Testosterone-Induced Hypertension in the Rat

Colby, Howard D.; Skelton, Floyd R.; Brownie, Alexander C.

doi:10.1210/endo-86-5-1093

Cited by 51 publications

(18 citation statements)

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“…One observable effect of metyrapone treatment was the increased size of adrenal glands in these animals. This hypertrophy is consistent with other reports of metyrapone suppression of corticoids in rodents [6,18,19] and with the effects of metyrapone in humans [14]. The lower absolute values of cortisol in the second experiment may have resulted from use of a more specific antibody in that RIA procedure and/or from the lack of daily social interaction tests which were part of the original experiment.…”

Section: Discussionsupporting

confidence: 90%

Pituitary/adrenal hormones do not influence bulbectomy-induced behavioural changes

Hull

L'Hommedieu

Kastaniotis

et al. 1979

Physiology & Behavior

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Section: Discussionsupporting

confidence: 90%

Pituitary/adrenal hormones do not influence bulbectomy-induced behavioural changes

Hull

L'Hommedieu

Kastaniotis

et al. 1979

Physiology & Behavior

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“…9,27 Furthermore, chronic testosterone treatment of normotensive, uninephrectomized female rats increases arterial blood pressure that was found not to be reversible, depending on the length of time the testosterone was given. 28,29 Thus, increases in androgens in humans and in normotensive and hypertensive rats lead to higher blood pressure.…”

Section: Mechanisms For Gender Differences In Blood Pressure Control:mentioning

confidence: 99%

Gender Differences in the Regulation of Blood Pressure

2001

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Abstract-Men are at greater risk for cardiovascular and renal disease than are age-matched, premenopausal women.Recent studies using the technique of 24-hour ambulatory blood pressure monitoring have shown that blood pressure is higher in men than in women at similar ages. After menopause, however, blood pressure increases in women to levels even higher than in men. Hormone replacement therapy in most cases does not significantly reduce blood pressure in postmenopausal women, suggesting that the loss of estrogens may not be the only component involved in the higher blood pressure in women after menopause. In contrast, androgens may decrease only slightly, if at all, in postmenopausal women. In this review the possible mechanisms by which androgens may increase blood pressure are discussed. Findings in animal studies show that there is a blunting of the pressure-natriuresis relationship in male spontaneously hypertensive rats and in ovariectomized female spontaneously hypertensive rats treated chronically with testosterone. The key factor in controlling the pressure-natriuresis relationship is the renin-angiotensin system (RAS). The possibility that androgens increase blood pressure via the RAS is explored, and the possibility that the RAS also promotes oxidative stress leading to production of vasoconstrictor substances and reduction in nitric oxide availability is proposed. Key Words: sex characteristics Ⅲ hypertension Ⅲ angiotensin II Ⅲ nitric oxide Ⅲ oxidative stress I n this review gender differences in blood pressure control are explored, including possible mechanisms by which androgens may increase blood pressure. Gender Differences in Blood Pressure Regulation in HumansMen are generally at greater risk for cardiovascular and renal disease than are age-matched, premenopausal women. Recent studies using the technique of 24-hour ambulatory blood pressure monitoring have shown that blood pressure is higher in men than in women at similar ages. As shown in Figure 1, Wiinber and colleagues 1 studied 352 normotensive (for age) Danish men and women, aged 20 to 79 years, and found that blood pressure increased with aging in both men and women, but that men had higher 24-hour mean blood pressure, by approximately 6 to 10 mm Hg, than did women, until the age of 70 to 79 years, when blood pressure was similar for men and women. Khoury and colleagues 2 performed ambulatory blood pressure monitoring on 131 men and women, aged 50 to 60 years, and found that men had higher blood pressure than did women. Findings were similar in a meta-analysis study performed by Staessen et al. 3 In addition, the Third National Health and Nutrition Evaluation Survey (NHANES III) showed that, in general, men had higher blood pressure than women through middle age. 4 Furthermore, the incidence of uncontrolled hypertension is also greater in men than in women. 5After menopause, however, blood pressure increases in women as well. The data from NHANES III, shown in Figure 2, confirmed that by 60 to 69 years of age, non-Hispanic black and Hi...

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“…In the mammalian organism testosterone or dihydrotestosterone functions to promote the growth of male accessory genital organs and the appearance of the secondary sexual characteristics. Recent studies have shown that chronic administration of androgenic hormones will induce hypertension in the rat by increasing secretion of 1 l -desoxycorticosterone (Colby et al 1970;Molteni et al 1970). The resultant hypernatremia cantributes considerably to the development of the hypertension.…”

Section: Introductionmentioning

confidence: 99%

Androgen-Induced Enhancement of Vascular Reactivity

Greenberg¹,

George²,

Kadowitz³

et al. 1974

Can. J. Physiol. Pharmacol.

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Impairment of testosterone metabolism or excretion has been found in some patients with essential hypertension (Nowacynski et al. Can. J. Biochem. (1968), 46, 1031–1038). The effects of testosterone (10 mg/kg, intramuscular (i.m.)), methyltestosterone (10 mg/kg, i.m.), and vehicle on heart rate, arterial pressure, and responses of perfused canine hindpaws to intra-arterial norepinephrine (0.1–3.0 μg), tyramine (50 and 200 μg), angiotensin (0.1, 0.3, and 1.0 μg), and nitroglycerin (10 and 100 μg) were studied in three groups of dogs (five per group), 5 days after single doses of androgen or vehicle. Plasma and tibial artery electrolytes were also measured. After testosterone, heart rate (157 ± 5 beats/min) was higher than in control dogs after vehicle (132 ± 6 beats/min). Mean arterial pressure was similar in the two groups. Methyltestosterone-treated dogs had a significantly greater heart rate (160 ± 8 beats/min) than vehicle-treated animals. However, mean arterial pressures were similar in the two groups. A second series of dogs that received propranolol (1 mg/kg) 30 min before evaluation of heart rate showed no significant differences in heart rate among the treatment groups. Mean arterial pressures were similar in the three experimental groups. Pressor responses (expressed as the percentage change in perfusion pressure from the base line) to norepinephrine and tyramine were significantly enhanced after testosterone treatment. Pressor responses to angiotensin- and nitroglycerin-induced vasodilatation were unchanged after testosterone treatment when compared with vehicle controls. Pressor responses to tyramine, but not to norepinephrine, were also enhanced after methyltestosterone when compared with control responses after vehicle. Responses to angiotensin and nitroglycerin were similar in the two groups of animals. Plasma and tibial artery electrolytes were not different in the three experimental groups. These data suggest that single doses of androgen sensitized these animals to exogenously administered and endogenously released catecholamines. The effects were not mediated by sodium retention or altered plasma or tissue calcium concentrations.

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Testosterone-Induced Hypertension in the Rat

Cited by 51 publications

References 0 publications

Pituitary/adrenal hormones do not influence bulbectomy-induced behavioural changes

Pituitary/adrenal hormones do not influence bulbectomy-induced behavioural changes

Gender Differences in the Regulation of Blood Pressure

Androgen-Induced Enhancement of Vascular Reactivity

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