Sex Differences In Pressure Research Articles

Chronic Angiotensin II Infusion in Lewis Rats Does Not Reveal Sex Differences in Blood Pressure or Renal Injury Apparent in the mRen2.Lewis Strain

Sexual dimorphism in blood pressure is evident in hypertensive mRen(2).Lewis (mRen2), but not the normotensive Lewis rat. As circulating and renal angiotensin II (Ang II) levels are higher in male mRen2, we determined whether Ang II infusion (300 ng/kg/min, osmotic minipump, 2 wks) would also reveal sex differences in pressure and proteinuria in male (M) and female (F) Lewis rats, as well as in ovariectomized (OVX) females. Ang II infusion significantly elevated systolic blood pressure in all groups (157 + 4, n=18 M/F/OVX vs. 112 + 1 mm Hg, n=10 M/F); however, pressure was not different between groups. Proteinuria was also comparable between the male and female Lewis rats following Ang II (M: 3.5+0.6; F: 4.0 +0.9 mg/mg creatinine), but was reduced in the OVX Lewis (0.7+0.2 mg/mg creatinine, p<0.05). Kidney angiotensin content was not different for Ang II or Ang‐(1‐7) in the renal cortex; however, medullary Ang II levels were lower in the OVX Lewis (OVX: 0.37+0.03; F: 0.66+0.16; M: 0.94+0.10 fmol/mg) while Ang‐(1‐7) content was higher in the female groups (OVX: 5.2+0.4; F: 5.3+0.3; M: 3.9+0.3 fmol/mg). In summary, chronic Ang II infusion in Lewis rats does not replicate the sex differences in pressure or proteinuria evident in the mRen2 strain. OVX increases blood pressure in the mRen2, but does not exacerbate pressure in female Lewis emphasizing key differences between models of Ang II infusion and genetic activation of the RAS.

Role of the gonads in control of blood pressure in chickens.

Blood pressure changes in gonadectomized and gonadotrophin-treated chicks were utilized to determine the role of the gonads in establishing and maintaining the sex difference in pressure of the adult chicken. By the 23rd week, 4–5 weeks after the normal rise in male pressure, both capon and poulard pressures had climbed to near the male level and significantly above the female. This confirms that androgen is not essential to the rise in pressure, and indicates that other than ovarian activity, nothing inherent in the female prevents the rise. Furthermore, elevated poulard pressures could be depressed to near female levels with estrogen or 2-amino,5-nitrothiazole, presumably through suppression of pituitary gonadotrophin secretion. Exogenous gonadotrophin failed to change the pressure of the chick prematurely, despite marked sexual stimulation, suggesting that chronological maturation, possibly independent of the pituitary-gonad interrelationship, is a prerequisite.

Development of the sex difference in blood pressure of the chick.

In order to establish the age and manner in which the sex difference in blood pressure of the adult white leghorn chicken develops, periodical blood pressure measurements were made on chicks between 3 and 34 weeks of age. There were no consistent differences in pressure between the sexes under 8 weeks of age. Between the 8th and 13th weeks, pressures began to diverge, and within 4–8 weeks a 26–30-mm sex difference in systolic pressure developed. Significant divergences occurred also in diastolic and pulse pressure. The sex divergence was due primarily to a rise in male pressure, the female level remaining comparatively stable. Net changes in male parameters during the period of rapid development of the sex difference in pressure were: body weight + 219 gm, systolic pressure + 26 mm, diastolic pressure + 16 mm and heart rate –22/ min. The age at which the sex difference in pressure begins and its rate of development appear to be related to sexual maturation in the male. However, no significant correlation between the rising male pressure and testes or comb size could be shown. Normal chick blood pressure values prior to the sex divergence differ within strains of white leghorns and for the two groups used here, between 7 and 9 weeks of age, were 150/130 and 162/136 mm Hg.