Possible Involvement of Androgen in Increased Norepinephrine Synthesis in Blood Vessels of Spontaneously Hypertensive Rats

Abstract

ABSTRACT-We investigated the effects of castration and testosterone propionate on sympathetic nervous systems in spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Four-week-old male rats were castrated. For replacement of androgen, testosterone propionate (500 pg/rat) was administered sub cutaneously 2 times a week to castrated rats after their 14th week. The systolic blood pressure of the castrated SHR (44 weeks) was significantly lower than those of intact SHR and testosterone-replaced SHR. The norepinephrine (NE) levels and the tyrosine hydroxylase (TH) activities in the abdominal aorta and mesenteric artery of castrated SHR (45 50 weeks) were significantly lower than those of intact SHR. The NE levels and the TH activities in these blood vessels of testosterone-replaced SHR recovered to the levels obtained in those of intact SHR. As well as the systolic blood pressure, the NE levels and TH activities in blood vessels of WKY were significantly lower than those of intact SHR and showed no significant difference among the three groups. These results suggest that androgen may contribute to the development of hyperten sion in SHR via sustained enhancement of TH activity in blood vessels leading to increased NE level.

Androgens Are Necessary for the Development of Fructose-Induced Hypertension

“…These results are consistent with the findings of other laboratories, which also showed that testosterone plays an important role in the development of hypertension in other hypertensive animal models. In these experiments, castration at a young age (3 to 5 weeks) attenuated the development of hypertension in SHR, 12,[25][26][27] in Dahl salt-sensitive hypertensive male rats, 14 in male rats subjected to 2-kidney, 1-clip maneuver, 28 and in male rats subjected to reduced renal mass. 29 Moreover, Reckelhoff et al reported that chronic blockade of the androgen receptor with flutamide attenuates BP in male SHR to the level found in female SHR, 13 and testosterone treatment of ovariectomized females or castrated males promoted hypertension.…”

Adult Levels of Testosterone Alter Catecholamine Innervation in an Animal Model of Attention-Deficit Hyperactivity Disorder

“…First, although during childhood ADHD is predominant in males, the disorder seems to persist into adulthood [21] in a higher proportion of females than males, with the ratios almost equal in adulthood [4]. Second, peripheral increases in TH levels have been reported in SHRs in response to androgens [22]. Third, SHRs seem to have a decrease in sensitivity to androgens in adulthood [23,24].…”

Serum Testosterone Levels and Arterial Blood Pressure in the Elderly

“…On the one hand, it is known that testosterone promotes noradrenaline synthesis and facilitates vasoconstriction (1,2); the abuse of high doses of anabolic steroids has been linked to sudden cardiac death (3); testosterone increases plasma total homocysteine levels, which in turn damages vascular endothelium (4); and men with complete androgen suppression showed improved endothelial function compared to controls (5). On the other hand, it has been demonstrated that the replacement of natural androgens inhibits atheroma formation in castrated male animals (6).…”

“…However, although androgens have been demonstrated to contribute to the development and severity of hypertension in some genetic and nongenetic rat models of hypertension (1,17) and in some forms of human secondary hypertension, few and contrasting findings have been reported in epidemiological trials regarding the relationship between androgens and essential hypertension; namely, some studies have shown reduced androgen levels in subjects with essential hypertension as compared to normotensive subjects (18−21), whereas other studies have not demonstrated a significant difference in this respect (22,23). The disparity among various reports might be due to the following factors: differences in the characteristics of the examined populations; differences in the methodologies used; and the lack of data control for age, body composition (adiposity), smoking habits, drug intake and history of previous sexual dysfunction, all of which may all represent confounding factors.…”