No abstract

TSH, T4, and T3 were measured by radioimmunoassay in plasma samples obtained from 77 young adult male and 114 female rats fed a Purina high-iodine diet and maintained in an isolated room, 2-4/cage, at 24 +/- 1 C with light from 0600-1800 h. In one experiment, 7 male and 7 female rats were decapitated every 3 h for 30 consecutive h and trunk blood was collected. There was a clear nyctohemeral rhythm of plasma TSH in both sexes characterized by a zenith at 1200 h and a nadir between 1800 and 2100 h. The plasma TSH cycle was approximately 180 degrees out of phase and negatively correlated (P less than .05) with that of plasma corticosterone (B) in both sexes. Although glucocorticoids have been reported to suppress TSH secretion, there was no causal relationship between plasma B and TSH in our experiments since the TSH cycles were normal in chronically adrenalectomized rats. Normal TSH cyclicity was not observed in severely iodine-deficient rats with extremely high plasma TSH levels although the nyctohemeral B rhythm was normal. Plasma TSH was approximately twice as high in males as in females (overall mean +/- SE: M = 149 +/- 11, F = 81 +/- 7 muU/ml, p less than 0.001). There was no significant difference (P greater than 0.05) in plasma TSH at different stages of the estrous cycle. Plasma T4 was slightly, but significantly, higher in males than females (overall mean +/- SE: M = 6.4 +/- 0.1, F = 6.0 +/- 0.1 mug/100 ml; P less than 0.001), while T3 was higher in females than in males (overall mean +/- SE: M = 69.5 +/- 1.7, F = 80.3 +/- 2.1 ng/100 ml; P less than 0.001). No significant nyctohemeral rhythm was observed in plasma T4 or T3 in either sex. These observations indicate that: 1) There is a nyctohemeral rhythm of plasma TSH which is independent of plasma B fluctuations and not associated with proportional changes in plasma thyroid hormones. 2) A sustained high rate of TSH secretion abolishes the normal nyctohemeral plasma TSH rhythm. 3) There are significant differences in plasma concentrations of TSH, T4, and T3 between male and female rats.

No abstract

Because vasopressin is one of the most potent naturally occurring pressor agents, and because of its importance in the regulation of blood volume and composition, we have undertaken a study of the role of vasopressin in the pathogenesis of the hypertension in the Okamoto-Aoki spontaneously hypertension (SH) rat. In SH rats, systolic blood pressure increased from 135 +/- 3 (SE) mmHg at age 33 days to 184 +/- 3 mmHg at age 75 days (P less than 0.01). In the Wistar-Kyoto (WKY) control rats, blood pressure increased from 100 +/- 2 to 120 +/- 2 mmHg (P less than 0.01). The differences in blood pressure between the SH and WKY rats at all ages were significant (P less than 0.01). During the age period 33-75 days, the 24-h urinary excretion of vasopressin in the SH rat was consistently more than twofold greater (P less than 0.01) than in the WKY rat. Plasma vasopressin concentration and pituitary vasopressin content were also elevated in the SH rat (P less than 0.01 and P less than 0.02, respectively). Changes in systolic blood pressure in the SH rat, however, were not paralleled by changes in the urinary excretion of vasopressin. The data indicate that the secretion of vasopressin is elevated in the SH rat. However, the magnitude of this elevation, in and of itself, may not be sufficient to account for the rising blood pressure in the young SH rat.

The participation of the amygdaloid complexes in the stress-induced release of ACTH was studied in the adult male rat. Unilateral and/or bilateral radiofrequency lesions were placed in the amygdalae or their efferent pathways. Plasma corticosterone concentrations were measured after either a leg break, tourniquet, or ether stress. Unilateral amygdaloid lesions did not block the effect of a contralaterally-applied tourniquet or leg break. Bilateral paired amygdaloid lesions blocked the effect of the leg break but not of ether or tourniquet. Bilateral paired lesions between the lateral hypothalamic area and the amygdalae also blocked the effect of the leg break but not ether or tourniquet, whereas bilateral lesions in the anterior portion of the striae terminali did not block the leg-break effect. These data suggest that the amygdalae facilitate rather than directly transmit neurogenic stress-induced signals (leg break) but not signals from systemic stresses (ether). Furthermore, one amygdaloid complex appears to be sufficient for achieving this effect. The pathway from the amygdalae to the hypothalamus involved in the facilitatory effect is probably a direct medial projection to the hypothalamus.