The effects of growth hormone on blood pressure and renin secretion in hypophysectomized rats.
The effects of hypophysectomy and GH on blood pressure and renin secretion were studied. Within 2 weeks after removal of the pituitary gland of rats, mean arterial blood pressure declined 30%, and heart rate fell 50%. No significant effect of hypophysectomy on blood volume or hematocrit was noted. Within 2 h after the iv administration of 10 micrograms ovine GH to hypophysectomized rats, blood pressure, but not heart rate, was restored to normal. Despite the hypotension, the PRA of hypophysectomized rats was not significantly greater than that of intact animals. This relatively low PRA could not be accounted for by a lack of renin per se, since kidneys of hypophysectomized rats contained at least as much renin as kidneys from intact rats. Neither the PRA of hypophysectomized rats nor the kidney renin content was significantly altered 24 h after a single injection of GH (100 micrograms, ip). When perfusions were performed at 100 mm Hg, the rate of renin secretion by isolated kidneys obtained from hypophysectomized rats was markedly lower than that of kidneys from intact rats. Reduction of mean perfusion pressure to 50 mm Hg or adding isoproterenol to the perfusate produced much smaller increases in renin secretion by kidneys of hypophysectomized rats than that observed in kidneys from intact rats. Kidneys obtained from hypophysectomized rats treated with GH 24 h earlier had a renin content similar to that of kidneys from untreated animals, but secreted renin at a much higher rate. Kidneys from hormone-treated hypophysectomized rats also exhibited a greater renin secretory response to low perfusion pressure or isoproterenol. These data indicate that hypophysectomy severely impairs the renin secretory response of the isolated kidney and that a single injection of GH can reverse this impairment. These observations suggest the possibility that the hypotension characteristic of hypophysectomized rats may, in part, reflect the lack of GH and alterations in the renin-angiotensin system.