Neither Hypertension nor Sexual Maturation is Responsible for Elevated Mesenteric Arterial Expression of TGF‐β in Female Spontaneously Hypertensive Rats (SHR)

TGF‐β has been implicated in vascular damage and hypertension. We have demonstrated that adult female SHR express more vascular TGF‐β than males. Moreover, TGF‐β expression increases as female SHR, but not males, age from 5 to 13 wks. This study tested the hypotheses that 1) increased TGF‐β expression in female SHR is due to hypertension not sexual maturation and 2) greater TGF‐β in females does not equate with greater fibrosis. To test our hypotheses 5 wk old female SHR were randomized to the following groups (N=4): vehicle vs hydralazine‐treated (50 mg/kg/day) or gonad‐intact vs ovariectomized (OVX). Mesenteric arteries were isolated at 13 wks and TGF‐β was measured by immunoblotting. TGF‐β expression was similar in vehicle and hydralazine treated SHR (densitometric units (DU): 27±1 vs 33±5, p=0.3) as well as between intact and OVX (DU: 17±2 vs 14±2, p=0.2). These data suggest that increased TGF‐β with age in female SHR is not dependent on hypertension or sexual maturation. Additional studies measured collagen expression by histological staining in 13 wk male and female SHR. Mesenteric arterial collagen deposition was similar in males and females (area μm 2 : 6632±898 vs 5507±522, p=0.3; N=3), suggesting that greater TGF‐β in females does not result in greater vascular injury. We propose that the increase in TGF‐β in females might instead be compensatory to offer vascular protection.