Abstract.
Adult male and female spontaneously hypertensive rats (SHR-Okamoto, Kyoto) were gonadectomized when they were 17 weeks old. Intact SHR showed a progressive increase of their blood pressure with growth, attaining systolic pressure levels of 194–208 in males and 163–173 mmHg in females when they were 29–30 weeks old. During this same period, the gonadectomized animals showed a significant reduction in blood pressure ranging from 168–175 in males and from 158–163 mmHg in females. These studies indicate that male and female SHR gonadectomized at 17 weeks of age do not show the progressive blood pressure rise that occurs in intact SHR. There was no change in heart rate in either sex. Corticosterone (B) levels in plasma were increased in the orchidectomized males, and 18-OH-DOC levels in plasma were increased in the adrenal glands of ovariectomized females indicating that these hormonal changes probably do not play a role in SHR hypertension. It appears that gonadal and other hormones are involved in the pathogenesis of SHR hypertension.
Adrenergic regulation of adenylate cyclase activities in the zona glomerulosa (the capsular fraction) and the zona fasciculata-reticularis (the decapsulated fraction) from rat adrenocortical glands has been investigated. Specific binding of [3H]dihydroalprenolol to the membrane from the capsular and the decapsulated fractions was saturable with dissociation constant (Kd) of 4.67 and 5.1 microM, respectively. The receptor density in the capsular and the decapsulated fractions was 230 and 235 fmol/mg protein, respectively. The potencies which isoproterenol, epinephrine, salbutamol, and norepinephrine competed with [3H]dihydroalprenolol binding sites indicted that adrenergic receptors of the capsular and the decapsulated membranes were of the beta 2-type. beta-Adrenergic stimulation of the adenylate cyclase system was observed only in the capsular fraction. This suggests that beta-adrenergic receptors of the capsular membrane are associated with their adenylate cyclase system, but those of the decapsulated membrane are not. Maximum stimulatory concentrations of ACTH and isoproterenol had no additive effect on the capsular adenylate cyclase, indicating that receptors for ACTH and beta-adrenergic agonists are coupled to a common pool of the cyclase.
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