology; Receptors, Adrenergic, alpha - pharmacology; Vasoconstriction - drug effects; Venules - drug effects
• ISSN: 0026-2862; 1095-9319
• DOI: 10.1016/0026-2862(81)90008-X

The neural and pharmacologic responses of the hepatic microvasculature were evaluated in Sprague-Dawley rats anesthetized with urethane or pentobarbital. Various concentrations of several potential vasoactive substances alone or in combination with appropriate blocking agents were administered topically to the livers of these rats while changes in the microvasculature were measured using in vivo microscopic methods. The results provided logarithmic dose-response data for these substances in order to establish the relative sensitivity of various segments of the microvasculature and demonstrated adrenergic receptors in the microvasculature. Alpha receptors were demonstrated on all segments of the microvasculature while beta receptors (beta 2) were isolated on portal venules and sinusoids. In the sinusoids, the lining cells were the site responsive to adrenergic substances. These cells appear to be the primary site for locally regulating flow through the sinusoids. Electrical stimulation of the celiac ganglion and the nerves associated with the celiac artery elicited alpha-mediated constriction of portal venules, hepatic arterioles, and sinusoids while stimulation of the nerves associated with the portal vein elicited responses of a lesser magnitude in these vessels. The constriction of hepatic arterioles was of a much larger magnitude than that of portal venules. All of the microvascular responses to neural stimulation were antagonized by alpha-receptor blockade.