Localization of vasopressin-neurophysin and norepinephrine in the supraoptic nucleus of spontaneously hypertensive rats.

Histological analysis of the catecholaminergic innervation of vasopressin neurons in the supraoptic nucleus (SON) was performed using catecholamine histofluorescence and immunocytochemistry of vasopressin specific neurophysin (VP-NP) in order to determine if spontaneously hypertensive rats (SHR) demonstrate alterations in the relationship between these two types of chemically defined neurons. Chronically hypertensive SHRs showed an increased density of catecholamine fluorescence particularly in the dorsal part of the SON in comparison to age-matched, normotensive, Wistar-Kyoto (WKY) rats, but not in comparison to age-matched Wistar rats. In addition, there was an increase in the area of distribution of VP-NP immunopositive neurons such that they extended into the dorsal portion of the nucleus in the SHR compared to the WKY. Comparator bridge analysis of immunocytochemical staining and catecholamine histofluorescence revealed a precise overlap of the two patterns in SHR. Thus, the more extensive distribution of catecholamine fluorescence in the dorsal SON in the SHR compared to WKY paralleled the more extensive distribution of VP neurons in this region. Quantitative analysis of the relative percentage of SON neurons which were VP-NP positive indicated that the increased representation of VP-NP positive neurons in the dorsal portion of the nucleus reflected a greater distribution of the VP-NP cell population throughout the SON rather than an increase in the number of VP-NP neurons in the SHR. In young SHRs (5 weeks old) the catecholamine fluorescence pattern in the SON was considerably smaller than that observed in older SHRs. This low density pattern, however, was comparable to that observed in young WKYs. Thus, the catecholamine fluorescence in the SON apparently increases in the SHR in parallel with the development of the hypertension. This observation and the finding of comparable catecholamine fluorescence in Wistars and SHRs suggest that the altered catecholamine innervation of VP neurons observed in chronically hypertensive SHRs is not causal to the hypertension but may reflect a response to the elevated blood pressure. A marked increase in the catecholamine innervation of cerebral arteries was also noted.