Trophic effect of norepinephrine on the rat portal vein in organ culture.

Abstract

SUMMARY Rat portal veins were maintained in organ culture to study the development of characteristic denervation changes and a possible trophic effect of the neurotransmitter norepinephrine (NE). Vessels maintained in organ culture for 2 days showed supersensitivity to NE and Ba 2+, a more rapid rate of relaxation from a Ba 2+ contracture, and partial depolarization of the myovascular cells. All of these changes except the quicker relaxation from Ba 2+ contracture could be prevented by incubating the preparations in a NE-containing medium. This evidence suggests that functional changes in vascular muscle cells are caused by the removal of a trophic influence of NE, but can be prevented by NE replacement. However, the failure of NE in the culture media to prevent the increased rate of relaxation from Ba 2+ contracture found after 2 days in organ culture suggests that NE is not the only trophic influence acting on the portal vein. In addition, incubation of veins in a NE-containing medium produced a marked subsensitivity to the contractile effects of NE, but not Ba 2+, and thus possible desensitization of noradrenergic receptors. The data thus support a trophic role for NE in the rat portal vein.

Deletion of the neuropeptide Y (NPY) Y 1 receptor gene reveals a regulatory role of NPY on catecholamine synthesis and secretion

“…We hypothesized three possibilities to explain these data: (i) an increase of chromaffin cell number and͞or size in the adrenal gland, (ii) a deficiency of catecholamine storage in chromaffin granules, or (iii) an increase of catecholamine turnover rate. The first hypothesis was supported by the increased catecholamine and NPY contents in the adrenals of Y 1 Ϫ͞Ϫ mice, because a trophic effect of catecholamines, especially NE, on the cardiovascular system has been demonstrated in several studies (20)(21)(22)(23)(24)(25)(26). Also, NPY was shown to induce DNA synthesis in a concentration-dependent manner and through the activation of Y 1 receptor in vascular smooth muscle cells (27)(28)(29), whereas in cardiomyocytes, the trophic effect of NPY is mediated through Y 5 receptors (30).…”

Sympathetic cross-innervation of SHR and genetic controls suggests a trophic influence on vascular muscle membranes.

“…This phenomenon has been observed in a variety of vascular muscles including the rat portal vein (Aprigliano and Hermsmeyer, 1977;Abel et al, 1980), rabbit saphenous artery (Abel et aL, 1976), and rabbit ear artery (Bevan and Tsuru, 1979). In addition, depolarization of the resting Em has been found to be associated with postjunctional super-sensitivity in both vascular (Abel et aL, 1976;Aprigliano and Hermsmeyer, 1977;Abel et al, 1980) and nonvascular (Fleming and Westfall, 1975;Urquilla et al, 1978) smooth muscles. The present study also demonstrates a postjunctional increase in sensitivity to NE of transplanted KNR caudal arteries when sympathetic innervation was eliminated.…”

“…The sympathetic nervous system may control some or all of these processes to alter the contractile response and thus the sensitivity of muscle cells. Changes in both Em (Aprigliano and Hermsmeyer, 1977;Abel et al, 1980) and calcium influx (Kaiman and Shibata, 1978) have been observed in denervated vascular muscle. In addition, Bevan (1975) has reported that.ehronic sympathetic denervation reduced the number of proliferating muscle cells in the rabbit ear artery, suggesting that sympathetic innervation may modulate the growth of vascular muscle.…”

Elevated Contractile Responses to Acetylcholine in Organ Cultured Rabbit Carotid Artery

“…In a study with rat tail arteries, Lindqvist et al18 reported that sensitivity to norepinephrine was higher in organ cultured arteries as compared to freshly isolated arteries. Abel et al19 also observed sensitization to norepinephrine in organ cultured portal veins. Rogers et al5 reported a sensitization to ACh in organ cultured canine colonic smooth muscle.…”