Angiotensins stimulate catecholamine release from the chromaffin tissue of the rainbow trout.

Immunohistochemical and pharmacological techniques were utilized to investigate the relationships between angiotensins and catecholamine release from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). Double labeling with [Asp1, Ile5]angiotensin II-fluorescein isothiocyanate (ANG II-FITC) and anti-dopamine beta-hydroxylase revealed specific ANG II binding sites on chromaffin cells. Injection (1 nmol/kg body wt) of either ANG II-FITC, [Asn1, Val5, Asn9]ANG I, [Asp1, Ile5, His9]ANG I, [Asn1, Val5]ANG II, [Asp1, Val5]ANG II, or [Asp1, Ile5]ANG II elicited catecholamine release from in situ perfusion preparations of the head kidney. Catecholamine release elicited by [Asn1, Val5]ANG II (10(-13) to 10(-7) mol/kg body wt) was dose dependent, and the secretion of epinephrine (Epi) was greater than that of norepinephrine (NE). Relative to the results obtained with the [Asn1, Val5]ANG II treatment (1 nmol/kg body wt), Epi release was 72 and 82% lower in response to injections (1 nmol/kg body wt) of [Asn1, Val5]ANG I [amino acid (AA) positions 1-7] and [Asn1, Val5]ANG I (AA 1-6), respectively. Pretreatment with either losartan (10(-5) M), PD-123319 (10(-5) M), or hexamethonium (10(-3) M) had no effect on [Asn1, Val5]ANG II-elicited catecholamine release. Pretreatment with captopril (10(-4) M) significantly reduced [Asn1, Val5, Asn9]ANG I-elicited Epi and NE release and decreased basal catecholamine release. These results provide direct evidence that angiotensins can elicit catecholamine release from the chromaffin tissue via specific ANG II binding sites and indicate that the synthesis of ANG II may be either local or systemic.

Fine structural correlates of vascular permeability of chromaffin cell transplants in CNS pain modulatory regions.

Adrenal medullary tissue, bovine chromaffin cells, and PC12 cells were transplanted into the pain modulatory regions of the rat midbrain periaqueductal gray (PAG) or dorsal spinal cord. Fine structural studies of vascular permeability of these grafts revealed that in all three cases, the capillary endothelium of the graft vasculature was attenuated and fenestrated, unlike that of the surrounding host CNS tissue. The intravascular injection of the protein marker, horseradish peroxidase (HRP), enters the grafted tissue parenchyma and is found in the extracellular space of the surrounding host CNS. In contrast, control gelfoam transplants, which become vascularized, do not contain vessels with fenestrated endothelium and do not leak HRP. Since cell suspension implants do not contain endothelial cells, the vasculature of the grafts must be derived from the host. However, as their morphological characteristics are similar to those of the in situ adrenal medulla, it appears that the tissue environment of the graft influences the permeability properties of the vascular bed. The increased permeability to HRP is apparently permanent and most likely is due to the passage through endothelial cell fenestrae.