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...

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Intracerebroventricular (icv) administration of carbachol into conscious rats evoked a substantial increase in vasopressin secretion and blood pressure in a dose-dependent manner. These effects were blocked by pretreatment with the muscarinic blocker, atropine (10 micrograms icv), but not by the nicotinic blocker, hexamethonium (10 micrograms icv). Hexamethonium did, however, block the increase in blood pressure, the decrease in heart rate, and the very small elevation in the plasma vasopressin concentration induced by nicotine (10 micrograms icv). These results indicate that stimulation of either central nicotinic or muscarinic receptors can affect the cardiovascular system and suggest that the cholinergic stimulation of vasopressin secretion may involve primarily muscarinic receptors in the conscious rat.

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There is considerable evidence to suggest that there is a cholinergic link in the neural control of vasopressin release, but the precise role for this link has not been adequately demonstrated in the intact animal. We have, therefore, examined in conscious unrestrained rats the effects of central cholinergic blockade on the stimulation of vasopressin release by increased plasma osmotality (iv infusion of 2.5 M NaCl at 0.1 mg/kg body weight.min for 30 min) and by decreased blood volume (2 successive hemorrhages of 10% of blood volume each). The vasopressin responses to these stimuli were unaffected by either intracerebroventricular (icv) atropine (10 micrograms; muscarinic blockade) or icv hexamethonium (10 micrograms; nicotinic blockade) in doses which block the vasopressin responses to icv cholinergic agonists. The implications of these findings are discussed.