Evidence for circulating factors as a cause of venous hypertrophy in spontaneously hypertensive rats

Increased contractility, decreased extensibility, and hypertrophy occur in portal veins (PV) obtained from spontaneously hypertensive rats (SHR). This study evaluates the potential existence of circulating humoral factors as mediators of these changes. SHR were parabiosed with normotensive Wistar-Kyoto rats (WKY) matched for sex and age. Blood pressure increased over a 3-wk to 5-mo period in 2-mo-old WKY parabiosed with SHR. Similar changes were absent in WKY parabiosed with WKY (WKY-WKY) or in SHR parabiosed with SHR (SHR-SHR). The functional blood flows between the parabiosed pairs were 1.4 +/- 0.21%. PV obtained from WKY-WKY developed less spontaneous tension, less tension in response to norepinephrine, potassium chloride, angiotensin II, an 9 alpha, 11 alpha-epoxymethano-prostaglandin H2, and were more extensible than PV obtained from SHR-SHR. In contrast, PV obtained from the WKY member of the WKY-SHR, developed changes similar to PV obtained from the SHR. The wet and dry weight and protein content increased in the PV of WKY-SHR, when compared with these parameters in the PV obtained from WKY-WKY. Light microscopy of the blood vessels demonstrated that PV obtained from the wKY parabiosed to SHR exhibited medial smooth muscle hypertrophy. These data support the conclusion that a circulating humoral factor in the SHR may initiate the venous smooth muscle derangements during the development of spontaneous hypertension.