SUMMARY To investigate a possible sex difference in the development of deoxycorticosterone (DOC)-salt hypertension in rats, systolic blood pressure was measured over 6 weeks in unilaterally nephrectomized male and female rats with or without DOC-salt treatment. Throughout the treatment, systolic blood pressure was significantly lower in female than in male DOC-salt rats (at the end of the sixth week: 190 ± 8 vs 163 ± 7 nun Hg, p < 0.05). The difference in blood pressure was also confirmed by the direct measurement of mean arterial pressure at the end of the experiment. The 24-hour urinary excretion of vasopressin was significantly higher in male control rats than in female control rats; however, no difference was observed between male and female DOC-salt rats, in which the urinary excretion of vasopressin was four to five times higher than in control rats. The plasma vasopressin concentration was higher in DOC-salt rats, but there were no differences between sexes. These were no differences in the metabolic clearance rate of vasopressin among the four groups of rats. This indicates that the elevated plasma vasopressin concentration in DOC-salt hypertensive rats is due to increased release of the hormone, rather than to impaired metabolism. Thus, although vasopressin plays a pivotal role in the pathogenesis of DOC-salt hypertension, the sexual dimorphism in this form of hypertension cannot be attributed to differences in the secretion, metabolism, or plasma concentration of vasopressin. (Hypertension 9: 172-177, 1987) KEY WORDS • deoxycorticosterone-salt hypertension metabolic clearance rate sex difference • vasopressin T HE lower incidence of hypertension in women before menopause than in men is an established epidemiological observation. 12 It has also been reported that in some genetic models of hypertension, such as spontaneously hypertensive rats 3 -4 and Dahl salt-sensitive rats, 5 the female is less hypertensive than the male rat. The mechanisms responsible for this sex difference have not been elucidated, but involvement of the gonadal hormones seems likely, since gonadectomy and treatment with gonadal steroids can influence the course of the hypertension in these genetic models.3 " 7In the present study, we investigated the question of whether there is sexual dimorphism in the develop- Received May 19, 1986; accepted August 19, 1986. ment of deoxycorticosterone (DOC)-salt hypertension in the rat. This issue has not, to our knowledge, been systematically investigated. Furthermore, since vasopressin is a prerequisite for the development and maintenance of this form of hypertension, 8 " 10 and since recent evidence" indicates that vasopressin secretion is higher in normotensive male than in female rats, experiments also were designed to determine whether any differences in the development of DOC-salt hypertension between male and female rats are accompanied by differences in the rate of secretion or metabolism of vasopressin. Materials and Methods Experiment 1Twenty male and 20 female 5-week-old Sp...
Atrial natriuretic factor (ANF, Arg 101-Tyr 126; 0.5 and 2.5 micrograms) administered into the lateral cerebral ventricle of conscious euhydrated and dehydrated rats resulted in a significant reduction in the plasma vasopressin concentration. The effect of ANF on vasopressin secretion was greater in the water-deprived animal. Central ANF was without effect on mean arterial blood pressure in both euhydrated and dehydrated rats. The data suggest that ANF occurring in the central nervous system may be important in the control of vasopressin secretion.
In order to investigate the role of central alpha 1- and alpha 2-adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.
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