Pressor responsiveness in rats with hypertension induced by mestranol.

The aim of this study was to determine if pressor hyper-responsiveness is associated with the hypertension that results from the ingestion of the synthetic estrogen, mestranol. Rats were fed a diet containing mestranol for 6 months, while control rats were fed the same diet without mestranol. Catheters were then placed in the carotid artery and jugular vein of all rats, under halothane anesthesia. When the rats had recovered from the anesthesia, blood pressure was measured through the carotid catheter in conscious rats. Each rat received IV injections of norepinephrine (NE) at 2, 4, 8, and 16 ng per 100 gm body weight, and the pressor responses were recorded. The rats fed mestranol had significantly higher arterial pressures than did the control rats. However, the pressor responses to NE were significantly less in the mestranol-treated rats than in the controls, indicating that pressor hyper-responsiveness does not contribute to this form of hypertension.

Arterial sodium concentration in rats with hypertension induced by mestranol.

Rats were made hypertensive by the oral ingestion of mestranol for 6 months. Carotid arteries from these hypertensive rats and from control rats were incubated in an extract of plasma from these rats, which contained 24Na and 14C-sucrose (an extracellular fluid marker). After sufficient time for equilibration, the vessels were removed and counted for 24Na; an aliquot of the incubation fluid was also counted for 24Na. At least 7 days later, after the 24Na had decayed away, the samples were counted for 14C-sucrose. By knowing the specific activity of the 24Na and the ratio of 24Na/14C in the bathing fluid, the amount of intracellular Na could be calculated for each carotid artery. The total protein content of each vessel was determined, and the results were expressed as nEq of Na per mg of vessel. The Na content of carotids from mestranol treated rats averaged 135 +/- 11 (SEM) while the carotids from the control rats averaged 125 +/- 8 nEq/mg protein. Because these values were not significantly different, this study provided no evidence that increases in arterial Na content contributed to the hypertension associated with the ingestion of mestranol in this rat model.

Total exchangeable sodium in rats with mestranol-induced hypertension.

Rats were fed a diet containing mestranol, an orally active estrogen, while control rats were fed the same diet without mestranol. After 6 months of these diets, the rats were weighed, blood pressures were measured, and total exchangeable sodium was determined by injecting 24Na and determining the amount of 24Na in the plasma, the plasma Na concentration, and the residual 24Na in each rat. The 16 mestranol-treated rats were hypertensive (mean arterial pressure 135 +/- 3 mm Hg) when compared with the 17 controls (116 +/- 3 mm Hg). Total exchangeable sodium in the mestranol-treated rats averaged 39.94 +/- 0.49 (SEM) mEq/kg body wt, which was very similar to the value of 39.87 +/- 0.63 mEq/kg found in the control rats. Thus, no changes in total exchangeable sodium in mestranol-hypertensive rats were found in these studies.

Hyperresponsiveness of arterial rings induced by renal prehypertensive rabbit plasma.

Vascular rings from normal rabbit renal arteries, when bathed in processed plasma from 3-day renal artery stenosis (RAS) rabbits, had greater contractile responses to norepinephrine than did matched rings bathed in processed plasma from sham-operated rabbits. This vascular hyperresponsiveness of the rings produced by 3-day RAS plasma was abolished by the angiotensin II (ANG II) antagonist [Sar1, Ile8] ANG II but not by [Sar1, Ala8] ANG II at a dose that completely blocked the contractile responses of the rings to ANG II. The addition of [Sar1, Ala8]-ANG II to rings bathed in normal rabbit plasma did not alter the contractile responses to norepinephrine, indicating a lack of agonistic action by this ANG II analogue. These studies demonstrated that the ANG II receptors involved in the hormonally mediated vascular hyperresponsiveness in 3-day RAS rabbits are contained in the tissues that comprise these renal arterial rings.