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Hypersecretion of Follicle-Stimulating Hormone (FSH) after Ovariectomy of Hypophysectomized, Pituitary-Grafted Rats: Implications for Local Regulatory Control of FSH*

1991; Oxford University Press; Volume: 128; Issue: 4 Linguagem: Inglês

10.1210/endo-128-4-1731

1945-7170

Louis V. DePaolo,

Estrogen and related hormone effects

Previous observations have shown that a portion of the acute (>12 h) FSH hypersecretion after ovariectomy (OVX) is LHRH independent, thereby suggesting that mechanisms governing the acute FSH hypersecretory response to OVX may reside largely within the anterior pituitary gland. Accordingly, the present studies were conducted to determine whether acute OVX-induced FSH hypersecretion can be elicited in an animal model in which the anterior pituitary gland is isolated from diencephalic chemical signals, and if so, whether the hypersecretion could be abated by the FSH-suppressing protein, follistatin. Adult female rats hypophysectomized (H) 1 week earlier received anterior pituitary grafts (H/G) (one to three glands per rat) under the kidney capsule. In order to increase ovarian secretion of negative feedback effector substances (i.e. estrogen, inhibin), some H/G rats were injected sc with 30 IU PMSG 4-6 days after receiving pituitary transplants, whereas Other rats were given the saline vehicle. Two days later (0830 h), a blood sample was obtained via an indwelling atrial catheter inserted the previous day. H/G rats given saline or PMSG then were further subdivided and either castrated or sham castrated. Additional blood samples were obtained from the catheter, and trunk blood was collected from decapitated rats 24 h after OVX for measurement of serum estradiol and PRL levels. For comparison, H rats not receiving renal pituitary transplants were subdivided into similar experimental groups as the H/G rats. Blood samples were also obtained after sham OVX or OVX of pituitary-intact, 4-day cycling rats on diestrous day 1. Ovariectomy of PMSG-treated H rats receiving either one or three pituitary allografts resulted in a significant (P < 0.01) increase in serum FSH levels by 12 h after OVX followed by a 2- to 3- fold increase in FSH levels by 24 h relative to either the pre- OVX FSH levels measured in this group or the FSH levels measured in PMSG-treated H/G rats 24 h after sham OVX. In contrast, OVX of saline-treated H/G rats failed to elicit FSH hypersecretion. Similarly, FSH hypersecretion was not observed after OVX of saline-or PMSG-treated H rats. Whereas serum LH levels were increased 24 h after OVX of diestrous rats, no such increases were detected 24 h after OVX of any H or H/G rats. In an additional experiment, H rats receiving two pituitary allografts were treated with PMSG and subsequently castrated. Twenty-four hours later, rats were injected iv with either 60 ng purified porcine follistatin or saline. Administration of follistatin suppressed serum FSH levels by approximately 40% 5 h after injection compared to FSH levels measured in saline-treated rats. These data clearly demonstrate that acute OVX-induced FSH hypersecretion can occur from transplanted pituitary tissue, thus providing support for an autonomous component of acute OVXinduced FSH hypersecretion in pituitary-intact rats. Furthermore, the transplanted pituitary tissue retains its responsiveness to FSH regulatory peptides as evidenced by the suppression of FSH release in H/G rats by follistatin. Importantly, in view of the potential existence of local modulators of FSH secretion, the experimental outcome of this study establishes a feasible in vivo model to study paracrine/autocrine regulation of FSH secretion. (Endocrinology128: 1731–1740,1991)