SUMMARY

Domestic ducks were adenohypophysectomized and 2–3 weeks later were loaded with hypertonic saline. Normal intact ducks and sham-operated ducks were similarly treated. For 2 hr. nasal gland secretion was almost completely inhibited (0·20 g.) in the adenohypophysectomized ducks and was significantly reduced (4·93 g.) in the sham-operated ducks compared with the normal intact controls (14·74 g.).

When the renal response of the adenohypophysectomized ducks was compared with that of the normal intact controls no significant difference was found as far as volume of urine and concentration of Na⁺ and K⁺ were concerned. When compared with sham-operated controls, however, these values were significantly lower in adenohypophysectomized ducks.

The adrenal weight was not significantly reduced in the adenohypophysectomized ducks, but the weights of thyroid, nasal gland and testis decreased significantly. Histological examination of the adrenal glands of the adenohypophysectomized ducks showed that the central regions were atrophic while the peripheral regions remained normal. Nasal glands, thyroid glands and testes were also examined.

It is concluded that the adenohypophysis plays a major part in regulating extrarenal excretion.

ABSTRACT

Confluent monolayers cultured from the rat cauda epididymidis have been shown to respond to angiotensin I (AI) and angiotensin II (AII) when studied under short-circuit conditions and bathed on both sides with Krebs–Henseleit solution. Both the decapeptide AI and the octapeptide AII elicited transient increases in short-circuit current (SCC) when added to the basolateral as well as to the apical surfaces, with the effect of basolateral application greater than that of apical application. The maximal responses produced by AI and AII were similar with median effective concentrations of 20 to 80 nmol/l. The increase in SCC by AII was dependent upon extracellular Cl⁻ and was inhibited by addition of a Cl⁻ channel blocker, diphenylamine 2-carboxylate, to the apical surface. These patterns of activity suggest that the SCC responses to angiotensins result from electrogenic chloride secretion. Pretreating the monolayers with captopril (100 nmol/l), an angiotensin-converting enzyme (ACE) inhibitor, reduced the response to basolateral application of AI, but completely abolished the response to AI added apically. These results suggest that the response to apical addition of AI was due to conversion of AI to AII which interacts with apical angiotensin receptors. This conversion was mediated by ACE which has been detected in epididymal monolayers. Of the endogenous ACE activity, 86% was found to be inhibited by captopril (100 nmol/l).

Responses of the epididymal monolayers to angiotensins were mediated by specific angiotensin receptors. [Sar¹,Ile⁸]-AII, a specific antagonist of the AII receptor, completely inhibited the responses to AI and All but had no effect on the responses to bradykinin and endothelin. The effects of All were mediated by eicosanoid formation since piroxicam, a cyclooxygenase inhibitor, inhibited the AII-induced increase in SCC. This is the first study to demonstrate an effect of angiotensin on epididymal functions. We propose that angiotensin formed locally in the epididymis may play a role in the regulation of electrolyte and fluid transport.

Journal of Endocrinology (1990) 125, 449–456